Inhibition by epinephrine of AVP- and cAMP-stimulated Na+ and water transport in Dahl rat CCD

C. T. Hawk, L. H. Kudo, A. J. Rouch, J. A. Schafer

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

We examined the effects of epinephrine in perfused cortical collecting ducts (CCD) isolated from inbred Dahl-Rapp salt-sensitive (SS) and salt- resistant (SR) rats and from Sprague-Dawley (SD) rats. Rats were treated with 2.5 mg deoxycorticosterone pivalate (DOC; depot injection 4-9 days before study), and the CCD were treated with 220 pM vasopressin (AVP) to maximize Na+ transport. In CCD from all three strains 10 μM epinephrine in the bathing solution completely inhibited net Na+ transport, osmotic water permeability (P(f)), and transepithelial voltage. In the SS CCD, epinephrine increased the fractional resistance of the luminal membrane to the same extent as 10 μM amiloride, indicating that it blocked the amiloride- sensitive conductance of the luminal membrane. Even at 100 nM epinephrine inhibited 80-100% of Na+ and water transport, and 1 μM yohimbine reversed or prevented these effects. In SS CCD, 0.1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) plus 0.1 mM 3-isobutyl-1-methylxanthine in place of AVP increased lumen-to-bath Na+ flux (J(1-b)) from 56 ± 5 to 143 ± 3 pmol · min-1 · mm-1 and P(f) from 6 ± 12 to 1067 ± 152 μm/s, but 100 nM epinephrine still significantly inhibited cAMP-stimulated J(1-b) and P(f) by 40 ± 5% and 31 ± 9%, respectively. Similar results were observed in the SR and SD rat CCD; however, the ability of yohimbine to reverse the epinephrine effect on cAMP-dependent transport was variable among the rat strains. We conclude that epinephrine acts via an α2-receptor to inhibit adenylate cyclase but that at least one additional intracellular second messenger system may be involved.

Original languageEnglish
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume265
Issue number3 34-3
StatePublished - 1 Jan 1993

Fingerprint

Inbred Dahl Rats
Epinephrine
Water
Salts
Yohimbine
Amiloride
Second Messenger Systems
Sprague Dawley Rats
8-Bromo Cyclic Adenosine Monophosphate
1-Methyl-3-isobutylxanthine
Desoxycorticosterone
Membranes
Vasopressins
Baths
Adenylyl Cyclases
Permeability
Injections

Keywords

  • α-adrenergic receptors
  • 3-isobutyl-1- methylxanthine
  • antidiuretic hormone
  • cortical collecting duct
  • forskolin
  • hypertension
  • mineralocorticoids
  • salt sensitivity
  • Sprague-Dawley rat
  • vasopressin
  • yohimbine

Cite this

@article{535c4d47cf48452b99ed3501b30cf909,
title = "Inhibition by epinephrine of AVP- and cAMP-stimulated Na+ and water transport in Dahl rat CCD",
abstract = "We examined the effects of epinephrine in perfused cortical collecting ducts (CCD) isolated from inbred Dahl-Rapp salt-sensitive (SS) and salt- resistant (SR) rats and from Sprague-Dawley (SD) rats. Rats were treated with 2.5 mg deoxycorticosterone pivalate (DOC; depot injection 4-9 days before study), and the CCD were treated with 220 pM vasopressin (AVP) to maximize Na+ transport. In CCD from all three strains 10 μM epinephrine in the bathing solution completely inhibited net Na+ transport, osmotic water permeability (P(f)), and transepithelial voltage. In the SS CCD, epinephrine increased the fractional resistance of the luminal membrane to the same extent as 10 μM amiloride, indicating that it blocked the amiloride- sensitive conductance of the luminal membrane. Even at 100 nM epinephrine inhibited 80-100{\%} of Na+ and water transport, and 1 μM yohimbine reversed or prevented these effects. In SS CCD, 0.1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) plus 0.1 mM 3-isobutyl-1-methylxanthine in place of AVP increased lumen-to-bath Na+ flux (J(1-b)) from 56 ± 5 to 143 ± 3 pmol · min-1 · mm-1 and P(f) from 6 ± 12 to 1067 ± 152 μm/s, but 100 nM epinephrine still significantly inhibited cAMP-stimulated J(1-b) and P(f) by 40 ± 5{\%} and 31 ± 9{\%}, respectively. Similar results were observed in the SR and SD rat CCD; however, the ability of yohimbine to reverse the epinephrine effect on cAMP-dependent transport was variable among the rat strains. We conclude that epinephrine acts via an α2-receptor to inhibit adenylate cyclase but that at least one additional intracellular second messenger system may be involved.",
keywords = "α-adrenergic receptors, 3-isobutyl-1- methylxanthine, antidiuretic hormone, cortical collecting duct, forskolin, hypertension, mineralocorticoids, salt sensitivity, Sprague-Dawley rat, vasopressin, yohimbine",
author = "Hawk, {C. T.} and Kudo, {L. H.} and Rouch, {A. J.} and Schafer, {J. A.}",
year = "1993",
month = "1",
day = "1",
language = "English",
volume = "265",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "0002-9513",
publisher = "American Physiological Society",
number = "3 34-3",

}

Inhibition by epinephrine of AVP- and cAMP-stimulated Na+ and water transport in Dahl rat CCD. / Hawk, C. T.; Kudo, L. H.; Rouch, A. J.; Schafer, J. A.

