Ck. Kost et al., VASCULAR REACTIVITY TO ANGIOTENSIN-II IS SELECTIVELY ENHANCED IN THE KIDNEYS OF SPONTANEOUSLY HYPERTENSIVE RATS, The Journal of pharmacology and experimental therapeutics, 269(1), 1994, pp. 82-88
The two aims of the present study were to: 1) explore the hypothesis t
hat the kidneys of spontaneously hypertensive rats (SHR) are more resp
onsive 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 a
nd right carotid artery were monitored in anesthetized SHR and WKY dur
ing 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 simil
ar extent in both strains during the Ang II infusion. Hindquarter (aor
tic) resistance was unaffected by Ang II in both strains. Carotid resi
stance was slightly increased by the peptide to a similar magnitude in
SHR and WKY. The renal and mesenteric vasculature of both strains wer
e highly sensitive to Ang II, with significant dose-related increases
in resistance during the infusion. The magnitude of the mesenteric res
ponse was not different between SHR and WKY. However, the renal vascul
ar response to Ang II was significantly greater in SHR than in WKY. In
conclusion, the enhanced responsiveness to i.v. Ang II occurred selec
tively in the kidney of SHR and not in the other vessels examined.