Electrical stimulation of carotid baroreceptors (baropacing) acutely decreases arterial pressure in patients with refractory hypertension. The reduction in blood pressure seems to be mediated through sympathetic inhibition with concomitant reduction in the activity of the renin-angiotensin system. Indeed, switching on and off the stimulation is accompanied by decreases and increases in central sympathetic vasoconstrictor outflow, respectively. Plasma renin concentration also decreases with acute electrical baroreflex stimulation. In some patients chronic baropacing is associated with long-term blood pressure reduction. However, there is sparse information as to the relative contribution of blood pressure regulating systems to account for the acute and chronic effects of baropacing. Sympathetic, renal, and vascular mechanisms are of special interest. Furthermore, technical aspects of electrical baroreflex stimulation may play a role, e.g. worsening of the electrical contact between the stimulating electrodes and the baroreceptor afferents. This study is designed to answer the following primary questions: 1. Does chronic electrical stimulation of carotid baroreceptors inhibit sympathetic vasoconstrictor tone also in the long-term? 2. Does sympathetic vasoconstrictor tone increase on switching off chronic baropacing? Such an increase would confirm electrical integrity of the system and proper contact to the baroreceptor afferents. 3. Does acute electrical baroreflex stimulation decrease renal vascular resistance? 4. Does acute electrical baroreflex stimulation influence glucose delivery to skeletal muscle and change insulin sensitivity? The study follows an open-label observational design and it is planned to recruit up to 30 patients over 3 years.
Study Type
OBSERVATIONAL
Enrollment
30
Hannover Medical School
Hanover, Germany
RECRUITINGThis platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.