Within the classic renin-angiotensin endocrine system, the enzyme renin is produced in the kidney and upon stimulation for its release, it acts upon circulating angiotensinogen which is produced in the liver. The resultant decapeptide angioteinsin I loses its terminal two peptides upon its circulation through the lung by the angiotensin converting enzyme to form the powerful pressor decapeptide angiotensin II which promotes potent vasoconstriction, stimulates the release of aldosterone from the adrenal gland and, in turn, the retention of sodium and water by the kidney.
Until recently, there has been much research concerning local renin angiotensin systems functioning within such organs as the heart, blood vessels, kidney, brain, and others. In addition, research has shown that some of these organs also seem to produce locally the steroidal hormone aldosterone. This very important area of research has now achieved major clinical attention because these local systems seem to account for such major biological actions as mitogenesis, cellular hypertrophy, fibrosis, apoptosis, and inflammation within those organs. Moreover, further research has demonstrated still more complicated aspects to the metabolic events associated with the cascade of hormonal substances that result from the biogenesis of the angiotensins. The clinical implications of these events are of great clinical significance and also important.
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