Rat vena cava alpha 1B-adrenoceptors: characterization by [3H]prazosin binding and contraction experiments.
We examined which subtypes of alpha 1-adrenoceptors are expressed in rat vena cava by using both functional and [3H]prazosin binding experiments. Pretreatment with chloroethylclonidine inactivated about 80% of the specific [3H]prazosin binding sites and reduced the maximal noradrenaline-induced contraction to the same extent. Competition with subtype-selective agonists and antagonists showed primarily the alpha 1B-adrenoceptor subtype in vena cava. The number of alpha 1-adrenoceptors estimated with [3H]prazosin binding and the maximal noradrenaline-induced contraction were dose-dependently inhibited by phenoxybenzamine, indicating the absence of receptor reserve for noradrenaline in vena cava. As the noradrenaline-induced contraction was largely inhibited in Ca(2+)-free solution, these results suggest that alpha 1B-adrenoceptors can be mainly linked to Ca2+ influx in rat vena cava.
Sayet
I
I
Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, URA CNRS 1489, Université de Bordeaux II, France.
Neuilly
G
G
Rakotoarisoa
L
L
Mironneau
J
J
Mironneau
C
C
D000818:Animals; D066298:In Vitro Techniques; D009638:Norepinephrine / Q000494:pharmacology; D011224:Prazosin / Q000378:metabolism*; D011869:Radioligand Assay; D051381:Rats; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism*; D014316:Tritium; D014661:Vasoconstriction / Q000187:drug effects*; D014684:Venae Cavae / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology
D018340:Receptors, Adrenergic, alpha-1; D014316:Tritium; D009638:Norepinephrine; D011224:Prazosin