To assess in vivo functional interactions of vasopressor substances, norepinephrine, vasopressin and angiotensin II with renal vasodepressor mechanisms, prostaglandins and kallikrein-kinin systems, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day, ip), vasopressin (7.2 u/kg/day, ip) and angiotensin IE (0. 9 mg/kg/day ip) on urinary excretion of prostaglandin E and kallikrein in conscious rats. Norepinephrine, vasopressin and angiotensin n mduced a sustained increase in systolic blood pressure. Norepinephrine and angiotensin n induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin n level was markedly increased by exogenous angiotensin II, but it was not changed by norepinephrine and was decreased by vasopressin. These results indicate that renal prostaglandin E changes independently of the renal kallikrein-kinin and renin∼angiotensin systems in response to norepinephrine, vasopressin and angiotensin II, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.
- angiotensin I
- renal kallikrein-kinin system
- renal prostaglandin E
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