Sympathetic control of renin release.

Area of Science:

• Physiology
• Renal Physiology
• Neuroendocrinology

Background:

• Sympathetic nervous system activity and circulating catecholamines significantly influence renal renin release.
• Renin release is modulated by both stimulatory (beta-adrenoceptor) and potentially inhibitory (alpha-adrenoceptor) mechanisms.
• Cardiopulmonary and arterial baroreceptors also play a role in regulating renin release, with complex interactions.

Purpose of the Study:

• To review the mechanisms by which sympathetic outflow influences renin release.
• To discuss the evidence for and against alpha-adrenoceptor mediated inhibition of renin release.
• To explore the role of vascular volume receptors and calcium in renin secretion.

Main Methods:

• Review of in vivo, isolated perfused kidney, and in vitro experimental findings.
• Analysis of pharmacological evidence identifying adrenoceptor subtypes.
• Consideration of studies investigating baroreceptor input and calcium's role.

Main Results:

• Beta-adrenoceptor stimulation, primarily via the beta 1-subtype in juxtaglomerular (JG) cells, activates adenyl cyclase, leading to renin release.
• Evidence suggests alpha-adrenoceptors may inhibit renin release, but their location and physiological significance remain controversial.
• Vascular volume receptors (low and high pressure) provide conflicting signals that can cancel each other's effects on renin release.

Conclusions:

• Sympathetic control of renin release involves complex interactions between beta- and alpha-adrenoceptors, vascular volume receptors, and intracellular signaling pathways.
• The precise role and location of alpha-adrenoceptors in regulating renin release require further investigation.
• Calcium plays a significant, albeit complex, role in the activation of renin release.