[Plasma renin activity and prostaglandin E2 in hypotension induced by sodium nitroprusside]

Sodium nitroprusside (SNP) is a potent, effective and readily reversible vasodilating agent frequently used in anaesthesia for deliberate hypotension. Moderate hypotension induced by SNP activated catecholamine and vasopressin secretions, and the renin-angiotensin system, resulting in partial antagonism of the hypotensive response to SNP. Furthermore, this increase in renin release was involved in the hypertensive rebound after SNP withdrawal. This activation of vasoconstrictor systems led to pharmacological associations aimed at reducing the risk of cyanide poisoning. The physiological interrelationship between prostaglandins and renin secretion has now been well established but, as far as we know, no paper existed concerning prostaglandins during SNP-induced hypotension. In such hypotension (Pa: -30%), monitored by invasive and non invasive haemodynamic techniques (pulsed Doppler), the variations in plasma renin activity (PRA) and in venous and arterial plasma PGE2 concentrations (V PGE2 and A PGE2), determined by radioimmunoassay, were studied in anaesthetized dogs. Invasive haemodynamic data were similar to previous reports. Common carotid diameter increased (p less than 0.05), with a constant common carotid blood flow. PRA (p less than 0.05), V PGE2 (p less than 0.05) and A PGE2 (p less than 0.05) increased. PRA and V PGE2 were highly correlated before and after SNP. SNP resulted in hypotension with reflex sympathetic activation and dilatation of large arteries. Carotid blood flow autoregulation was maintained. Whilst pulmonary removal of PGE2 remained unchanged, an increase in A PGE2 may have been involved in the vasodilator mechanisms.