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Titolo:
REGULATION OF THE RENAL NA-HCO3 COTRANSPORTER .7. MECHANISM OF THE CHOLINERGIC STIMULATION
Autore:
RUIZ OS; QIU YY; CARDOSO LR; ARRUDA JAL; WANG LJ;
Indirizzi:
UNIV ILLINOIS,DEPT MED,NEPHROL SECT,820 S WOOD ST CHICAGO IL 60612 UNIV ILLINOIS,DEPT MED,NEPHROL SECT CHICAGO IL 60612 VET ADM W SIDE MED CTR CHICAGO IL 60680
Titolo Testata:
Kidney international
fascicolo: 4, volume: 51, anno: 1997,
pagine: 1069 - 1077
SICI:
0085-2538(1997)51:4<1069:ROTRNC>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROXIMAL CONVOLUTED TUBULE; PROTEIN-KINASE-C; NA-H ANTIPORTER; RESPIRATORY-ACIDOSIS; TRANSPORT; GLUCOCORTICOIDS; MODULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
23
Recensione:
Indirizzi per estratti:
Citazione:
O.S. Ruiz et al., "REGULATION OF THE RENAL NA-HCO3 COTRANSPORTER .7. MECHANISM OF THE CHOLINERGIC STIMULATION", Kidney international, 51(4), 1997, pp. 1069-1077

Abstract

Cholinergic agents regulate proximal tubule acidification but the mechanism responsible for this effect is unclear. We examined the effect of the cholinergic agent carbachol on the activity of the Na-HCO, cotransporter in primary cultures of the proximal tubule of the rabbit. The activity of the cotransporter was assayed either as HCO3-dependent Na-22 uptake or as the recovery of intracellular pH in cells perfused continuously with C1-free physiologic solution containing amiloride to block the Na-H antiporter. Carbachol caused a dose-dependent stimulation of the cotransporter activity with a maximum increase of 90% above control values at 10(-5) M and half maximal stimulation at 10(-7) M. The stimulation was blocked by atropine and pirenzepine indicating an effect through the M1 muscarinic receptor. Carbachol increased intracellular calcium fourfold and the rise in cytosolic calcium was preventedby the intracellular calcium chelator, BAPTA. BAPTA also blocked the effect of carbachol on the cotransporter. Because carbachol activates phospholipase C and protein kinase C, we examined the effect of carbachol in the presence of the phospholipase C inhibitor, U73122, or the PKC inhibitor, calphostin C, or PKC depletion. The phospholipase C inhibitor prevented both the effect of carbachol on the cotransporter and on the intracellular Ca. Calphostin C and PKC depletion also preventedthe stimulation of the cotransporter. Carbachol increased PKC activity and caused translocation of the PKC to the particulate fraction. We also examined the effect of the phosphatase inhibitor, calyculin A or the calmodulin kinase inhibitor, W-13 on carbachol stimulation. Calyculin A and W13 likewise prevented the carbachol-induced stimulation of the cotransporter. These results demonstrate that cholinergic stimulation modulated the activity of the cotransporter through multiple pathways including phospholipase C/PKC and phosphatase systems.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 13:27:11