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(Hypertension. 1996;27:893-896.)
© 1996 American Heart Association, Inc.
Articles |
L-Arginine Restores Dilator Responses of the Basilar Artery to Acetylcholine During Chronic Hypertension
From the Departments of Internal Medicine and Pharmacology, Cardiovascular Center, University of Iowa College of Medicine, and Veterans Administration Medical Center, Iowa City.
Correspondence to Donald D. Heistad, MD, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA 52242.
Abstract The objective of this study was to test the hypothesis that administration of L-arginine, a substrate for nitric oxide synthase, restores acetylcholine-induced dilatation of the basilar artery in chronically hypertensive rats. Basilar artery diameter was measured through a cranial window in anesthetized stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) aged 6 to 7 months (adult) and 12 months (older adult). Under control conditions, baseline basilar artery diameter was smaller in SHRSP (adult, 239±30 µm; older adult, 198±13 µm) (mean±SE) than in WKY (adult, 261±10 µm; older adult, 259±7 µm) (P<.05 versus SHRSP). Topical application of acetylcholine (10-5 mol/L) produced dilatation of the basilar artery in WKY, which was impaired in both adult and older SHRSP (P<.05). Topical L-arginine (10-3 mol/L for 30 minutes) did not affect responses to acetylcholine in adult SHRSP but enhanced vasodilatation in response to acetylcholine (10-5 mol/L) in older SHRSP without affecting responses to sodium nitroprusside. In contrast, D-arginine did not affect acetylcholine-induced vasodilatation in older SHRSP. These results suggest that impaired dilatation of the basilar artery in response to acetylcholine in older SHRSP is restored toward normal by L-arginine, a substrate for nitric oxide synthase.
Key Words: cerebral arteries • endothelium-derived factor • rats, stroke-prone SHR • acetylcholine • arginine • nitric oxide
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