Hypertension, Resistant to Conventional TherapyChemoBarNCT02587533
Peripheral Chemoreflex/Arterial Baroreflex Interaction in Patients With Electrical Carotid Sinus Stimulation
A study testing Hypoxia without dopamine, Hypoxia with dopamine and Hyperoxia without dopamine in people with Hypertension, Resistant to Conventional Therapy, run by Hannover Medical School at 1 site in Germany.
Trial summary
Peripheral chemoreceptors and baroreceptors are located in close proximity in the carotid artery wall at the level of the carotid bifurcation. Baroreceptor stimulation lowers sympathetic activity and blood pressure. In contrast, chemoreceptor stimulation raises sympathetic activity and blood pressure. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Hypertension, Resistant to Conventional Therapy
- What is being tested?
- Hypoxia without dopamine, Hypoxia with dopamine and Hyperoxia without dopamine
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 11 participants
- Where
- 1 siteGermany
- Study dates
- Nov 2015to Dec 2017
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Implanted device for electrical baroreflex stimulation.
- The patient is a 'responder', i. e. carotid-sinus stimulation causes a drop in systolic arterial pressure by at least 15 mmHg.
- The patient gave informed consent.
Who cannot join
- The patient is an investigator or any sub-investigator, research assistant, pharmacist, study coordinator, other staff or relative thereof directly involved in the conduct of the protocol.
- The mental condition renders the patient unable to understand the nature, scope, and possible consequences of the study.
- The patient is unlikely to comply with the protocol.
- The patient is pregnant or breast-feeding.
- Hypoxic conditions for half an hour are considered harmful, e. g. in patients with shunts.
- History of drug or alcohol abuse.
- Discontinuation of diuretic medication for one day is considered harmful. (Reason: Bladder distension is a sympathoexcitatory stimulus and shortens experimental time. In order to prevent these shortcomings three measures are taken: Dispensation with beverages and diuretics as well as complete bladder voiding immediately before the experiment.)
Trial locations and contacts
1 site in 1 country.
About this study
Peripheral chemoreceptors and baroreceptors are located in close proximity in the carotid artery wall at the level of the carotid bifurcation. Baroreceptor stimulation lowers sympathetic activity and blood pressure. In contrast, chemoreceptor stimulation raises sympathetic activity and blood pressure. Thus, beneficial effects of electrical carotid sinus stimulation on blood pressure could be diminished by chemoreceptor overactivity and/or concomitant chemoreceptor activation through the device. Therefore, our study will assess baroreflex/chemoreflex interactions in patients with resistant hypertension equipped with carotid sinus stimulators. The study will inform us of potential additional anti-hypertensive benefits of simultaneous chemoreceptor denervation during electrode placement. Furthermore, the results may provide information about suitable electrode design to spare co-activation of peripheral chemoreceptors. Taken together, the study will help develop strategies for improving responder rate and efficacy of carotid sinus stimulators in patients with resistant hypertension.
Read the detailed description
Patients with implanted devices for electrical baroreflex stimulation are recruited according to inclusion and exclusion criteria until good quality recordings have been obtained in 10 out of maximally 15 patients. After obtaining written informed consent patients will be investigated in the laboratory on one day. In up to 20% of the patients we may fail to find an appropriate nerve recording position. In these cases we will ask the patient to repeat the experiment.
Patients will be investigated in the post-absorptive state after emptying their bladder. During instrumentation and measurements they will rest in supine position. We will fix chest electrodes for ECG and impedance cardiography. A peripheral venous catheter will be introduced for later dopamine infusion. Cuffs will be used at the upper arm and the finger in order to monitor blood pressure and to allow for pulse-contour analysis. Finally, we will search for a suitable nerve recording position in the peroneal nerve for recordings of muscle sympathetic nerve activity (MSNA, postganglionic vasoconstrictor sympathetic drive). All bioelectric signals will be recorded continuously for the duration of the experiments.
