Figure 219

Cellular mechanism of the medullary collecting tubule (MCT). Sodium (Na) and water are reabsorbed along the MCT. Atrial natri-uretic peptide (ANP) is the best-characterized hormone that affects Na absorption along this segment [22]. Data on the effects of arginine vasopressin (AVP) and aldosterone are not as consistent [46,49]. Prostaglandin E2 (PGE2) inhibits Na transport by inner medullary collecting duct cells and may be an important intracellu-lar mediator for the actions of endothelin and interleukin-1 [50,51]. ANP inhibits medullary Na transport by interacting with a G-pro-tein-coupled receptor that generates cyclic guanosine monophosphate (cGMP). This second messenger inhibits a luminal Na channel that is distinct from the Na channel expressed by the principal cells of the cortical collecting tubule, as shown in Figure 2-18 [52,53]. Under normal circumstances, ANP also increases the glomerular filtration rate (GFR) and inhibits Na transport by way of the effects on the renin-angiotensin-aldosterone axis, as shown in Figures 2-7 to 2-10. These effects increase Na delivery to the MCT. The combination of increased distal Na delivery and inhibited distal reabsorption leads to natriuresis. In patients with congestive heart failure, distal Na delivery remains depressed despite high levels of circulating ANP. Thus, inhibition of apical Na entry does not lead to natri-uresis, despite high levels of MCT cGMP. AR—ANP receptor; GC—guanylyl cyclase; K—potassium; V2—receptors.

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