Regulation (renin release)

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