Interaction between the natriuretic effects of renal perfusion pressure and the antinatriuretic effects of angiotensin and aldosterone in control of sodium excretion.
Aldosterone has been recognized as an important sodium retaining hormone for many years. Recently we have demonstrated that angiotensin II has a much more powerful antinatriuretic effect than that of aldosterone. The importance of angiotensin II in regulation of sodium excretion has been observed in experiments in which angiotensin II has been infused intravenously or into the renal artery in acute and chronic situations, and in studies involving blockade of angiotensin II formation. In other experiments we have studied the effects of changes in renal perfusion pressure on sodium excretion. While earlier work by others indicated that an acute 10 mm Hg increase in perfusion pressure would increase sodium excretion 60%-70% we observed that a chronic 10 mm Hg change in perfusion pressure would result in a 300% change in sodium excretion. In view of evidence suggesting that changes in the ability of the kidney to excrete sodium normally at normal arterial pressure is an important element in hypertension we studied the effects of aldosterone and angiotensin II on arterial pressure regulation in normal dogs. High physiological levels of each hormone were infused intravenously for several weeks. Both produced sustained hypertension. Aldosterone hypertension was a typical volume loading type with sodium retention, increased blood volume and extracellular fluid volume and a slow rise in arterial pressure. Angiotensin hypertension was a typical vasoconstrictor type with high peripheral resistance, normal or decreased blood volume, decreased cardiac output, a rapid rise in arterial pressure and only initial sodium retention.(ABSTRACT TRUNCATED AT 250 WORDS)
D000315:Adrenalectomy; D000450:Aldosterone / Q000008:administration & dosage / Q000494:pharmacology*; D000804:Angiotensin II / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007261:Infusions, Intra-Arterial; D007668:Kidney / Q000502:physiology*; D009318:Natriuresis / Q000187:drug effects*; D010477:Perfusion; D011312:Pressure; D012077:Renal Artery / Q000502:physiology; D014882:Water-Electrolyte Balance
D000804:Angiotensin II; D000450:Aldosterone