Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of prostaglandin (PG) E2 on cell swelling were studied in isolated perfused tubules of rabbit kidney. PGE2 (1 microM) added to the bath induced cell swelling by 13.4, 7.2, and 9.6% in the connecting tubule, distal convoluted tubule, and cortical collecting duct, respectively, but it had no effect on the proximal convoluted tubule and cortical thick ascending limb. The response was dose dependent in the range of 1 nM to 1 microM. PGI2 exerted a similar effect, but PGF2 alpha had no effect. The swelling was completely blocked by basolateral Na+ removal and was attenuated by bilateral Cl- removal, suggesting that the swelling was mediated by basolateral Na+ entry in association with Cl- entry. In all segments except proximal tubule, PGE2 caused an initial transient peak followed by a sustained increase in intracellular Ca2+. Intracellular Ca2+ chelation or inhibition of Ca2+ release from intracellular stores abolished the PGE2-induced cell swelling, but extracellular Ca2+ removal did not. An inhibitor of the Na(+)-Ca2+ exchanger (3',4'-dichlorobenzamil, 100 microM) in the bath completely inhibited PGE2-induced cell swelling. Neither furosemide (1 mM) nor amiloride (1 mM) added to bath abolished the response, indicating that neither Na(+)-K(+)-2Cl- cotransport nor Na(+)-H+ exchange is involved in the action of PGE2. The swelling response to PGE2 was observed even in the presence of ouabain, indicating that the effect of PGE2 is independent of Na(+)-K(+)-adenosinetriphosphatase inhibition. Nicardipine added to bath partially inhibited the swelling response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of PGE2-induced cell swelling in distal nephron segments. 133 3

Calcium channel blockers have diuretic and natriuretic properties in normal animals and humans. The renal mechanism by which this natriuresis is produced has not yet been completely defined although dihydropyridine derivatives evoke it in experimental animals independently of any effects on renal blood flow or on the glomerular filtration rate. Injections or infusions into the renal artery indicate that the renal excretory effect is secondary to a direct action on renal tubular water and solute reabsorption but not to renal hemodynamic changes. Studies undertaken to localize the site of action of dihydropyridine calcium antagonists on renal tubules by renal clearance and micropuncture techniques suggest that both proximal and distal tubular sites are involved. Primary sites of action in distal convoluted tubules and in the collecting duct have been identified for felodipine and nisoldipine during sodium infusion, whereas sites for nitrendipine in proximal tubules have been demonstrated in strict hydropenia. Both changes in the tubuloglomerular feedback setting and suppression of aldosterone secretion have been proposed to explain some of these effects. The changes do not, however, seem to be dependent on renal innervation. In normal humans, the degree and duration of natriuresis and diuresis correlate with the dose of dihydropyridine derivatives and the extent of systemic pressure reduction. Clearance studies of normal subjects indicate an effect of different dihydropyridine derivatives on tubular fluid and electrolyte reabsorption. Nicardipine and nifedipine are reported to exert proximal tubular actions based either on urate and phosphate excretion or water and lithium clearance. The measurement of tubular indices following felodipine administration suggests a proximal tubular site of action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular effects of calcium antagonists. 161 68