Hypertension, Vol 22, 688-698, Copyright © 1993 by American Heart Association
EK Jackson and WA Herzer
The purpose of this study was to compare the effects of prostaglandin I2 on
several cardiovascular parameters and to compare the ability of
prostaglandin I2 to modify angiotensin II-induced changes in these
cardiovascular parameters in spontaneously hypertensive versus normotensive
rats. Studies were conducted in adult, age-matched, indomethacin-, and
captopril-pretreated spontaneously hypertensive and normotensive rats that
had been prepared for assessment of arterial blood pressure, cardiac output
(thermodilution), and renal and mesenteric blood flows (transit-time flow
probes). In both normotensive and hypertensive rats, intravenous infusions
of prostaglandin I2 (0.003, 0.03, 0.3, 1, 3, and 10 micrograms/kg per
minute) dose- dependently reduced mean arterial blood pressure, total
peripheral resistance, and mesenteric vascular resistance but not renal
vascular resistance. Only minor differences were detected between
normotensive versus hypertensive rats with regard to the effects of
prostaglandin I2 on baseline cardiovascular parameters (ie, in the absence
of angiotensin II). In both rat strains, an intravenous infusion of
angiotensin II (300 ng/kg per minute) increased mean arterial blood
pressure, total peripheral resistance, and renal and mesenteric vascular
resistances, and these effects of angiotensin II were similar in the two
strains in the absence of prostaglandin I2. In both strains, prostaglandin
I2 inhibited angiotensin II-induced changes in mean arterial blood
pressure, total peripheral resistance, and renal and mesenteric vascular
resistances. However, in the renal, but not mesenteric, vasculature of
hypertensive rats, the ability of prostaglandin I2 to attenuate angiotensin
II-induced vasoconstriction was strikingly reduced. These results indicate
that although in general spontaneously hypertensive rats respond normally
to prostaglandin I2, in the kidney of spontaneously hypertensive rats the
ability of prostaglandin I2 to attenuate angiotensin II-induced
vasoconstriction is reduced. This selective renal defect may relate to the
pathogenesis of high blood pressure in this genetic model of hypertension.
ARTICLES
Angiotensin II/prostaglandin I2 interactions in spontaneously hypertensive rats
Center for Clinical Pharmacology, University of Pittsburgh, PA Medical Center 15261.
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