Angiotensin II stimulates water and NaCl intake through separate cell signalling pathways in rats

Exp Physiol. 2009 Jan;94(1):130-7. doi: 10.1113/expphysiol.2008.044446. Epub 2008 Aug 22.

Abstract

Angiotensin II (AngII) stimulation of water and NaCl intake is a classic model of the behavioural effects of hormones. In vitro studies indicate that the AngII type 1 (AT(1)) receptor stimulates intracellular pathways that include protein kinase C (PKC) and mitogen-activated protein (MAP) kinase activation. Previous studies support the hypotheses that PKC is involved in AngII-induced water, but not NaCl intake and that MAP kinase plays a role in NaCl consumption, but not water intake, after injection of AngII. The present experiments test these hypotheses in rats using central injections of AngII in the presence or absence of a PKC inhibitor or a MAP kinase inhibitor. Pretreatment with the PKC inhibitor chelerythrine attenuated AngII-induced water intake, but NaCl intake was unaffected. In contrast, pretreatment with U0126, a MAP kinase inhibitor, had no effect on AngII-induced water intake, but attenuated NaCl intake. These data support the working hypotheses and significantly extend our earlier findings and those of others. Perhaps more importantly, these experiments demonstrate the remarkable diversity of peptide receptor systems and add support for the surprising finding that intracellular signalling pathways can have divergent behavioural relevance.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Angiotensin II / pharmacology*
  • Animals
  • Benzophenanthridines / pharmacology
  • Butadienes / pharmacology
  • Dose-Response Relationship, Drug
  • Drinking Behavior / drug effects
  • Male
  • Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Nitriles / pharmacology
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Angiotensin / metabolism
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology*
  • Sodium Chloride / metabolism*
  • Time Factors
  • Vasoconstrictor Agents / pharmacology*
  • Water / metabolism*

Substances

  • Benzophenanthridines
  • Butadienes
  • Nitriles
  • Receptors, Angiotensin
  • U 0126
  • Vasoconstrictor Agents
  • Water
  • Angiotensin II
  • Sodium Chloride
  • chelerythrine
  • Protein Kinase C
  • Mitogen-Activated Protein Kinase Kinases