Effect of quinidine on Na, H+, and water transport by the turtle and toad bladders

Abstract

The effect of quinidine on Na and H+ transport by the turtle bladder and water transport by the toad bladder was examined. Quinidine inhibited the short-circuit current and the potential difference in a dose-dependent fashion. The effect of quinidine on the short-circuit was not dependent on extracellular calcium concentration and was not reversible with removal of the drug. Quinidine inhibited H+ secretion in a dose-dependent fashion. The effect of quinidine on H+ secretion also was not dependent on extracellular calcium concentration and was not reversible, either with removal of the drug or with stimulation of H+ secretion with 5% CO2. The effect of quinidine on Na or H+ transport could not be elicited by an equivalent dose of tetracaine, suggesting that the inhibitory effect of quinidine is not dependent on its anesthetic properties. Quinidine also inhibited vasopressin and cyclic AMP stimulated water flow in the toad bladder. Quinidine did not alter calcium uptake by the turtle bladder but increased calcium efflux by the turtle and toad bladders. These observations suggest that a rise in cytosolic calcium is responsible for the inhibitory effect of quinidine on Na, H+, and water transport.

Roles of Ca2+ and Na+ on the modulation of antidiuretic hormone action on urea permeability in toad urinary bladder.

“…Quinidine does not increase Ca2+ uptake by the cells, but increases cytosolic Ca2+ activity by inducing its release from intracellular pools (14). We have confirmed these assertions in isolated epithelial cells of toad urinary bladder using Quin-2 and chlorotetracycline as fluorescent probes of intracellular Ca2+ activity (see above): quinidine decreases Ca2+ activity in intracellular organelles and elicits a large and sustained increase in cytosolic Ca2+ activity (Hardy, M. A., W. Jy, and D. H. Haynes, unpublished results).…”

“…These agents increase cytosolic Ca2+ activity by releasing Ca2+ from, and decreasing its uptake by, intracellular stores (14,17,19,(20)(21)(22)(23). Metabolic inhibitors may additionally increase cellular Ca2+ activity by depressing Ca2" extrusion across the plasma membrane (21).…”

“…Extensive studies have been done on the cationic requirements of the effect of ADH on water permeability (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). Different maneuvers dissociate the effect of ADH on the apical permeation pathways for water and urea (1)(2)(3)(4).…”

Physiological role of apical potassium ion channels in frog skin.

“…Recently, it has been shown that the addition of quinidine to the serosal medium (4 x 10-4 M) ofthe isolated urinary bladder impairs Na+ transport through this epithelium (Taylor & Windhager, 1979;Windhager & Taylor, 1983;Arruda, 1983). The reduction of Na+ transport is associated with an increase of Ca2+ release (Arruda & Sabatini, 1980). It was therefore suggested that quinidine causes a release of Ca2+ from intracellular organelles, thus increasing cytosolic Ca2+ concentration which is responsible for the reduction of Na+ transport.…”

Biochemistry and Pathophysiology of Vanadium

“…Whether N a+-K + ATPase activation is involved in microtubule function is not known, but in some tissues, N a+-K + ATPase inhibition decreases the rate of N a/C a exchange increasing cytosolic calcium. A rise in cytosolic calcium in the toad bladder, regardless of the mechanism, results in the inhibition of vasopressin-stimulated water flow [82][83][84],…”