Cyclic AMP inhibits Na+/H+ exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss, Luis

doi:10.1085/jgp.85.3.409

Cited by 106 publications

(46 citation statements)

References 28 publications

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“…However, this was never the case in the present study: i.e., the cytosol pH was usually raised by db-cAMP (Table 6). Similarly, REUSS and PETERSEN (1985) found that in gallbladder epithelium of Necturus, the intracellular pH was elevated for the first 2 min but lowered by about 0.1 pH with theophylline application for several minutes. Although they explained that pH elevation was not due to cAMP, but to the effect of the drug entry of theophylline (pKa = 8.8), our data showed that cytosol alkalosis was induced without theophylline application.…”

Section: Discussionmentioning

confidence: 72%

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

et al. 1988

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Using a direct cellular micropuncture technique with doublebarreled ion-selective microelectrodes, we investigated the effect of dibutyryl-cyclic AMP (db-cAMP) on the membrane potential and the transport of Na +, K +, and H + in doubly-perfused bullfrog proximal tubules. The peritubular membrane potential difference (EM) and the intracellular K+, Na+ activities ((K);, (Na);) or intracellular and luminal pH were monitored continuously after peritubular administration of dbcAMP (10-3-10-4 M). Results: 1) db-cAMP hyperpolarized the EM by 8.0 mV with an increase of (K); by 4.8 mEq/l; 2) the peritubular administration of high K + (13.5 and 50 mM) solutions depolarized the EM by 11.5 and 41.5 mV, respectively. The high K + perfusate with db-cAMP produced a depolarization to the same level as that in simple high K + perfusion without db-cAMP; 3) db-cAMP transiently blocked the luminal acidification concomitantly with a cellular alkalinization by about 0.1 pH; and 4) db-cAMP caused a decrease of (Na); by 5.0 mEq/l. Conclusions: 1) cAMP causes an increase of K+ permeability in the peritubular membrane; 2) cAMP induces a cytosol alkalosis by enhancing incorporation of H+ into the subcellular vesicles, thus favoring the activation of Na+/K+ pump; and 3) cAMP, in effect, suppresses the Na+/H+ exchange mechanism in the luminal membrane and transiently blocks the proximal urinary acidification.

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Section: Discussionmentioning

confidence: 72%

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

et al. 1988

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“…Necturus gallbladder (33). However, whether cAMP inhibits apical Na'-H' exchange in the medullary thick ascending limb has not been determined.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of bicarbonate absorption by peptide hormones and cyclic adenosine monophosphate in rat medullary thick ascending limb.

Good

1990

J. Clin. Invest.

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In vitro microperfusion experiments were performed to examine the effects of peptide hormones on bicarbonate and ammonium transport by the medullary thick ascending limb (MTAL) of the rat. Arginine vasopressin (AVP, 2.8 X 10-10 M in the bath) reduced bicarbonate absorption by 50% (from 7.8 to 3.7 pmol/min per mm). AVP caused a similar reduction in bicarbonate absorption in tubules perfused with i0' M furosemide to inhibit net NaCI absorption. Glucagon (2 X 10' M in the bath) also reduced bicarbonate absorption (from 11.7 to 7.6 pmol/min per mm). The inhibition of bicarbonate absorption could be reproduced with either exogenous 8-bromocAMP or forskolin. With 8-bromo-cAMP (i0-3 M) in the bath, addition of vasopressin to the bath did not significantly affect bicarbonate absorption. PTH significantly inhibited bicarbonate absorption, but the extent of inhibition was less than that observed with either AVP or glucagon. Vasopressin had no effect on net ammonium absorption in MTAL perfused and bathed with 4 mM NH4C1. These findings indicate that: (a) vasopressin, glucagon, and PTH directly inhibit bicarbonate absorption in the MTAL of the rat; (b) this inhibition occurs independent of effects on net NaCI absorption and appears to be mediated in part by cAMPF, and (c) HCO3 and NW absorption can be regulated independently in the MTAL. (J.

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“…Maximal doses of 8-bromo-CAMP, of the phosphodiesterase inhibitor theophylline, or of the adenylate cyclase activator forskolin inhibited Na'/H' exchange by~50% . The effect involved a decrease in the V.,, of the exchanger (Reuss and Petersen, 1985).…”

Section: Introductionmentioning

confidence: 99%

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

Reuss

1987

The Journal of General Physiology

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Intracellular microelectrode techniques were employed to study the effect of cyclic AMP on apical membrane Ci-/HCOi exchange and electrodiffusive HCOi transport in Necturus gallbladder epithelium, lntracellular cAMP levels were raised by addition of either the phosphodiesterase inhibitor theophyiline (3 x 10 -s M) or the adenylate cyclase activator forskolin (10 -5 M) to the serosal bathing solution. Measurements of pH in a poorly buffered control mucosal solution upon stopping superfusion show acidification, owing to secretion of both H + and HCOL When the same experiment is performed after addition of amiloride or removal of Na + from the mucosal bathing medium, alkalinization is observed since H + transport is either inhibited or reversed, whereas HCOi secretion persists. The changes in pH in both amiloride or Na-free medium were significantly decreased in theophylline-treated tissues. Theophylline had no effect on the initial rates of fall of intracellular CIactivity (aCl 0 upon reducing mucosal solution [CI-] to either 10 or 0 mM, although membrane voltage and resistance measurements were consistent with stimulation of apical membrane electrodiffusive CI-permeability. Estimates of the conductive flux, obtained by either reducing simultaneously mucosal [CI-] and [HCOg] or lowering [C1-] alone in the presence of a blocker of anion exchange (diphenylamine-2-carboxylate), indicate that elevation of intracellular cAMP inhibited the anion exchanger by ~50%. Measurements of net CI-uptake upon increasing mucosal C1-from nominally zero to levels ranging from 2.5 to 100 mM suggest that the mechanism of inhibition is a decrease in Vmax. Consistent with these results, the rate of intracellular alkalinization upon reducing external C1-was also inhibited significantly by theophylline. Reducing mucosal solution [HCO~] from 10 to 1 mM under control conditions caused intracellular acidification and an increase in aCll. Theophylline inhibited both changes, by 62 and 32%, respectively. These data indicate that elevation of intracellular cAMP inhibits apical membrane anion (CI-/HCOg) exchange. Studies of the effects of rapid changes in mucosal [HCOg] on membrane voltages and the apparent ratio of membrane resistances, both in the presence and in Address reprint requests to Dr.

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Cyclic AMP inhibits Na+/H+ exchange at the apical membrane of Necturus gallbladder epithelium.

Cited by 106 publications

References 28 publications

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

The effect of cAMP on ion transport in the proximal tubular cells in bullfrog kidney.

Inhibition of bicarbonate absorption by peptide hormones and cyclic adenosine monophosphate in rat medullary thick ascending limb.

Cyclic AMP inhibits Cl-/HCO3- exchange at the apical membrane of Necturus gallbladder epithelium.

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