After the preparations baseline recordings will be performed. Subsequently, the electrical baroreflex stimulator is switched OFF and ON repeatedly (toggling) under normoxic conditions. Every OFF and ON state will last for 4 minutes. Oscillometric blood-pressure readings are taken every two minutes so as to acquire two readings per stimulation period. Toggling under normoxia is meant to ensure that the patient is a responder at the experimental day and to rule out that the blood pressure rises are too high off stimulation (safety concern). Afterwards, the breathing gas will be changed in order to have the patient inhale a hypoxic or hyperoxic mixture in a blinded manner. After reaching a stable ventilatory and autonomic state, stimulator toggling and blood-pressure measurements will be repeated. The same procedures will take place after establishing the opposite oxygenation state. Stimulation will be ON in between the oxygen states implying that the first switches will be OFF switches with all oxygenation conditions. Afterwards, the last oxygenation state will be maintained and additional low-dose dopamine infusion will be applied. Again, the electrical baroreflex stimulator will be switched off and on repeatedly and blood-pressure readings are taken. During the last two stimulator toggling states of each oxygenation level, venous blood samples are drawn for hormone measurements and inert gas rebreathing will take place for cardiac output determination. Finally, the correct positioning of the microneurography electrode is checked again.
The duration of such an experiment depends on the time needed to find the sympathetic nerve bundles before the measurements and during the experiment, in case the recording position gets lost. However, experiments will rarely exceed 5 hours in total.
- Being tested
- Hypoxia without dopamine, Hypoxia with dopamine, Hyperoxia without dopamine, Hyperoxia with dopamine
- Keywords
- Baroreflex, Chemoreflex, Autonomic nervous system, Sympathetic activity, Muscle sympathetic nerve activity (MSNA), Microneurography, Electrical baroreflex stimulation, Resistant hypertension, Device-based therapy
- Medical subject headings
- Hypertension Resistant to Conventional Therapy
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Hypoxia without dopamineOther
Target hemoglobin oxygen saturation (SpO2) 80%.
Hypoxia with dopamineOther
Target hemoglobin oxygen saturation (SpO2) 80%. Dopamine dose 3 µg/kg/min.
Hyperoxia without dopamineOther
Nearly complete hemoglobin oxygen saturation.
Hyperoxia with dopamineOther
Nearly complete hemoglobin oxygen saturation. Dopamine dose 3 µg/kg/min.
| Study group | Role | What they receive |
|---|---|---|
| Hypoxia without dopamine | Active comparator | Target hemoglobin oxygen saturation (SpO2) 80%. No pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. Receives: Other: Hypoxia without dopamine |
| Hypoxia with dopamine | Active comparator | Target hemoglobin oxygen saturation (SpO2) 80%. Counteracting pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. Receives: Other: Hypoxia with dopamine |
| Hyperoxia without dopamine | Active comparator | Nearly complete hemoglobin oxygen saturation. No additional pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. Receives: Other: Hyperoxia without dopamine |
| Hyperoxia with dopamine | Active comparator | Nearly complete hemoglobin oxygen saturation. Additional pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. Receives: Other: Hyperoxia with dopamine |
What is being measured
The primary outcome is the main question the study is designed to answer.
Muscle sympathetic nerve activity (MSNA)
Muscle sympathetic nerve activity (MSNA) will be determined as burst frequency, i. e. as the number of bursts per minute [bursts/min]. In responders, electrical carotid sinus stimulation will lead to a decline in MSNA: [-]MSNA. According to our primary hypothesis, [-]MSNA during hyperoxic conditions ([-]MSNA_hyperoxia) is larger than during hypoxia ([-]MSNA_hypoxia). Therefore, the primary endpoint of the study is the difference [-]MSNA_hyperoxia - [-]MSNA_hypoxia. The study is successful as soon as the difference between the reduction in the hyperoxic and the hypoxic condition is significantly different from zero. A positive value would confirm our primary hypothesis. In case of a negative difference, we would conclude that the potency of electrical baroreflex stimulation to lower sympathetic activity is larger under conditions of an activated chemoreflex.
Measured: Over 24 minutes of stable de/oxygenation +/- dopamine infusion.
Secondary outcomes (1)
Systolic blood pressure (SBP)
In responders, electrical carotid sinus stimulation will lead to a decline in systolic blood pressure: [-]SBP. According to our primary hypothesis, [-]SBP during hyperoxic conditions ([-]SBP_hyperoxia) is larger than during hypoxia ([-]SBP_hypoxia). Therefore, the secondary endpoint of the study is the difference [-]SBP_hyperoxia - [-]SBP_hypoxia. A positive value would confirm our secondary hypothesis. If the difference turns out to be negative, we would conclude that the potency of electrical baroreflex stimulation to lower blood pressure is larger under conditions of an activated chemoreflex. However, such a finding would not necessarily imply that chemoreceptor activation is a prerequisite for optimal baroreflex activation therapy because SBP *level* could be lower with *inactive* chemoreceptors.