In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 265, No. 3 34-3, 01.01.1993.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inhibition by epinephrine of AVP- and cAMP-stimulated Na+ and water transport in Dahl rat CCD

AU - Hawk, C. T.

AU - Kudo, L. H.

AU - Rouch, A. J.

AU - Schafer, J. A.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - We examined the effects of epinephrine in perfused cortical collecting ducts (CCD) isolated from inbred Dahl-Rapp salt-sensitive (SS) and salt- resistant (SR) rats and from Sprague-Dawley (SD) rats. Rats were treated with 2.5 mg deoxycorticosterone pivalate (DOC; depot injection 4-9 days before study), and the CCD were treated with 220 pM vasopressin (AVP) to maximize Na+ transport. In CCD from all three strains 10 μM epinephrine in the bathing solution completely inhibited net Na+ transport, osmotic water permeability (P(f)), and transepithelial voltage. In the SS CCD, epinephrine increased the fractional resistance of the luminal membrane to the same extent as 10 μM amiloride, indicating that it blocked the amiloride- sensitive conductance of the luminal membrane. Even at 100 nM epinephrine inhibited 80-100% of Na+ and water transport, and 1 μM yohimbine reversed or prevented these effects. In SS CCD, 0.1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) plus 0.1 mM 3-isobutyl-1-methylxanthine in place of AVP increased lumen-to-bath Na+ flux (J(1-b)) from 56 ± 5 to 143 ± 3 pmol · min-1 · mm-1 and P(f) from 6 ± 12 to 1067 ± 152 μm/s, but 100 nM epinephrine still significantly inhibited cAMP-stimulated J(1-b) and P(f) by 40 ± 5% and 31 ± 9%, respectively. Similar results were observed in the SR and SD rat CCD; however, the ability of yohimbine to reverse the epinephrine effect on cAMP-dependent transport was variable among the rat strains. We conclude that epinephrine acts via an α2-receptor to inhibit adenylate cyclase but that at least one additional intracellular second messenger system may be involved.

AB - We examined the effects of epinephrine in perfused cortical collecting ducts (CCD) isolated from inbred Dahl-Rapp salt-sensitive (SS) and salt- resistant (SR) rats and from Sprague-Dawley (SD) rats. Rats were treated with 2.5 mg deoxycorticosterone pivalate (DOC; depot injection 4-9 days before study), and the CCD were treated with 220 pM vasopressin (AVP) to maximize Na+ transport. In CCD from all three strains 10 μM epinephrine in the bathing solution completely inhibited net Na+ transport, osmotic water permeability (P(f)), and transepithelial voltage. In the SS CCD, epinephrine increased the fractional resistance of the luminal membrane to the same extent as 10 μM amiloride, indicating that it blocked the amiloride- sensitive conductance of the luminal membrane. Even at 100 nM epinephrine inhibited 80-100% of Na+ and water transport, and 1 μM yohimbine reversed or prevented these effects. In SS CCD, 0.1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) plus 0.1 mM 3-isobutyl-1-methylxanthine in place of AVP increased lumen-to-bath Na+ flux (J(1-b)) from 56 ± 5 to 143 ± 3 pmol · min-1 · mm-1 and P(f) from 6 ± 12 to 1067 ± 152 μm/s, but 100 nM epinephrine still significantly inhibited cAMP-stimulated J(1-b) and P(f) by 40 ± 5% and 31 ± 9%, respectively. Similar results were observed in the SR and SD rat CCD; however, the ability of yohimbine to reverse the epinephrine effect on cAMP-dependent transport was variable among the rat strains. We conclude that epinephrine acts via an α2-receptor to inhibit adenylate cyclase but that at least one additional intracellular second messenger system may be involved.

KW - α-adrenergic receptors

KW - 3-isobutyl-1- methylxanthine

KW - antidiuretic hormone

KW - cortical collecting duct

KW - forskolin

KW - hypertension

KW - mineralocorticoids

KW - salt sensitivity

KW - Sprague-Dawley rat

KW - vasopressin

KW - yohimbine

UR - http://www.scopus.com/inward/record.url?scp=0027381050&partnerID=8YFLogxK

M3 - Article

C2 - 8105698

AN - SCOPUS:0027381050

VL - 265

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

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

SN - 0002-9513

IS - 3 34-3

ER -