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FIGURE 3 Renin secretion and the regulation of ECF volume and blood pressure. Renin is secreted by JG cells in the afferent arteriole in response to reductions in blood pressure, ECF volume, and GFR. Blood pressure is sensed directly by stretch receptors in the afferent arteriole. Decreased stretch results in a fall in intracellular Ca2+ and increased renin release. Renin secretion is also activated by increases in cAMP produced by increased sympathetic nerve input and circulating catecholamines, and by ATP and/or adenosine from macula densa cells. Elevated plasma angiotensin II produced by the release of renin acts to restore ECF volume and blood pressure by increasing Na+ reabsorption through two mechanisms. Angiotensin II has a direct effect on proximal tubular cells to increase Na+ reabsorption and stimulates the release of aldosterone from the adrenal cortex, which in turn increases Na+ reabsorption by the aldosterone-responsive distal nephron.

FIGURE 3 Renin secretion and the regulation of ECF volume and blood pressure. Renin is secreted by JG cells in the afferent arteriole in response to reductions in blood pressure, ECF volume, and GFR. Blood pressure is sensed directly by stretch receptors in the afferent arteriole. Decreased stretch results in a fall in intracellular Ca2+ and increased renin release. Renin secretion is also activated by increases in cAMP produced by increased sympathetic nerve input and circulating catecholamines, and by ATP and/or adenosine from macula densa cells. Elevated plasma angiotensin II produced by the release of renin acts to restore ECF volume and blood pressure by increasing Na+ reabsorption through two mechanisms. Angiotensin II has a direct effect on proximal tubular cells to increase Na+ reabsorption and stimulates the release of aldosterone from the adrenal cortex, which in turn increases Na+ reabsorption by the aldosterone-responsive distal nephron.

receptor isoforms, drug development is focusing on specific receptor blockers that may differentiate, for example, between vascular and adrenal cortical angio-tensin II receptors.

Natriuretic Hormones

The idea that there might be a circulating natriuretic hormone came from classical animal experiments in which both the GFR and plasma aldosterone concentration were kept constant during the infusion of isotonic saline. Despite the absence of changes in GFR or aldosterone levels, the infusion resulted in a natriuresis. In parallel experiments, it was found that a small volume of plasma from a volume-expanded animal produced natriuresis in a second animal that had not been volume expanded and in which GFR and aldosterone were held constant. Thus, it was proposed that a third factor (i.e., in addition to changes in GFR and aldosterone) must be involved in the regulation of Na+ excretion—a natriure-tic hormone that was released in response to volume expansion and caused decreased reabsorption of salt and water. It now appears that there are two classes of natriuretic factors, peptide hormones and ouabain-like factors.

After two decades of trial and error, evidence for the first natriuretic factor, which was called atrial natriuretic peptide (ANP), was published in 1980. It was subsequently found that the circulating form of ANP is a 28-amino-acid peptide with a molecular weight of about 3000 Da, and radioimmunoassays indicate a normal circulating concentration in the human of 3-5 pM. ANP is stored in granules in the myocytes of the left and right atria and is released in response to increased atrial filling, which occurs with extracellular volume expansion. Similar peptides are also produced by the brain, the heart, and the kidney, the latter being called urodilatin. When ANP is given in pharmacologic doses, rapid and marked natriuresis is observed, but the physiologic role of ANP has been questioned. It appears that physiologic concentrations of ANP can produce a natriuresis only in the presence of true ECF volume expansion, and then produce only a three- to fivefold increase in Na+ excretion. Furthermore, the permissive volume expansion must be sufficient to elevate the blood pressure and/or renal blood flow. It is for this reason that ANP is ineffective in counteracting the volume expansion in functional hypovolemia.

The effects of ANP on the kidney are due to a small increase in GFR that, for the reasons discussed earlier, would automatically increase Na+ excretion and inhibit Na+ reabsorption in the inner medullary collecting duct. The increase in GFR may be due to a slight increase in the ultrafiltration coefficient (Kf), accompanied by an increase in efferent arteriolar resistance with or without an increase in afferent arteriolar resistance. Receptors for ANP are also present in many areas of the brain, and they may have other effects through neural efferent arcs. ANP also causes a decrease in renin release, which promotes natriuresis.

There appears to be a second type of natriuretic factor that is biochemically almost identical to ouabain, which is a member of the class of drugs referred to as cardiac glycosides. There is evidence that this ouabain-like factor (OLF) is synthesized and released by the brain and/or by the adrenal cortex in response to expansion of the ECF volume. (Because the cardiac glycosides are structurally quite similar to steroids, the latter site seems plausible.) It is proposed that OLF, as all cardiac glycosides, is an Na+,K+-ATPase inhibitor and thereby decreases Na+ reabsorption, possibly in all segments of the nephron.

these hormones have primary actions in other organ systems, and their effects on proximal tubular reabsorption may be relatively slow in onset and not directly related to changes in ECF balance. The main regulators of proximal tubular volume reabsorption appear to be the renal nerves, the renin-angiotensin system, and the Starling forces that are responsible for the uptake of reabsorbed fluid into the peritubular capillaries.

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