Measured: Over 24 minutes of stable de/oxygenation +/- dopamine infusion.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 Oct 2015 (estimated)
- Study startNov 2015
- Primary completionDec 2017
- Study completionDec 2017
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (20)Papers the sponsor has linked to this study.
- Other trials for Hypertension, Resistant to Conventional TherapyStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind
- Who is masked
- Participant
- Enrolment
- 11 participants (actual)
Sponsor and investigators
- Lead sponsor
- Hannover Medical School
- Sponsor type
- University, hospital or other
- Collaborators
- Charite University, Berlin, Germany, Vanderbilt University School of Medicine, Mayo Clinic, University of Bristol
- Responsible party
- Sponsor
- Investigators
- Jens Tank, MD, Principal investigator, Hannover Medical School
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02587533
- Sponsor's protocol ID
- CRC-KliPha-004
- Acronym
- ChemoBar
- Status last verified
- Jan 2018
- First submitted
- 13 Oct 2015
- Last updated
- 9 Jan 2018
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Grassi G. Counteracting the sympathetic nervous system in essential hypertension. Curr Opin Nephrol Hypertens. 2004 Sep;13(5):513-9. doi: 10.1097/00041552-200409000-00006.
PubMed 15300157Eckberg DL. Carotid baroreflex function in young men with borderline blood pressure elevation. Circulation. 1979 Apr;59(4):632-6. doi: 10.1161/01.cir.59.4.632.
PubMed 421303Somers VK, Mark AL, Abboud FM. Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects. Hypertension. 1988 Jun;11(6 Pt 2):608-12. doi: 10.1161/01.hyp.11.6.608.
PubMed 3391673Trzebski A, Tafil M, Zoltowski M, Przybylski J. Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension. Cardiovasc Res. 1982 Mar;16(3):163-72. doi: 10.1093/cvr/16.3.163.
PubMed 6805956McBryde FD, Abdala AP, Hendy EB, Pijacka W, Marvar P, Moraes DJ, Sobotka PA, Paton JF. The carotid body as a putative therapeutic target for the treatment of neurogenic hypertension. Nat Commun. 2013;4:2395. doi: 10.1038/ncomms3395.
PubMed 24002774Abdala AP, McBryde FD, Marina N, Hendy EB, Engelman ZJ, Fudim M, Sobotka PA, Gourine AV, Paton JF. Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. J Physiol. 2012 Sep 1;590(17):4269-77. doi: 10.1113/jphysiol.2012.237800. Epub 2012 Jun 11.
PubMed 22687617Sinski M, Lewandowski J, Przybylski J, Bidiuk J, Abramczyk P, Ciarka A, Gaciong Z. Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension. Hypertens Res. 2012 May;35(5):487-91. doi: 10.1038/hr.2011.209. Epub 2011 Dec 8.
PubMed 22158114Paton JF, Deuchars J, Li YW, Kasparov S. Properties of solitary tract neurones responding to peripheral arterial chemoreceptors. Neuroscience. 2001;105(1):231-48. doi: 10.1016/s0306-4522(01)00106-3.
PubMed 11483315Somers VK, Mark AL, Abboud FM. Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans. J Clin Invest. 1991 Jun;87(6):1953-7. doi: 10.1172/JCI115221.
PubMed 2040688Paton JF, Sobotka PA, Fudim M, Engelman ZJ, Hart EC, McBryde FD, Abdala AP, Marina N, Gourine AV, Lobo M, Patel N, Burchell A, Ratcliffe L, Nightingale A. The carotid body as a therapeutic target for the treatment of sympathetically mediated diseases. Hypertension. 2013 Jan;61(1):5-13. doi: 10.1161/HYPERTENSIONAHA.111.00064. Epub 2012 Nov 19. No abstract available.
PubMed 23172927Despas F, Lambert E, Vaccaro A, Labrunee M, Franchitto N, Lebrin M, Galinier M, Senard JM, Lambert G, Esler M, Pathak A. Peripheral chemoreflex activation contributes to sympathetic baroreflex impairment in chronic heart failure. J Hypertens. 2012 Apr;30(4):753-60. doi: 10.1097/HJH.0b013e328350136c.
PubMed 22241144Wennergren G, Little R, Oberg B. Studies on the central integration of excitatory chemoreceptor influences and inhibitory baroreceptor and cardiac receptor influences. Acta Physiol Scand. 1976 Jan;96(1):1-18. doi: 10.1111/j.1748-1716.1976.tb10166.x.
