Interaction between cholinergic and nitrergic vasodilation: a novel mechanism of blood pressure control

Details

Ressource 1Download: serval:BIB_B61C908981AB.P001 (78.60 [Ko])
State: Public
Version: author
License: Not specified
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
Serval ID
serval:BIB_B61C908981AB
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Interaction between cholinergic and nitrergic vasodilation: a novel mechanism of blood pressure control
Journal
Cardiovascular Research
Author(s)
Lepori  M., Sartori  C., Duplain  H., Nicod  P., Scherrer  U.
ISSN
0008-6363 (Print)
Publication state
Published
Issued date
09/2001
Volume
51
Number
4
Pages
767-72
Notes
Clinical Trial
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep
Abstract
OBJECTIVE: Cholinergic vasodilation has been thought to play little if any role in the regulation of blood pressure in humans. Autonomic denervation potentiates the vasoconstriction evoked by nitric oxide synthase inhibition in humans, but the mechanism is unclear. We hypothesized that this may be related to loss of neuronal, non-nitric-oxide-dependent vasodilation. METHODS: To test this hypothesis, we examined effects of cholinergic blockade on blood pressure, heart rate and peripheral vascular responses to systemic infusion of the nitric-oxide-dependent vasoconstrictor L-NMMA (0.5 mg/kg/min over 15 min) in eight normal subjects. RESULTS: The L-NMMA-induced increase in mean (+/-S.E.) arterial pressure was roughly three times larger (P=0.002) in the presence than in the absence of cholinergic blockade (38+/-6 vs. 13+/-2 mmHg). Similarly, the increase in systemic and calf vascular resistance was more than twofold larger during L-NMMA-atropine. This potentiation was specific for nitric-oxide-dependent vasoconstriction, because atropine did not alter the responses to phenylephrine infusion. Cholinergic blockade also altered (P=0.004) the heart rate response to nitric oxide synthase inhibition; during L-NMMA alone heart rate decreased by 10+/-2 beats/min, whereas during L-NMMA-atropine infusion it increased by 14+/-4 beats/min. CONCLUSION: Cholinergic mechanisms play an important hitherto unrecognized role in offsetting the hypertension and cardiac sympathetic activation caused by nitric oxide synthase inhibition in humans. Decreased parasympathetic activity and impaired nitric oxide synthesis characterize several cardiovascular disease states, as well as normal aging. The conjunction of these two defects could trigger sudden death and contribute to the hypertension of the elderly.
Keywords
Adrenergic beta-Antagonists/pharmacology Adult Arginine/*pharmacology Atropine/*pharmacology Cardiac Output/drug effects Enzyme Inhibitors/pharmacology Female Hemodynamic Processes/drug effects Humans Leg Male Muscarinic Antagonists/*pharmacology Nitric Oxide Synthase/*antagonists & inhibitors Phenylephrine/pharmacology Propranolol/pharmacology Regional Blood Flow/drug effects Statistics, Nonparametric Vasoconstrictor Agents/*pharmacology omega-N-Methylarginine/*pharmacology
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 13:44
Last modification date
25/09/2019 6:10
Usage data