|Budget Amount *help
¥2,100,000 (Direct Cost : ¥2,100,000)
Fiscal Year 1987 : ¥1,000,000 (Direct Cost : ¥1,000,000)
Fiscal Year 1986 : ¥1,100,000 (Direct Cost : ¥1,100,000)
We studied the role of diminished sympathetic nervous system(SKS) activity and endogenous opiate activation in the hypotensive action of taurine, a sulfur amino acid, in deoxycorticorticosterone acetate (DOCA)-salt hypertensive rats. Supplementation of taurine could prevent the development of DOCA-salt hypertension in rats, but failed to change blood pressure in vehicle-treated control rats. Cardiao norepinephrine (NE) turnover, which was determined from the rate of deoline of tissue NE concentration after the administration of <alpha> -methl-p-thyrosine, was markedly accelerated in DOCA-salt rats, but 1% taurine supplement restored it normal. Moreover, naloxone (img/kg), the specific opiate antagonist, increaed blood pressure in taurine-treated DOCA-salt rats, restoring it to levels approximately in the DOCA-salt rats. In contrast,neither taurine decreased cardiao NE turnover in the control rats, nor naloxone increased blood pressure in the taurine-treated control rats. Moreover, suppiementation of taurine increased both <beta> -endorphin-like immunoreactive material and taurine contents in the hypothalamus of DOCA -salt rats,whereas it did not increases <beta> -endorphin in that of control rats despite increased taurine contents. Thus, taurine not only normalized the increased cardiac SNS activity but also elicited an opiate-mediated vasodepressor response only in DOCA-salt rats. It is suggested, therefore, that endogenous opiate activation, which is intimately realated to SNS suppression, may contribute to the antihypertensive effect of taurine in sodium-ohloride hypertension.