PubMed 1251739Heusser K, Tank J, Engeli S, Diedrich A, Menne J, Eckert S, Peters T, Sweep FC, Haller H, Pichlmaier AM, Luft FC, Jordan J. Carotid baroreceptor stimulation, sympathetic activity, baroreflex function, and blood pressure in hypertensive patients. Hypertension. 2010 Mar;55(3):619-26. doi: 10.1161/HYPERTENSIONAHA.109.140665. Epub 2010 Jan 25.
PubMed 20101001Schroeder C, Heusser K, Brinkmann J, Menne J, Oswald H, Haller H, Jordan J, Tank J, Luft FC. Truly refractory hypertension. Hypertension. 2013 Aug;62(2):231-5. doi: 10.1161/HYPERTENSIONAHA.113.01240. Epub 2013 May 20. No abstract available.
PubMed 23690343Jordan J, Heusser K, Brinkmann J, Tank J. Electrical carotid sinus stimulation in treatment resistant arterial hypertension. Auton Neurosci. 2012 Dec 24;172(1-2):31-6. doi: 10.1016/j.autneu.2012.10.009. Epub 2012 Nov 9.
PubMed 23146623
Study at a glance
From the registry record, last updated by the sponsor on 9 Jan 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Peripheral Chemoreflex/Arterial Baroreflex Interaction in Patients With Electrical Carotid Sinus Stimulation
- ClinicalTrials.gov ID
- NCT02587533
- Acronym / sponsor ID
- ChemoBar / CRC-KliPha-004
- Keywords
- Baroreflex, Chemoreflex, Autonomic nervous system, Sympathetic activity, Muscle sympathetic nerve activity (MSNA), Microneurography, Electrical baroreflex stimulation, Resistant hypertension
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 11 participants (actual)
- Lead sponsor
- Hannover Medical SchoolUniversity, hospital or other
- Collaborators
- Charite University, Berlin, Germany, Vanderbilt University School of Medicine, Mayo Clinic, University of Bristol
- Study start
- Nov 2015
- Primary completion
- Dec 2017 (actual)
- Study completion
- Dec 2017 (actual)
- First posted
- 27 Oct 2015 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Peripheral chemoreceptors and baroreceptors are located in close proximity in the carotid artery wall at the level of the carotid bifurcation. Baroreceptor stimulation lowers sympathetic activity and blood pressure. In contrast, chemoreceptor stimulation raises sympathetic activity and blood pressure. Thus, beneficial effects of electrical carotid sinus stimulation on blood pressure could be diminished by chemoreceptor overactivity and/or concomitant chemoreceptor activation through the device. Therefore, our study will assess baroreflex/chemoreflex interactions in patients with resistant hypertension equipped with carotid sinus stimulators. The study will inform us of potential additional anti-hypertensive benefits of simultaneous chemoreceptor denervation during electrode placement. Furthermore, the results may provide information about suitable electrode design to spare co-activation of peripheral chemoreceptors. Taken together, the study will help develop strategies for improving responder rate and efficacy of carotid sinus stimulators in patients with resistant hypertension.
Detailed description
Patients with implanted devices for electrical baroreflex stimulation are recruited according to inclusion and exclusion criteria until good quality recordings have been obtained in 10 out of maximally 15 patients. After obtaining written informed consent patients will be investigated in the laboratory on one day. In up to 20% of the patients we may fail to find an appropriate nerve recording position. In these cases we will ask the patient to repeat the experiment.
Patients will be investigated in the post-absorptive state after emptying their bladder. During instrumentation and measurements they will rest in supine position. We will fix chest electrodes for ECG and impedance cardiography. A peripheral venous catheter will be introduced for later dopamine infusion. Cuffs will be used at the upper arm and the finger in order to monitor blood pressure and to allow for pulse-contour analysis. Finally, we will search for a suitable nerve recording position in the peroneal nerve for recordings of muscle sympathetic nerve activity (MSNA, postganglionic vasoconstrictor sympathetic drive). All bioelectric signals will be recorded continuously for the duration of the experiments.
