Neuronal prostacyclin is an autocrine regulator of arterial baroreceptor activity

Vladislav SNITSAREV; Carol A WHITEIS; Mark W CHAPLEAU; Francois M ABBOUD

doi:10.1161/01.HYP.0000175475.17666.26

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Neuronal prostacyclin is an autocrine regulator of arterial baroreceptor activity

Journal article

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Neuronal prostacyclin is an autocrine regulator of arterial baroreceptor activity

Vladislav SNITSAREV, Carol A WHITEIS, Mark W CHAPLEAU and Francois M ABBOUD

Hypertension (Dallas, Tex. 1979), Vol.46(3), pp.540-546

2005

DOI: 10.1161/01.HYP.0000175475.17666.26

PMID: 16061731

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Abstract

We tested the hypothesis that neuronal prostacyclin is an autocrine regulator of arterial baroreceptor neuronal activity. In isolated rat aortic nodose baroreceptor neurons, mechanical stimulation depolarized 12 neurons by 13.1+/-3.4 mV and triggered action potentials in 5 of them, averaging 18.2+/-9.5 spikes. Current injections depolarized 21 neurons by 29.9+/-8.0 mV and triggered action potentials averaging 17.0+/-2.4 spikes. After a period of prolonged neuronal activation with pulses of 1 nA at 20 Hz for 1 minute, the action potential responses to mechanical stimulation and to current injections were first markedly suppressed (0.2+/-0.2 and 2.1+/-0.7 spikes, respectively) and then enhanced, reaching levels above control (29.0+/-8.0 and 21.7+/-2.6 spikes, respectively) over the subsequent 15 minutes. In contrast, there was no inhibition of the depolarizations caused by mechanical stimulation or current injections. The recovery and enhancement of action potentials, which reached 150+/-5.4% of control values at 15 minutes (n=13), were abrogated by 10 micromol/L of indomethacin and replaced by sustained inhibition for over 15 minutes. Carbacyclin (10 micromol/L) reversed the inhibition and restored action potential responses. Prostacyclin production by cultured nodose neurons was enhanced by arachidonic acid and electrical field stimulation and inhibited by indomethacin. We conclude that prostacyclin provides an autocrine feedback that restores and enhances the responsiveness of arterial baroreceptor neurons after their inhibition from excessive neuronal activation. We speculate that reduced synthesis of neuronal prostacyclin contributes to the resetting phenomenon and the suppressed activity of arterial baroreceptors in hypertension.

Fundamental and applied biological sciences. Psychology

Cardiology. Vascular system

Arterial hypertension. Arterial hypotension

Blood vessels and receptors

Biological and medical sciences

Medical sciences

Vertebrates: cardiovascular system

Blood and lymphatic vessels

Experimental diseases

Details

Title: Subtitle: Neuronal prostacyclin is an autocrine regulator of arterial baroreceptor activity
Creators: Vladislav SNITSAREV - Cardiovascular Center and the Department of Internal Medicine, University of Iowa, Iowa City, United States
Carol A WHITEIS - Cardiovascular Center and the Department of Internal Medicine, University of Iowa, Iowa City, United States
Mark W CHAPLEAU - Cardiovascular Center and the Department of Internal Medicine, University of Iowa, Iowa City, United States
Francois M ABBOUD - Cardiovascular Center and the Department of Internal Medicine, University of Iowa, Iowa City, United States
Resource Type: Journal article
Publication Details: Hypertension (Dallas, Tex. 1979), Vol.46(3), pp.540-546
DOI: 10.1161/01.HYP.0000175475.17666.26
PMID: 16061731
NLM abbreviation: Hypertension
ISSN: 0194-911X
eISSN: 1524-4563
Publisher: Lippincott; Philadelphia, PA; Hagerstown, MD
Language: English
Date published: 2005
Academic Unit: Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
Record Identifier: 9984025423302771

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