Na+ transport in isolated rat CCD: Effects of bradykinin, ANP, clonidine, and hydrochlorothiazide

Alexander J. Rough, L. U. Chen, Susan L. Troutman, James A. Schafer

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We examined the effects of bradykinin (BK), atrial natriuretic peptide (ANP), hydrochlorothiazide (HCTZ), and clonidine on Na+ transport in isolated perfused cortical collecting ducts from rats treated with deoxycorticosterone. Arginine vasopressin was present in the bathing solution at 220 pM. Clonidine (1 μM, bathing solution) depolarized transepithelial potential difference (PDT) from -11.9 ± 2.0 (SE) to -7.4 ± 1.7 mV (P < 0.001), hyperpolarized basolateral membrane potential difference (PDbl) from -85 ± 1 to -87 ± l mV (P < 0.01), and increased the fractional resistance of the apical membrane (FA.) from 0.81 ± 0.02 to 0.86 ± 0.02 (P < 0.03), indicating that it inhibited the Na+ conductance of the luminal membrane. BK (1 or 10 nM) or ANP (10 nM) in the bathing solution had no effect on PDT, PDbl, or FRa. BK, ANP, or 0.1 mM luminal HCTZ also had no effect on lumen-to-bath 22Na+ flux (Jl→b), whereas we showed previously that clonidine inhibits Jl→b by 30% (L. Chen, M. Paris, S. K. Williams, M. C. Reif, and J. A. Schafer. Kidney Int. 37: 366, 1990). Luminal addition of Na+ channel blockers amiloride (10 μM) or benzamil (1 μM) reduced Jl→b, to a level not significantly different from bath-to-lumen 22Na+ flux measured previously (M. Reif, S. L. Troutman, and J. A. Schafer. J. Clin. Invest. 77:1291-1298,1986), and neither BK nor HCTZ had any further effect. These results show that transcellular Na+ transport occurs exclusively through the apical membrane amiloride-sensitive channel, and this conductance is inhibited by clonidine but not by BK, ANP, or HCTZ.

Original languageEnglish
Pages (from-to)F86-F95
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number1 29-1
StatePublished - 1991


  • Adrenergic agonist
  • Cortical collecting duct
  • Electrophysiology
  • Sodium channel
  • Sodium chloride cotransport
  • Sodium reabsorption


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