RT Journal Article
SR Electronic
T1 Vascular reactivity to angiotensin II is selectively enhanced in the kidneys of spontaneously hypertensive rats.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 82
OP 88
VO 269
IS 1
A1 C K Kost, Jr
A1 W A Herzer
A1 P Li
A1 E K Jackson
YR 1994
UL http://jpet.aspetjournals.org/content/269/1/82.abstract
AB The two aims of the present study were to: 1) explore the hypothesis that the kidneys of spontaneously hypertensive rats (SHR) are more responsive to angiotensin II (Ang II) than are the kidneys of normotensive Wistar Kyoto rats (WKY) and 2) determine whether other vascular beds of SHR exhibit enhanced responsiveness to Ang II, relative to WKY. SHR and WKY received captopril from 4 weeks of age until the time of the experiment to prevent vascular alterations secondary to hypertension. Blood pressure, heart rate, cardiac output and blood flow through the superior mesenteric artery, left renal artery, lower abdominal aorta and right carotid artery were monitored in anesthetized SHR and WKY during acute i.v. administration of Ang II at doses of 0, 3, 10, 30, 100 and 300 ng kg-1 min-1. The heart rate and cardiac output were not significantly affected but the blood pressure was increased to a similar extent in both strains during the Ang II infusion. Hindquarter (aortic) resistance was unaffected by Ang II in both strains. Carotid resistance was slightly increased by the peptide to a similar magnitude in SHR and WKY. The renal and mesenteric vasculature of both strains were highly sensitive to Ang II, with significant dose-related increases in resistance during the infusion. The magnitude of the mesenteric response was not different between SHR and WKY. However, the renal vascular response to Ang II was significantly greater in SHR than in WKY. In conclusion, the enhanced responsiveness to i.v. Ang II occurred selectively in the kidney of SHR and not in the other vessels examined.