Ca2(+)-dependent inhibition of sodium transport in rabbit cortical collecting tubules.
Experiments were carried out to test whether maneuvers believed to increase intracellular Ca2+ concentration [( Ca2+]cell) inhibit Na transport in cortical collecting tubules (CCTs). Unidirectional Na efflux (JNa1----b) and Na influx (JNab----1) were measured isotopically in isolated perfused renal CCTs of rabbits. The animals were either untreated or pretreated with deoxycorticosterone (DOC) for 1-3 wk. To raise [Ca2+]cell, ionomycin or quinidine were added to, or [Na] reduced in, pertubular fluid. In control DOC-pretreated CCTs JNa1----b tended to saturate as luminal Na concentration was increased, reaching 22.9 +/- 1.2 pmol.cm-1.s-1 at 145 mM. In addition, in these CCTs, in contrast to non-DOC-treated tubules, the apical cell membrane was not found to be rate limiting for Na reabsorption as neither amphotericin B nor vasopressin further enhanced JNa1----b. In non-DOC-treated CCTs 10(-6) M ionomycin inhibited JNa1----b by 44.7%. When DOC-pretreated CCTs were exposed to either 10(-6)M ionomycin or 10(-4)M quinidine, JNa1----b was inhibited by 27 and 26%, respectively, while JNab----1 remained unchanged. This ionomycin-induced inhibition was Ca dependent. Exposure of DOC-pretreated CCTs to 5 mM Na-Ringer solution (Na replaced by choline or N-methyl-D-glucamine) for 30 min reduced JNa1----b by 18-30%. The inhibition of JNa1----b caused by any of the three maneuvers was fully reversed upon addition of amphotericin B to the luminal fluid. The results are consistent with the view that a sustained increase in [Ca2+]cell reduces Na transport by inhibition of the rate of Na+ entry across the apical cell membrane.
Frindt
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G
Department of Physiology, Cornell University Medical College, New York, New York 10021.
Windhager
E E
EE
D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology; D003900:Desoxycorticosterone / Q000494:pharmacology; D004553:Electric Conductivity; D015759:Ionomycin / Q000494:pharmacology; D007684:Kidney Tubules / Q000378:metabolism*; D007685:Kidney Tubules, Collecting / Q000378:metabolism* / Q000502:physiology / Q000648:ultrastructure; D009994:Osmolar Concentration; D011802:Quinidine / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology
D014667:Vasopressins; D003900:Desoxycorticosterone; D015759:Ionomycin; D000666:Amphotericin B; D012964:Sodium; D011802:Quinidine; D002118:Calcium