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We studied the role of diminished sympathetic nervous system (SNS) activity and endogenous opiate activation in the hypotensive action of taurine, a sulfur amino acid, in deoxycorticosterone 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. Cardiac NE turnover, which was determined from the rate of decline of tissue NE concentration after the administration of alpha-methyl-p-tyrosine, was markedly accelerated in DOCA-salt rats, but 1% taurine supplement restored it to normal. Moreover, naloxone (2 mg/kg), the specific opiate antagonist, increased blood pressure in taurine-treated DOCA-salt rats, restoring it to levels similar to those in the DOCA-salt rats. In contrast, taurine did not decrease cardiac NE turnover in the control rats, nor did naloxone increase blood pressure in the taurine-treated control rats. Moreover, supplementation of taurine increased both beta-endorphin-like immunoreactive material and taurine contents in the hypothalamus of DOCA-salt rats, whereas it did not increase 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 related to SNS suppression, may contribute to the antihypertensive effect of taurine in sodium chloride hypertension.

Hypotensive effect of taurine. Possible involvement of the sympathetic nervous system and endogenous opiates.