Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Heinemann, A; Horina, G; Stauber, RE; Pertl, C; Holzer, P; Peskar, BA.
Lack of effect of a selective vasopressin V1A receptor antagonist SR 49,059, on potentiation by vasopressin of adrenoceptor-mediated pressor responses in the rat mesenteric arterial bed.
BRIT J PHARMACOL 1998 125: 1120-1127.
Doi: 10.1038/sj.bjp.0702167
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- Führende Autor*innen der Med Uni Graz
- Heinemann Akos
- Co-Autor*innen der Med Uni Graz
- Holzer Peter
- Peskar Bernhard
- Stauber Rudolf
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- Abstract:
- The vasopressin receptor subtype involved in the enhancement by vasopressin of adrenoceptor-mediated vasoconstriction was investigated in rat isolated perfused mesenteric arteries. [Arg8]vasopressin (1-10 nM) dose-dependently increased the perfusion pressure and enhanced the pressor response to the adrenoceptor agonist methoxamine (40 nmol) or electrical stimulation of periarterial nerves (16 Hz), at the concentration of 10 nM of [Arg8]vasopressin up to 4 and 3 fold, respectively. During prolonged exposure (45 min) the direct vasoconstrictor effect of [Arg8]vasopressin (10 nM) rapidly declined whereas the potentiation of methoxamine-induced vasoconstriction was maintained. The selective vasopressin V1A receptor antagonist SR 49,059 (1-3 nM) and the non-selective V1A/B and oxytocin receptor antagonist [deamino-Pen1,Tyr(Me)2,Arg8]vasopressin (15-45 nM) inhibited the direct vasoconstrictor action of [Arg8]vasopressin but had no effect on the enhancement of the pressor response to methoxamine or electrical stimulation. The V1B receptor agonist [deamino-Cys1,beta-(3-pyridyl)-D-Ala2,Arg8]vasopressin (100-1000 nM) and the V2 receptor agonist [deamino-Cys1,D-Arg8]vasopressin (1-10 nM) were devoid of any pressor activity and did not potentiate methoxamine-evoked vasoconstriction. In contrast, [1-triglycyl,Lys8]vasopressin (100 - 1000 nM) potentiated the methoxamine responses without per se inducing vasoconstriction. In arteries precontracted with methoxamine (7.5 microM) pressor responses to [Arg8]vasopressin (3-10 nM) were not inhibited by a dose of SR 49,059 (3 nM) which abolished the peptide's vasoconstrictor effect under control conditions. These data show that the direct vasoconstrictor effect of [Arg8]vasopressin is mediated by V1A receptors while the enhancement of adrenoceptor-mediated pressor responses is insensitive to V1A, V1B, and oxytocin receptor antagonists and is not mimicked by selective agonists of V1B and V2 receptors. In conclusion, an unusual interaction of vasopressin with V1A receptors, or even the existence of a novel receptor subtype, has to be considered.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Argipressin - pharmacology
- Blood Pressure - drug effects
- Drug Synergism - drug effects
- Hormone Antagonists - pharmacology
- Indoles - pharmacology
- Male - pharmacology
- Mesenteric Arteries - drug effects
- Methoxamine - pharmacology
- Perfusion - pharmacology
- Pressoreceptors - drug effects
- Pyrrolidines - pharmacology
- Rats - pharmacology
- Rats, Sprague-Dawley - pharmacology
- Receptors, Adrenergic - drug effects
- Receptors, Vasopressin - antagonists and inhibitors
- Research Support, Non-U.S. Gov't - antagonists and inhibitors
- Vasoconstriction - drug effects
- Vasoconstrictor Agents - pharmacology