22 February 2002
Regulation of renal tubular sodium transport by cardiac natriuretic peptides:two decades of research.Jerzy Bełtowski, Grazyna Wójcicka
Med Sci Monit 2002; 8(2): RA39-52 :: ID: 420919
This review presents the current state of our knowledge regarding the regulationof renal tubular sodium transport by natriuretic peptides, with special emphasis on recent findings inthis field. Natriuretic peptides constitute a complex system involved in the regulation of sodium balanceand blood pressure. The natriuretic peptide family consists of atrial peptides, such as atrial natriureticfactor (ANF, ANP(99-126)), long-acting natriuretic peptide (ANP(1-30)), vessel dilator (ANP(31-67)) andkaliuretic peptide (ANP(79-98)), as well as brain or B-type natriuretic peptide (BNP), C-type natriureticpeptide (CNP) and urodilatin. Natriuretic peptides act on target cells through A-type and B-type receptorsand stimulate cyclic GMP synthesis. ANF stimulates natriuresis mainly by inhibiting sodium reabsorptionin the inner medullary collecting duct. The effect results from coordinate inhibition of apical sodiumchannels and basolateral Na+, K+-ATPase. Additional effects on sodium transport occur in more proximalnephron segments and on glomerular filtration when hormone concentration is elevated. BNP and urodilatinshare the same mechanism of action. CNP synthetized in several nephron segments acts through specificB-type natriuretic peptide receptors, which are also expressed in renal tubule, but have a differentdistribution than A-type receptors. ANP(1-30), ANP(31-67) and ANP(79-98) decrease Na+, K+-ATPase activityin tubular cells through a prostaglandin E2-dependent mechanism.
Keywords: Ion Transport, Kidney Tubules, Natriuretic Agents, Sodium
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