Anti-hypertensive actions of d:\winwrd2\dotfiles\paper.dot in
spontaneously hypertensive rats.
Benter, Ibrahim F., Carlos M. Ferrario, Mariana Morris Anddebra I.
Diz.
Hypertension Center and Department of Physiology & Pharmacology,
The Bowman Gray School of Medicine of, Wake Forest University,
Winston-Salem, North Carolina 27157-1032
APStracts 2:0061H, 1995.
Observations that angiotensin-(1-7) [Ang-(1-7)] may oppose the
vasoconstrictor actions of angiotensin II (Ang II) prompted an
investigation of the effects of the heptapeptide on the maintenance
of elevated blood pressure in spontaneously hypertensive rats (SHR).
Ang-(1-7) was infused into the jugular vein of 13 week old SHR (n =
64), Wistar Kyoto (WKY, n = 50) and Sprague-Dawley (SD, n = 18) rats
for two weeks at a dose of 24 [mu]g/kg/hr using osmotic minipumps.
Blood pressure, fluid and electrolyte balance, plasma vasopressin and
urinary excretion of prostaglandin E2 and 6-keto-PGF1 were measured
at days 2, 7 and 12 of the infusion. Ang-(1-7) caused a sustained and
significant reduction in plasma vasopressin concentration that was
associated with an increase in urinary prostaglandin E2 and 6-keto
-PGF1 excretion at day 2 after the commencement of the infusion in
SHR. These changes were accompanied by diuresis and natriuresis
during the first three days of infusion in SHR but not in WKY or SD
rats. Direct measurments of arterial pressure confirmed the lowering
effect of Ang-(1-7) on systolic pressure of SHR day 2 of treatment
witha restoration of the pressure by days 7 and 12. These findings,
along with our previous demonstration that Ang-(1-7) is an active
depressor peptide in the intact animal, suggest that Ang-(1-7) may
play a significant role as a vasodepressor system opposing the
hemodynamic actions of Ang II in this genetic form of experimental
hypertension.
Received 16 March 1994; accepted in final form 14 February 1995.
APS Manuscript Number H254-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.