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
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