α2-Adrenergic-mediated inhibition of water and urea permeability in the rat IMCD

Alexander J. Rough, Lúcia H. Kudo

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

These studies were conducted to determine whether the ag-agonists epinephrine and dexmedetomidine inhibit osmotic water permeability (Pf) and urea permeability (Pu) in the rat inner medullary collecting duct (IMCD). Wistar rat IMCD segments were perfused via standard methods, and Pf and Pu were determined in separate studies. The control period was followed by adding 220 pM arginine vasopressin (AVP) or 10-4 M dibutyryladenosine 3′,5′-cyclic monophosphate (DBcAMP) to the bath. Epinephrine or dexmedetomidine, both at 1 μM, was then added to the bath, and this period was followed by adding 1 μM atipamezole, a selective α2-antagonist. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine was present in all experiments with DBcAMP. Epinephrine inhibited AVP- and DBcAMP-stimulated Pf by 90% and 80%, respectively. Dexmedetomidine inhibited AVP- and DBcAMP-stimulated Pf by 98% and 97%, respectively. Epinephrine inhibited AVP- and DBcAMP-stimulated Pu by 70% and 60%, respectively. Dexmedetomidine failed to affect Pu. Atipamezole reversed all inhibitory effects. These data confirm an α2-mediated mechanism in the IMCD that modulates Pf and Pu, and they indicate that inhibition occurs via post-cAMP cellular events.

Original languageEnglish
Pages (from-to)F150-F157
JournalAmerican Journal of Physiology
Volume271
Issue number1 PART 2
StatePublished - 1 Dec 1996

Fingerprint

Bucladesine
Dexmedetomidine
Adrenergic Agents
Arginine Vasopressin
Urea
Permeability
Epinephrine
Water
Baths
Phosphodiesterase 3 Inhibitors
Wistar Rats

Keywords

  • 5′-cyclic monophosphate
  • Arginine vasopressin
  • Atipamezole
  • Dexmedetomidine
  • Dibutyryladenosine 3′
  • Epinephrine
  • Terminal inner medullary collecting duct
  • α-adrenoceptor

Cite this

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abstract = "These studies were conducted to determine whether the ag-agonists epinephrine and dexmedetomidine inhibit osmotic water permeability (Pf) and urea permeability (Pu) in the rat inner medullary collecting duct (IMCD). Wistar rat IMCD segments were perfused via standard methods, and Pf and Pu were determined in separate studies. The control period was followed by adding 220 pM arginine vasopressin (AVP) or 10-4 M dibutyryladenosine 3′,5′-cyclic monophosphate (DBcAMP) to the bath. Epinephrine or dexmedetomidine, both at 1 μM, was then added to the bath, and this period was followed by adding 1 μM atipamezole, a selective α2-antagonist. The phosphodiesterase inhibitor 3-isobutyl-l-methylxanthine was present in all experiments with DBcAMP. Epinephrine inhibited AVP- and DBcAMP-stimulated Pf by 90{\%} and 80{\%}, respectively. Dexmedetomidine inhibited AVP- and DBcAMP-stimulated Pf by 98{\%} and 97{\%}, respectively. Epinephrine inhibited AVP- and DBcAMP-stimulated Pu by 70{\%} and 60{\%}, respectively. Dexmedetomidine failed to affect Pu. Atipamezole reversed all inhibitory effects. These data confirm an α2-mediated mechanism in the IMCD that modulates Pf and Pu, and they indicate that inhibition occurs via post-cAMP cellular events.",
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α2-Adrenergic-mediated inhibition of water and urea permeability in the rat IMCD. / Rough, Alexander J.; Kudo, Lúcia H.

In: American Journal of Physiology, Vol. 271, No. 1 PART 2, 01.12.1996, p. F150-F157.

Research output: Contribution to journalArticle

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