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If it is possible to single out one substance as being the most important in the control of sodium excretion and blood pressure, then that substance would be angiotensin II It is a potent vasoconstrictor and a mediator of multiple actions in the kidneys that affect sodium excretion Thus, it affects blood pressure directly as a vasoconstrictor and indirectly via regulation of renal sodium excretion There are many local RAS in individual tissues, including the kidneys, brain, and the heart There is also a global or systemic RAS which we normally consider to be the major renal regulator of blood pressure All RAS, whether global or local, consist of a large protein substrate called angiotensinogen, several enzymes and several products The key product is angiotensin II When angiotensin II binds to cell surface receptors, it initiates actions that affect blood pressure and excretion of sodium The first key enzyme in all RAS is renin It acts on angiotensinogen to produce a small (10-amino-acid) product called angiotensin I Angiotensin I is acted upon by another enzyme, angiotensin-converting enzyme (ACE), to produce the highly active 8-amino-acid peptide angiotensin II In the global RAS, the source of angiotensinogen circulating in the blood is the liver The source of circulating renin is the granule cells in the kidney Renin is secreted both into the interstitium of the kidney and into the lumen of the afferent arterioles, where it acts on circulating angiotensinogen to produce circulating angiotensin I ACE, which is expressed on the luminal surface of endothelial cells in many parts of the vasculature, particularly in the lungs, then converts angiotensin I to angiotensin II We will describe the regulation of RAS in terms of the global system, in part because more is known about it Investigators agree, however, that locally produced angiotensin II (and some related peptides) is the more important source in terms of regulating the kidneys because the levels of angiotensin II in renal tissues are far higher than can be accounted for by a systemic source It is presumed that global angiotensin II arriving in the renal blood supply acts synergistically with local angiotensin II as a regulator of function Circulating levels of angiotensinogen are usually fairly high and ACE activity usually converts most angiotensin I into angiotensin II Therefore, the primary determinant of circulating levels of angiotensin II is the amount of renin available to convert angiotensinogen to angiotensin I Consequently, to understand angiotensin II regulation of blood pressure, we require an understanding of the regulation of renin secretion What determines how much renin is secreted Two primary regulators have been described The first are the neural baroreceptors, which produce signals via the renal sympathetic nerves that stimulate granular cells: Activation of 1-adrenergic receptors on the granular cells stimulates renin secretion via a cyclic adenosine monophosphate and protein kinase A-dependent process (In addition, the activity of renal sympathetic nerves causes afferent arteriolar constriction and reduction in renal blood flow) The second regulators of.

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renin secretion are the intrarenal baroreceptors, ie, granular cells that deform in response to changes in afferent arteriolar pressure; when the pressure falls, renin production increases Thus, as mentioned previously, granular cells act both as detectors (of renal arteriolar pressure) and as signal generators (releasing renin) in response to changes in pressure and sympathetic activity The signals from the vasomotor system to the renin-producing granular cells ensures that there is tight coordination between the rapid activity of the baroreceptor reflex and the slower acting RAS; ie, the short-term regulation and the intermediate-term regulation have at least one common set of detectors However, the intrarenal pressure detector can function in the absence of renal innervation (eg, after a renal transplant) There is also a third detector mechanism that regulates renin release It is also intrarenal, but it does not detect blood pressure Rather, it measures the amount of sodium chloride that leaves the thick ascending limb, directly bathing the macula densa cells of the juxtaglomerular apparatus and delivered to the distal convoluted tubule This amount of sodium chloride depends on both the rate of filtration and the rate of sodium reabsorption in all the nephron elements preceding the macula densa When sodium chloride delivery (a combination of concentration and flow rate) to the luminal surface of macula densa cells increases, renin production decreases This is due to increased uptake of NaCl by the cells with subsequent osmotic swelling Osmotic swelling (Figure 7 3) causes the release of transmitter agents (see later discussion) that inhibit renin release This load detector, therefore, does not generate signals that directly regulate blood pressure However, it does contribute to the regulation of renin secretion

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