l-Arginine-induced hypotension in the rat: evidence that NO synthesis is not involved

l‐Arginine is the biological precursor for nitric oxide (NO). NO is formed continuously in endothelial cells and maintains a certain degree of vasodilator tone under physiological conditions. Although the formation of NO is not primarily controlled by precursor availability, the extent to which extr...

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Bibliographic Details
Published in:Acta physiologica Scandinavica 1994-12, Vol.152 (4), p.385-390
Main Authors: JUN, T., WENNMALM, Å.
Format: Article
Language:English
Subjects:
Animals
Arginine - analogs & derivatives
Arginine - metabolism
Arginine - pharmacology
Biological and medical sciences
blood pressure
Blood Pressure - drug effects
endothelium
Erythrocytes - chemistry
Fundamental and applied biological sciences. Psychology
Glycated Hemoglobin A - analysis
Glycated Hemoglobin A - drug effects
Glycated Hemoglobin A - metabolism
Hemodynamics. Rheology
Hypotension - drug therapy
Hypotension - physiopathology
Male
NG-Nitroarginine Methyl Ester
nitrate
Nitric Oxide - analysis
Nitric Oxide - antagonists & inhibitors
Nitric Oxide - biosynthesis
Nitric Oxide - metabolism
Rats
Rats, Wistar
vascular resistance
Vertebrates: cardiovascular system
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Summary:l‐Arginine is the biological precursor for nitric oxide (NO). NO is formed continuously in endothelial cells and maintains a certain degree of vasodilator tone under physiological conditions. Although the formation of NO is not primarily controlled by precursor availability, the extent to which extra supplementation with l‐arginine may affect endothelial NO formation, and hence, vasodilator tone and systemic blood pressure, is not entirely clear. To address this issue, we infused l‐arginine i.v. in anaesthetized normotensive rats pretreated with NG‐nitro‐l‐arginine methyl ester (l‐NAME, 50 or 200 mg‐1) and in untreated controls, under continued recording of mean arterial pressure (MAP). In control animals l‐arginine (25 or 100 mg kg‐1 min‐1) had no effect on systemic MAP (111 ± 3 mm Hg), while l‐arginine (200 mg kg‐1 min‐1) lowered MAP (to 70 ± 6mmHg). D‐Arginine (200 mg kg‐1 min‐1) also induced hypotension; during infusion of D‐arginine MAP fell from 106 ± 4 to 64 ± 4 mm Hg. Pretreatment with l‐NAME (50 and 200mgkg‐1) elevated MAP to 140 ± 2 and 147 ± 3 mm Hg, respectively, but failed to affect the hypotensive response to l‐arginine; during infusion of l ‐arginine (200 mg kg‐1 min‐1) in rats pretreated with l‐NAME (50 and 200 mg kg‐1) MAP fell to 86 ± 9 and 104 ± 6 mm Hg, respectively. Plasma levels of the NO metabolite, nitrate, were 18 ± 4 and 17 ± 3μmol l‐1, respectively, before and after infusion of l‐arginine (200 mg kg‐1 min‐1). Trapping of NO to haemoglobin (HbNO) could not be detected, either before or after infusion of l‐arginine (200 mg kg‐1 min‐1). We conclude that a high dose of l‐arginine may act hypotensive in normotensive rats. This effect does, however, not seem to be based on an augmented formation of NO.
ISSN:0001-6772
1365-201X
DOI:10.1111/j.1748-1716.1994.tb09820.x