Postsynaptic alpha 2-adrenergic receptor-mediated vasoconstriction in SHR tail arteries in vitro.

Abstract

In isolated perfused tail arteries of spontaneously hypertensive rats (SHR), the selective alpha 2-adrenergic receptor antagonist idazoxan ( RX781094 ) at low concentrations antagonized vasoconstrictor responses induced by norepinephrine (NE) and low frequency periarterial field stimulation. The vasoconstrictor responses to the selective alpha 2-adrenergic receptor agonist TL99 or to phenylephrine were also antagonized by low concentrations of idazoxan . In contrast, idazoxan did not antagonize responses induced by the alpha 1-adrenergic receptor agonists amidephrine or methoxamine in perfused tail arteries of SHR. The alpha 1-adrenergic receptor antagonist prazosin was very potent against methoxamine or phenylephrine and responses to periarterial field stimulation in SHR and Wistar-Kyoto (WKY) rat tail arteries, but only showed a modest selectivity for TL99 -induced responses in SHR arteries. The results support the contention that postjunctional alpha 2-adrenergic receptors can be demonstrated in arterial smooth muscle in vitro and are particularly evident in arteries from hypertensive animals. In SHR tail arteries, postsynaptic alpha 2-adrenergic receptors contribute to the vasoconstrictor responses to exogenous NE and may be activated by endogenously released NE.