After the preparations baseline recordings will be performed. Subsequently, the electrical baroreflex stimulator is switched OFF and ON repeatedly (toggling) under normoxic conditions. Every OFF and ON state will last for 4 minutes. Oscillometric blood-pressure readings are taken every two minutes so as to acquire two readings per stimulation period. Toggling under normoxia is meant to ensure that the patient is a responder at the experimental day and to rule out that the blood pressure rises are too high off stimulation (safety concern). Afterwards, the breathing gas will be changed in order to have the patient inhale a hypoxic or hyperoxic mixture in a blinded manner. After reaching a stable ventilatory and autonomic state, stimulator toggling and blood-pressure measurements will be repeated. The same procedures will take place after establishing the opposite oxygenation state. Stimulation will be ON in between the oxygen states implying that the first switches will be OFF switches with all oxygenation conditions. Afterwards, the last oxygenation state will be maintained and additional low-dose dopamine infusion will be applied. Again, the electrical baroreflex stimulator will be switched off and on repeatedly and blood-pressure readings are taken. During the last two stimulator toggling states of each oxygenation level, venous blood samples are drawn for hormone measurements and inert gas rebreathing will take place for cardiac output determination. Finally, the correct positioning of the microneurography electrode is checked again.
The duration of such an experiment depends on the time needed to find the sympathetic nerve bundles before the measurements and during the experiment, in case the recording position gets lost. However, experiments will rarely exceed 5 hours in total.
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind (participant)
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| Hypoxia without dopamine | Active comparator | Other: Hypoxia without dopamineTarget hemoglobin oxygen saturation (SpO2) 80%. No pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. |
| Hypoxia with dopamine | Active comparator | Other: Hypoxia with dopamineTarget hemoglobin oxygen saturation (SpO2) 80%. Counteracting pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. |
| Hyperoxia without dopamine | Active comparator | Other: Hyperoxia without dopamineNearly complete hemoglobin oxygen saturation. No additional pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. |
| Hyperoxia with dopamine | Active comparator | Other: Hyperoxia with dopamineNearly complete hemoglobin oxygen saturation. Additional pharmacologic suppression of chemoreflex afferents. Readout: Responses to electrical baroreflex stimulation. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- Implanted device for electrical baroreflex stimulation.
- The patient is a 'responder', i. e. carotid-sinus stimulation causes a drop in systolic arterial pressure by at least 15 mmHg.
- The patient gave informed consent.
Key exclusion criteria (7 listed)
- The patient is an investigator or any sub-investigator, research assistant, pharmacist, study coordinator, other staff or relative thereof directly involved in the conduct of the protocol.
- The mental condition renders the patient unable to understand the nature, scope, and possible consequences of the study.
- The patient is unlikely to comply with the protocol.
- The patient is pregnant or breast-feeding.
- Hypoxic conditions for half an hour are considered harmful, e. g. in patients with shunts.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Hypoxia without dopamineTarget hemoglobin oxygen saturation (SpO2) 80%. | Other | Hypoxia without dopamine |
| Hypoxia with dopamineTarget hemoglobin oxygen saturation (SpO2) 80%. Dopamine dose 3 µg/kg/min. | Other | Hypoxia with dopamine |
| Hyperoxia without dopamineNearly complete hemoglobin oxygen saturation. | Other | Hyperoxia without dopamine |
| Hyperoxia with dopamineNearly complete hemoglobin oxygen saturation. Dopamine dose 3 µg/kg/min. | Other | Hyperoxia with dopamine |
Primary outcome
Muscle sympathetic nerve activity (MSNA)
Time frame: Over 24 minutes of stable de/oxygenation +/- dopamine infusion.
Muscle sympathetic nerve activity (MSNA) will be determined as burst frequency, i. e. as the number of bursts per minute [bursts/min]. In responders, electrical carotid sinus stimulation will lead to a decline in MSNA: [-]MSNA. According to our primary hypothesis, [-]MSNA during hyperoxic conditions ([-]MSNA_hyperoxia) is larger than during hypoxia ([-]MSNA_hypoxia). Therefore, the primary endpoint of the study is the difference [-]MSNA_hyperoxia - [-]MSNA_hypoxia. The study is successful as soon as the difference between the reduction in the hyperoxic and the hypoxic condition is significantly different from zero. A positive value would confirm our primary hypothesis. In case of a negative difference, we would conclude that the potency of electrical baroreflex stimulation to lower sympathetic activity is larger under conditions of an activated chemoreflex.
1 secondary outcome
Systolic blood pressure (SBP)
Time frame: Over 24 minutes of stable de/oxygenation +/- dopamine infusion.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 9 Jan 2018.
- Background: PubMed 15300157Grassi G. Counteracting the sympathetic nervous system in essential hypertension. Curr Opin Nephrol Hypertens. 2004 Sep;13(5):513-9. doi: 10.1097/00041552-200409000-00006.
- Background: PubMed 421303Eckberg DL. Carotid baroreflex function in young men with borderline blood pressure elevation. Circulation. 1979 Apr;59(4):632-6. doi: 10.1161/01.cir.59.4.632.
