regulation (renin release)

Last reviewed 11/2023

Renin release is controlled by:

• intrarenal response:
• blood pressure is sensed by an unknown mechanism in the afferent arteriole of the JGA. An increased blood pressure leads to reduced renin secretion, and vice-versa.
• sodium concentration detected at the macula densa; an elevated sodium concentration associated with increased glomerular filtration leads to reduced renin secretion and vice-versa. This mechanism underlies the pathophysiology of renal artery hypertension.
• prostaglandins, particularly PGI2, may be involved in one or both mechanisms

• sympathetic response:
• the JGA is in close proximity to renal sympathetic nerve afferents; there are beta-adrenergic receptors on its surface which may be a drug target
• increased renin release occurs in response to increased sympathetic nerve signals directly on renin-containing cells, and possibly by the intrarenal response (described above) due to reduced renal perfusion
• increased sympathetic output may be secondary to:
• decreased stimulation of low pressure receptors in the atria and great veins
• decreased stiumlation of high pressure arterial baroreceptors within the carotid sinus

• hormonal response:
• adrenaline and noradrenaline act directly on the beta-receptors of cells containing renin to increase its release; hence, beta-blocker drugs may diminish renin release
• renin release may be inhibited directly by:
• angiotensin II - negative feedback loop
• aldosterone - negative feedback loop
• atrial natriuretic peptide