L-ARGININE RESTORES DILATOR RESPONSES OF THE BASILAR ARTERY TO ACETYLCHOLINE DURING CHRONIC HYPERTENSION

The objective of this study was to test the hypothesis that administra tion of L-arginine, a substrate for nitric oxide synthase, restores ac etylcholine-induced dilatation of the basilar artery in chronically hy pertensive rats. Basilar artery diameter was measured through a crania l window in anesthetized stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY) aged 6 to 7 months (a dult) and 12 months (older adult). Under control conditions, baseline basilar artery diameter was smaller in SHRSP (adult, 239+/-30 mu m; ol der adult, 198+/-13 mu m) (mean+/-SE) than in WKY (adult, 261+/-10 mu m; older adult, 259+/-7 mu m) (P<.05 versus SHRSP). Topical applicatio n of acetylcholine (10(-5) mol/L) produced dilatation of the basilar a rtery 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 resp onses to acetylcholine in adult SHRSP but enhanced vasodilatation in r esponse to acetylcholine (10(-5) mol/L) in older SHRSP without affecti ng responses to sodium nitroprusside. In contrast, -arginine did not a ffect acetylcholine-induced vasodilatation in older SHRSP. These resul ts suggest that impaired dilatation of the basilar artery in response to acetylcholine in older SHRSP is restored toward normal by L-arginin e, a substrate for nitric oxide synthase.