Adrenergic regulation of renin release and effects on angiotensin and aldosterone.

This survey discloses the main mechanisms regulating renin release from the kidneys. Stimulation or inhibition of renin at least during a normal sodium intake seems to depend mostly on the sympathetic nervous system and be mediated through beta 1-adrenoceptors. The suppression of renin release is maintained during long-term treatment with both selective (beta 1) and non-selective (beta 1 + beta 2)-adrenoceptor blocking drugs. The role of alpha-adrenoceptors on renin release is less clear, both stimulating and suppressive effects having been described after treatment with alpha 1-adrenoceptor blocking therapy (i.e. prazosin). In certain conditions, i.e. when renal vascular resistance is increased or renal perfusion pressure augmented, renal prostaglandins (PG) especially PGE2, may play an important part in renin release. Angiotensin II (A II) and aldosterone generally follow the shifts in renin release. Thus, a decrease in both A II and plasma aldosterone is seen during long-term treatment with beta-adrenoceptor-blockade and may contribute to the blood-pressure lowering effect of these drugs.