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

Alexander Rouch, L. Chen, S. L. Troutman, J. A. Schafer

Research output: Contribution to journalArticle

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Abstract

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 (PD(T)) from -11.9 ± 2.0 (SE) to -7.4 ± 1.7 mV (P < 0.001), hyperpolarized basolateral membrane potential difference (PD(bl)) from -85 ± 1 to -87 ± 1 mV (P < 0.01), and increased the fractional resistance of the apical membrane (FR(a)) 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 PD(T), PD(bl), or FR(a). BK, ANP, or 0.1 mM luminal HCTZ also had no effect on lumen-to-bath 22Na+ flux (J(l→b)), whereas we showed previously that clonidine inhibits J(l→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 J(l→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
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume260
Issue number1 29-1
StatePublished - 1 Jan 1991

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Hydrochlorothiazide
Clonidine
Atrial Natriuretic Factor
Bradykinin
Membranes
Amiloride
Baths
Transcytosis
Desoxycorticosterone
Arginine Vasopressin
Membrane Potentials
Kidney

Keywords

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

Cite this

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title = "Na+ transport in isolated rat CCD: Effects of bradykinin, ANP, clonidine, and hydrochlorothiazide",
abstract = "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 (PD(T)) from -11.9 ± 2.0 (SE) to -7.4 ± 1.7 mV (P < 0.001), hyperpolarized basolateral membrane potential difference (PD(bl)) from -85 ± 1 to -87 ± 1 mV (P < 0.01), and increased the fractional resistance of the apical membrane (FR(a)) 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 PD(T), PD(bl), or FR(a). BK, ANP, or 0.1 mM luminal HCTZ also had no effect on lumen-to-bath 22Na+ flux (J(l→b)), whereas we showed previously that clonidine inhibits J(l→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 J(l→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.",
keywords = "Adrenergic agonist, Cortical collecting duct, Electrophysiology, Sodium channel, Sodium chloride cotransport, Sodium reabsorption",
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year = "1991",
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Na+ transport in isolated rat CCD : Effects of bradykinin, ANP, clonidine, and hydrochlorothiazide. / Rouch, Alexander; Chen, L.; Troutman, S. L.; Schafer, J. A.

In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 260, No. 1 29-1, 01.01.1991.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Na+ transport in isolated rat CCD

T2 - Effects of bradykinin, ANP, clonidine, and hydrochlorothiazide

AU - Rouch, Alexander

AU - Chen, L.

AU - Troutman, S. L.

AU - Schafer, J. A.

PY - 1991/1/1

Y1 - 1991/1/1

N2 - 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 (PD(T)) from -11.9 ± 2.0 (SE) to -7.4 ± 1.7 mV (P < 0.001), hyperpolarized basolateral membrane potential difference (PD(bl)) from -85 ± 1 to -87 ± 1 mV (P < 0.01), and increased the fractional resistance of the apical membrane (FR(a)) 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 PD(T), PD(bl), or FR(a). BK, ANP, or 0.1 mM luminal HCTZ also had no effect on lumen-to-bath 22Na+ flux (J(l→b)), whereas we showed previously that clonidine inhibits J(l→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 J(l→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.

AB - 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 (PD(T)) from -11.9 ± 2.0 (SE) to -7.4 ± 1.7 mV (P < 0.001), hyperpolarized basolateral membrane potential difference (PD(bl)) from -85 ± 1 to -87 ± 1 mV (P < 0.01), and increased the fractional resistance of the apical membrane (FR(a)) 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 PD(T), PD(bl), or FR(a). BK, ANP, or 0.1 mM luminal HCTZ also had no effect on lumen-to-bath 22Na+ flux (J(l→b)), whereas we showed previously that clonidine inhibits J(l→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 J(l→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.

KW - Adrenergic agonist

KW - Cortical collecting duct

KW - Electrophysiology

KW - Sodium channel

KW - Sodium chloride cotransport

KW - Sodium reabsorption

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M3 - Article

C2 - 1847013

AN - SCOPUS:0025972087

VL - 260

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 0002-9513

IS - 1 29-1

ER -