In Conn's syndrome there is increased production of aldosterone. This causes an increase in the aldosterone to renin level as the aldosterone level is high and the renin low.
- Renin is a proteolytic enzyme that is released into the circulation primarily by the kidneys
- Control of Blood pressure
- Renin is formed from preprorenin and then prorenin and then converted to renin by the kidney
- Renin is a glycoprotein acid protease released by the Juxtaglomerular cells of the kidney.
- Renin cleaves angiotensinogen to the inactive decapeptide angiotensin I
- ACE converts the inactive decapeptide angiotensin I to the active octapeptide Angiotensin II
- Angiotensin II - acts via type 1 Angiotensin II receptors
- Effects of Angiotensin II include - increased arterial tone and increased sodium reabsorption and cell growth and sympathetic stimulation and increases thirst and ADH release
- ATII blockers act only at the type 1 Angiotensin II receptors and not the type 2 Angiotensin II receptors
Therapeutic agents that work on RAS
- ACE inhibitors e.g. Lisinopril
- Angiotensin II blockers e.g. Losartan
- New Renin-inhibitors currently being developed