Integrated response of the kidneys to changes in extracellular fluid (ECF) volume. This composite figure illustrates natriuretic and antinatriuretic mechanisms. For simplicity, the systems are shown operating only in one direction and not all pathways are shown. The major antinatriuretic systems are the renin-angiotensin-aldos-terone axis and increased efferent renal sympathetic nerve activity (ERSNA). The most important natriuretic mechanism is pressure natriuresis, because the level of renal perfusion pressure (RPP) determines the magnitude of the response to all other natriuretic systems. Renal interstitial hydrostatic pressure (RIHP) is a link between the circulation and renal tubular sodium reabsorption. Atrial natriuretic peptide (ANP) is the major systemic natriuretic hormone. Within the kidney, kinins and renomedullary prostaglandins are important modulators of the natriuretic response of the kidney. AVP—arginine vasopressin; FF—filtration fraction. (Modified from Gonzalez-Campoy and Knox [7].)


Overview of the renin-angiotensin-aldosterone system [8,9]. Angiotensinogen (or renin substrate) is a 56-kD glycoprotein produced and secreted by the liver. Renin is produced by the juxtaglomerular apparatus of the kidney, as shown in Figures 2-8 and 2-9. Renin cleaves the 10 N-terminal amino acids from angiotensinogen. This decapeptide (angiotensin I) is cleaved by angiotensin converting enzyme (ACE). The resulting angiotensin II comprises the 8 N-terminal amino acids of angiotensin I. The primary amino acid structures of angiotensins I and II are shown in single letter codes. Angiotensin II increases systemic vascular resistance (SVR), stimulates aldosterone secretion from the adrenal gland (indicated in gray), and increases sodium (Na) absorption by renal tubules, as shown in Figures 2-15 and 2-17. These effects decrease urinary Na (and chloride excretion; UNaV).

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