Barorezeptorstimulation bei therapierefraktärem Bluthochdruck

J. Jordan; J. Tank

doi:10.1055/s-0038-1628498

Nervenheilkunde, Table of Contents

Nervenheilkunde 2013; 32(04): 206-208
DOI: 10.1055/s-0038-1628498

Autonomes Nervensystem

Schattauer GmbH

Barorezeptorstimulation bei therapierefraktärem Bluthochdruck

Baroreceptor stimulation in treatment resistant arterial hypertension

J. Jordan

¹Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover

,

J. Tank

¹Institut für Klinische Pharmakologie, Medizinische Hochschule Hannover

› Author Affiliations

Abstract

Zusammenfassung

Therapierefraktärer Bluthochdruck liegt vor, wenn eine Behandlung mit mindestens drei Antihypertensiva in ausreichender Dosierung, von denen eines ein Diuretikum sein sollte, den Blutdruck nicht kontrolliert und keine sekundären Hypertonieursachen vorliegen. Für medikamentös austherapierte Patienten und bei hohem kardiovaskulärem Risiko wurde die elektrische Baroreflexstimulation entwickelt. Dabei soll dem Gehirn mittels einer elektrischen Stimulation von Barorezeptoren vorgegaukelt werden, dass der Blutdruck ansteigt, um so eine reflektorische Reduktion der Sympathikusaktivität zu erzielen. Tatsächlich bewirkt eine elektrische Stimulation des Karotissinus eine akute Reduktion von mikroneurografisch abgeleiteter Sympathikusaktivität und Blutdruck bei Patienten mit refraktärem Bluthochdruck. Gleichzeitig reduziert sich die Reninkonzentration im venösen Blut, was für eine Hemmung der renalen Sympathikusaktivität spricht. Die physiologische Baroreflexregulation von Herzfrequenz und Sympathikus bleibt erhalten. Erste Langzeiterfahrungen in klinischen Studien sprechen dafür, dass mittels Baroreflexstimulation bei einem Teil der Patienten eine langfristige Blutdrucksenkung erreicht werden kann. Die Daten aus kontrollierten klinischen Studien sind jedoch nicht hinreichend, um einen breiteren klinischen Einsatz zu rechtfertigen.

Summary

Treatment resistant arterial hypertension is diagnosed when concurrent use of three properly dosed antihypertensive medications including a diuretic is not sufficient to control blood pressure. Secondary causes have to be excluded. Electrical carotid sinus stimulation has been developed for high risk patients not responding to maximal antihypertensive therapy. In the brain, electrical baroreceptor stimulation is perceived as further blood pressure increase, which leads to reflex sympathetic inhibition. Indeed, electrical carotid sinus stimulation acutely reduces muscle sympathetic nerve activity and blood pressure in patients with treatment resistant hypertension. Moreover, venous renin concentration decreases suggesting that renal sympathetic activity is also attenuated. Physiological baroreflex control is not perturbed. Results from clinical trials suggest that electrical carotid sinus stimulation elicits a sustained blood pressure reduction in a subgroup of patients. However, data from controlled clinical trials are not yet sufficient to justify widespread clinical use.

Schlüsselwörter

Baroreflex - sympathisches Nervensystem - arterielle Hypertonie

Keywords

Baroreflex - sympathetic nervous system - arterial hypertension

Full Text

References

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