Angiotensin and prostaglandins in the pressure-natriuresis response in rats

Abstract

The possible roles of angiotensin and prostaglandins as humoral mediators of the pressure-natriuresis response were studied in anesthetized Sprague-Dawley rats. Neural and other hormonal influences on the kidney were held constant by denervating the kidney and by maintaining fixed high plasma levels of aldosterone, corticosterone, vasopressin and norepinephrine by continuous intravenous infusion. Acute elevation of arterial pressure by tightening the ligature placed around the abdominal aorta below the renal artery produced marked increases in urine flow and sodium excretion with no detectable changes in renal blood flow or glomerular filtration rate. In rats undergoing a saline diuresis, the pressure-natriuresis response was markedly inhibited by intravenous infusion of angiotensin II at a rate of 10 ng/kg/min. Blockade of prostaglandin synthesis with indomethacin also reduced the pressure-natriuresis response in the presence of low-dose (2 ng/kg/min) of angiotensin II, but indomethacin alone did not affect significantly. On the other hand, in rats with hydropenia indomethacin alone significantly inhibited the sodium excretory response to changes in arterial pressure. This indomethacin-induced inhibitory effect on the pressure-natriuresis response was completely attenuated in rats treated with captopril. These results indicate that angiotensin II is a powerful modulator of the pressure-natriuresis response. In addition, it has been suggested that prostaglandins are also capable of modulating the response only in the presence of the renin-angiotensin system. However, neither angiotensin nor prostaglandins appears to be essential for the basic pressure-natriuresis phenomenon since the pressure-natriuresis response can occur during blockade of both the renin-angiotensin and prostaglandin systems.(ABSTRACT TRUNCATED AT 250 WORDS)