- Background: PubMed 3391673Somers VK, Mark AL, Abboud FM. Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects. Hypertension. 1988 Jun;11(6 Pt 2):608-12. doi: 10.1161/01.hyp.11.6.608.
- Background: PubMed 6805956Trzebski A, Tafil M, Zoltowski M, Przybylski J. Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension. Cardiovasc Res. 1982 Mar;16(3):163-72. doi: 10.1093/cvr/16.3.163.
- Background: PubMed 24002774McBryde FD, Abdala AP, Hendy EB, Pijacka W, Marvar P, Moraes DJ, Sobotka PA, Paton JF. The carotid body as a putative therapeutic target for the treatment of neurogenic hypertension. Nat Commun. 2013;4:2395. doi: 10.1038/ncomms3395.
- Background: PubMed 22687617Abdala AP, McBryde FD, Marina N, Hendy EB, Engelman ZJ, Fudim M, Sobotka PA, Gourine AV, Paton JF. Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat. J Physiol. 2012 Sep 1;590(17):4269-77. doi: 10.1113/jphysiol.2012.237800. Epub 2012 Jun 11.
- Background: PubMed 22158114Sinski M, Lewandowski J, Przybylski J, Bidiuk J, Abramczyk P, Ciarka A, Gaciong Z. Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension. Hypertens Res. 2012 May;35(5):487-91. doi: 10.1038/hr.2011.209. Epub 2011 Dec 8.
- Background: PubMed 11483315Paton JF, Deuchars J, Li YW, Kasparov S. Properties of solitary tract neurones responding to peripheral arterial chemoreceptors. Neuroscience. 2001;105(1):231-48. doi: 10.1016/s0306-4522(01)00106-3.
- Background: PubMed 2040688Somers VK, Mark AL, Abboud FM. Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans. J Clin Invest. 1991 Jun;87(6):1953-7. doi: 10.1172/JCI115221.
- Background: PubMed 23172927Paton JF, Sobotka PA, Fudim M, Engelman ZJ, Hart EC, McBryde FD, Abdala AP, Marina N, Gourine AV, Lobo M, Patel N, Burchell A, Ratcliffe L, Nightingale A. The carotid body as a therapeutic target for the treatment of sympathetically mediated diseases. Hypertension. 2013 Jan;61(1):5-13. doi: 10.1161/HYPERTENSIONAHA.111.00064. Epub 2012 Nov 19. No abstract available.
- Background: PubMed 22241144Despas F, Lambert E, Vaccaro A, Labrunee M, Franchitto N, Lebrin M, Galinier M, Senard JM, Lambert G, Esler M, Pathak A. Peripheral chemoreflex activation contributes to sympathetic baroreflex impairment in chronic heart failure. J Hypertens. 2012 Apr;30(4):753-60. doi: 10.1097/HJH.0b013e328350136c.
- Background: PubMed 1251739Wennergren G, Little R, Oberg B. Studies on the central integration of excitatory chemoreceptor influences and inhibitory baroreceptor and cardiac receptor influences. Acta Physiol Scand. 1976 Jan;96(1):1-18. doi: 10.1111/j.1748-1716.1976.tb10166.x.
Related trials for Hypertension, Resistant to Conventional Therapy
RecruitingPhase 4
Antihypertensive Mechanisms of Minocycline in Resistant Hypertension
Hypertension, Resistant to Conventional Therapy
Not yet recruiting
Expand Management of Blood Pressure With Renal Denervation in Patients Undergoing Staged PCI for Advanced Coronary Artery diseasE
Multivessel Coronary Artery Disease, Hypertension Resistant to Conventional Therapy
Recruiting
Physical Activity Program for Reducing Blood Pressure in Sleep Apnea Patients With Resistant Hypertension
Hypertension, Resistant to Conventional Therapy, Sleep Apnea
Active, not recruiting
RADIANCE Continued Access Protocol
Hypertension, Hypertension, Resistant to Conventional Therapy
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Jens Tank, MD principal investigator
Hannover Medical School
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Hypoxia without dopamine, Hypoxia with dopamine and Hyperoxia without dopamine in people with Hypertension, Resistant to Conventional Therapy, run by Hannover Medical School at 1 site in Germany.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 7 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 9 Jan 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Germany. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Muscle sympathetic nerve activity (MSNA) (time frame: Over 24 minutes of stable de/oxygenation +/- dopamine infusion.). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02587533, which also lists 20 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 9 Jan 2018.