Sodium acetate produced a direct, dose-related decrease in myocardial contractile force in the dog and isolated rabbit papillary muscle. In the dog, there was also a decrease in blood pressure which was attributed primarily to the fall in contractile force. However, sodium acetate was found to have weak vasodilator properties as shown by the decreases in hind-limb perfusion pressure.

1. The cardiovascular effects of sodium glutamate were investigated in anaesthetized dogs with bolus injections, intravenous infusions and rabbit isolated papillary muscles. 2. The intravenous bolus injections of sodium glutamate resulted in slight, transient decreases in contractile force at doses of 58 and 117 mg/kg, which were followed by brief increases in blood pressure. 3. Sodium glutamate had no effect on contractile responses of isolated papillary muscles at any of the concentrations used. 4. Infusions of glutamate produced no change in blood pressure, an increase in cardiac output, and a decrease in heart rate, total peripheral resistance and femoral vascular resistance. 5. The infusion of sodium glutamate into animals with no renal function resulted in an increased plasma osmolality and a decreased haematocrit. 6. The results from this study show that sodium glutamate had minimal cardiovascular effects. The results from the infusion data suggest that glutamate increases intravascular volume by an osmotic effect.

Reserpine has been previously shown to generally enhance femoral arterial vasodilator responses as indicated by increased slopes of regression lines relating decreases in resistance produced by injections of vasodilator agents to resistance prior to the injections. We have examined the same parameters in dogs pretreated with 6-hydroxydopamine. In contrast, 6-hydroxydopamine either decreased (nitroglycerin, adenosine) or had no effect (isoproterenol, acetylcholine) on femoral arterial vasodilator responses. In a second set of animals, reserpine was administered after pretreatment with 6-hydroxydopamine, and reserpine again tended to augment responses to vasodilator agents. These data suggest that reserpine’s effects on vasodilator responses may be a direct effect on vascular smooth muscle and was not dependent on its effects on sympathetic innervation of the femoral bed. The decreased vasodilator responses to certain agents induced by 6-hydroxydopamine, in contrast, may have been attributable to loss of a presynaptic component of their mechanism(s) of vasodilator action.