Efficacy of Electrical Baroreflex Activation Is Independent of Peripheral Chemoreceptor Modulation
Karsten Heusser1, Arvo Thöne2, Axel Lipp3
1From the Institute of Aerospace Medicine, German Aerospace Center, Cologne, Germany (K.H., F.H., J.J., J.T.).
Insights
Electrical carotid sinus stimulation treats resistant hypertension. Moderate peripheral chemoreflex activation, induced by hypoxia, did not reduce baroreflex efficacy in patients with resistant hypertension.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Neuroautonomic Function
Background:
- Arterial baroreflex activation via electrical carotid sinus stimulation is a treatment for resistant hypertension.
- Peripheral chemoreflex activation may inhibit baroreflex responses in hypertensive patients.
- The interaction between baroreflex and chemoreflex in hypertension is not fully understood.
Purpose of the Study:
- To investigate whether peripheral chemoreflex activation attenuates baroreflex efficacy during electrical carotid sinus stimulation in patients with resistant hypertension.
- To explore baroreflex-chemoreflex interactions in humans with resistant hypertension.
Main Methods:
- 11 patients with resistant hypertension and implanted electrical carotid sinus stimulators were studied.
- Baroreflex responses to electrical stimulation were assessed under normoxia, isocapnic hypoxia, and hyperoxia.
- Measurements included blood pressure, heart rate, ventilation, and muscle sympathetic nerve activity.
Main Results:
- Electrical baroreflex activation reduced blood pressure, heart rate, and muscle sympathetic nerve activity during normoxia.
- Hypoxia activated the peripheral chemoreflex, increasing blood pressure, heart rate, muscle sympathetic nerve activity, and ventilation.
- Responses to electrical carotid sinus stimulation were similar during hypoxia and hyperoxia, indicating no attenuation by chemoreflex activation.
Conclusions:
- Moderate peripheral chemoreflex activation does not attenuate acute responses to electrical baroreflex activation therapy in patients with resistant hypertension.
- These findings provide novel insights into human baroreflex-chemoreflex interactions in the context of resistant hypertension.
Abstract:
Arterial baroreflex activation through electrical carotid sinus stimulation has been developed for the treatment of resistant hypertension. Previous studies suggested that the peripheral chemoreflex is tonically active in hypertensive patients and may inhibit baroreflex responses. We hypothesized that peripheral chemoreflex activation attenuates baroreflex efficacy evoked by electrical carotid sinus stimulation. We screened 35 patients with an implanted electrical carotid sinus stimulator. Of those, 11 patients with consistent acute depressor response were selected (7 men/4 women, age: 67±8 years, body mass index: 31.6±5.2 kg/m2, 6±2 antihypertensive drug classes). We assessed responses to electrical baroreflex stimulation during normoxia, isocapnic hypoxia (SpO2: 79.0±1.5%), and hyperoxia (40% end-tidal O2 fraction) by measuring heart rate, blood pressure, ventilation, oxygen saturation, end-tidal CO2 and O2 fractions, and muscle sympathetic nerve activity. During normoxia, baroreflex activation reduced systolic blood pressure from 164±27 to 151±25 mm Hg (mean±SD, P<0.001), heart rate from 64±13 to 61±13 bpm (P=0.002), and muscle sympathetic nerve activity from 42±12 to 36±12 bursts/min (P=0.004). Hypoxia increased systolic blood pressure 8±12 mm Hg (P=0.057), heart rate 10±6 bpm (P<0.001), muscle sympathetic nerve activity 7±7 bursts/min (P=0.031), and ventilation 10±7 L/min (P=0.002). However, responses to electrical carotid sinus stimulation did not differ between hypoxic and hyperoxic conditions: systolic blood pressure: -15±7 versus -14±8 mm Hg (P=0.938), heart rate: -2±3 versus -2±2 bpm (P=0.701), and muscle sympathetic nerve activity: -6±4 versus -4±3 bursts/min (P=0.531). We conclude that moderate peripheral chemoreflex activation does not attenuate acute responses to electrical baroreflex activation therapy in patients with resistant hypertension. These patients provided insight into human baroreflex-chemoreflex interactions that could not be gained otherwise.
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