| Inhibition of nitric oxide synthesis augments centrally induced sympathetic coronary vasoconstriction in cats. | |
| | |
MedLine Citation:
|
PMID: 7943371 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The principal effect of sympathetic activation on the coronary circulation is an alpha-adrenergic coronary vasoconstriction in the presence of beta-receptor blockade. Secondary effects include vasodilation due to beta-adrenoceptor stimulation and alpha 2-mediated release of endothelium-derived relaxing factor (EDRF) from the coronary vascular endothelium. We hypothesized that blockade of nitric oxide synthesis (nitro-L-arginine methyl ester, L-NAME) would augment coronary vasoconstriction to sympathetic stimulation as a result of a decrease in alpha 2-mediated EDRF release. In chloralose-anesthetized cats, hypothalamic stimulation produced increases in coronary vascular resistance [maximum 26 +/- 9% (SE)] and arterial pressure (41 +/- 7%) and a decrease in coronary blood flow velocity (15 +/- 6%). L-NAME (3 mg/kg iv) increased baseline arterial pressure from 69 +/- to 92 +/- 7 mmHg (P < 0.05). After L-NAME, a greater increase in coronary vascular resistance (55 +/- 20%, P < 0.05), a decrease in coronary blood flow velocity (24 +/- 7%, P < 0.05), and a similar pressor response (34 +/- 7%) were observed in response to hypothalamic stimulation. L-Arginine reversed the effect of L-NAME on coronary vasoconstriction to hypothalamic stimulation. Similar increases in arterial pressure (from 73 +/- 3 to 91 +/- 5 mmHg, P < 0.05) with vasopressin (0.01-0.05 U/min) failed to enhance coronary vasoconstriction to activation in anterior hypothalamus. We conclude that inhibition of EDRF synthesis augments centrally induced sympathetic coronary vasoconstriction in the cat. |
| | |
Authors:
|
A R Goodson; J M Leibold; D D Gutterman |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
|
Title: The American journal of physiology Volume: 267 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1994 Oct |
Date Detail:
|
Created Date: 1994-11-18 Completed Date: 1994-11-18 Revised Date: 2007-11-14 |
Medline Journal Info:
|
Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: H1272-8 Citation Subset: IM |
Affiliation:
|
Veterans Administration Medical Center, Iowa City, Iowa. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Arginine / analogs & derivatives*, pharmacology Blood Flow Velocity / drug effects Blood Pressure / drug effects, physiology Cats Coronary Vessels / drug effects, innervation, physiology* Electric Stimulation Female Hypothalamus / drug effects, physiology* Male Muscle, Smooth, Vascular / drug effects, innervation, physiology* NG-Nitroarginine Methyl Ester Nitric Oxide / antagonists & inhibitors, biosynthesis*, secretion Sympathetic Nervous System / drug effects, physiology* Time Factors Vascular Resistance / drug effects, physiology Vasoconstriction / drug effects* Vasodilation / drug effects Vasopressins / pharmacology* Vena Cava, Inferior / physiology |
| Grant Support | |
ID/Acronym/Agency:
|
HL-032295/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
|
10102-43-9/Nitric Oxide; 11000-17-2/Vasopressins; 50903-99-6/NG-Nitroarginine Methyl Ester; 74-79-3/Arginine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Physiological assessment of augmented vascularity induced by VEGF in ischemic rabbit hindlimb.
Next Document: Regional changes in myocyte structure in model of canine right atrial hypertrophy.