Alpha-adrenoceptor- and prostaglandin-mediated modulation of vascular adrenergic neurotransmission in spontaneously hypertensive rats.
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概要
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The modulation of vascular adrenergic neurotransmission in the spontaneously hypertensive rat (SHR) and Wistar-Kyoto rat (WKY) mediated by alpha-adrenoceptor and prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>) were evaluated. The pressor responses of the perfused mesenteric vascular bed to perivascular adrenergic nerve stimulation (NS) and infusion of norepinephrine (NE) and the NS-induced <SUP>3</SUP>H-efflux in preparations pretreated with <SUP>3</SUP>H-norepinephrine were determined. In both SHR and WKY, a selective alpha<SUB>2</SUB> agonist, B-HT 920 (30-300 nM), inhibited neurogenic vasoconstriction, and B-HT 920 (100-300 nM) potentiated the pressor response to NE in a dose-dependent manner. The effects of B-HT 920 did not significantly differ in SHR and WKY. Another alpha<SUB>2</SUB> agonist, clonidine (100 nM), decreased the <SUP>3</SUP>H-efflux approximately by 30% both in SHR and WKY. A selective alpha<SUB>2</SUB> blocking agent, yohimbine (3-300 nM), potentiated the neurogenic vasoconstriction and inhibited the pressor response to NE equally in SHR and WKY. No difference in enhancement of <SUP>3</SUP>H-efflux by yohimbine (30-300 nM) was seen between SHR and WKY either in the absence or presence of cocaine (10 μM) and metanephrine (20 μM). PGE<SUB>2</SUB> (0.1-1 μM) potentiated pressor responses to NS and NE in SHR and WKY, but this compound (1 μM) did not affect the NS-induced <SUP>3</SUP>H-efflux in either group of rats. It appears that adrenergic neurotransmission is inhibited presynaptically via an alpha<SUB>2</SUB> receptor mechanism and facilitated postsynaptically by PGE<SUB>2</SUB> in the rat mesenteric vascular bed. The hypertensive state in SHR can not be accounted for by alteration of these modulator mechanisms.
- 公益社団法人 日本薬理学会の論文
著者
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Kubo Takao
Department Of Pharmacology Showa College Of Pharmaceutical Sciences
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SU Che
Department of Pharmacology, Southern Illinois University School of Medicine
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Su Che
Department of Pharmacology, Southern Illinois University School of Medicin
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