Synthesis and structures of the angiotensins.
Three generally accepted mechanisms are involved in the regulation of renin secretion (Fig. 18.2). The first depends on renal afferent arterioles that act as stretch receptors or baroreceptors. Increased intravascular pressure and increased volume in the afferent arteriole inhibits the release of renin. The second mechanism is the result of changes in the amount of filtered sodium that reaches the macula densa of the distal tubule. Plasma renin activity correlates inversely with dietary sodium intake. The third renin secretory control mechanism is neurogenic and involves the dense sympathetic innervation of the juxtaglomerular cells in the afferent arteriole; renin release is increased following activation of ^-adrenoceptors by the neurotransmitter norepi-nephrine.
Angiotensin II, the primary end product of the renin-angiotensin system, acts on the juxtaglomerular cells to inhibit the release of renin; this process is therefore a negative feedback mechanism. The half-life of renin in the circulation is 10 to 30 minutes, with inacti-vation occurring primarily in the liver. Small amounts of renin are eliminated by the kidneys. Pure human renin
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