Cardiovascular responses of the taurine-depleted rat to vasoactive agents

The objective of this study was to assess the effect of taurine-depletion o n cardiovascular responses of rat to vasoactive agents. Male Wistar-Kyoto ( WKY) rats were given either tap water (control) or 3% beta -alanine (taurin e-depleted) for three weeks. Thereafter, mean arterial pressure (MAP) and h eart rate of the freely moving animal were measured in response to vasoacti ve agents. Administration of phenylephine (5-40 mug/kg/min; i.v.) resulted in a similar and significant increase in MAP but a reduction in heart rate in both control and taurine-depleted groups. On the other hand, administrat ion of sodium nitroprusside (15-30 mug/kg/min; i.v.) elicited a similar and significant reduction in MAP but increased heart rate in both groups. Lack of a differential response to phenylephrine and sodium nitroprusside betwe en the two groups suggests that baroreflex regulation of cardiovascular fun ction is not adversely affected by taurine-depletion. Administration of ang iotensin II (0.1-3.0 mug/kg/min; i.v.) resulted in a dose-related increase in the presser response and a decrease in heart rate in both groups. Howeve r, angiotensin II-induced presser response was reduced in the taurine-deple ted compared to the control rats (p < 0.05); heart rate was similarly reduc ed in both groups. Acute exposure to p-alanine (3g/kg; i.v., 30-minutes) di d not alter angiotensin II-induced hemodynamic responses. Similarly, incuba tion of aortic rings with <beta>-alanine (40mM, 30 minutes) did not affect the contractile responses to angiotensin II. The results suggest that p-ala nine, per se, does not affect angiotensin II-induced responses in rat. Howe ver, P-alanine-induced taurine depletion is associated with a reduction in the presser response to angiotensin II without impairing baroreflex functio n.