A pressor amine (methoxamine) which produces peripheral vasoconstriction, while lacking a significant, direct, positive inotropic effect upon ventricular heart muscle, has been shown to produce hemodynamic effects that are in distinct contrast to those resulting from the injection or infusion ofl-epinephrine andl-norepinephrine in “physiologic” concentrations or of mephentermine sulfate. The latter 3 amines, possessing a positive inotropic action in addition to varying vasoconstrictor effects, decrease right and left atrial mean pressures while increasing femoral and pulmonary arterial pulse and mean pressures, right and left ventricular stroke works and the cardiac index.Methoxamine injection or infusion, in contrast, resulted in linear increases in the calculated total peripheral resistance and left and right atrial mean pressures. There was a simultaneous rise in right and left ventricular stroke works which were maintained until a maximum rise in the mean arterial pressure was reached. The average stroke volume indices were maintained at near control values in both blocked and unblocked animals. The cardiac index of the normal unblocked dogs decreased in proportion to the decrease in heart rate.Following the peak pressor response to methoxamine, a progressive fall in mean femoral arterial pressure occurred resulting from ventricular failure rather than “tachyphylaxis” to the vasoconstrictor activity of methoxamine. This decrease in systemic arterial pressure was accompanied by: (1) a further rise in calculated total peripheral resistance and in right and left atrial mean pressures, and (2) a fall in right and left ventricular stroke work and stroke volume indices and in the cardiac indices.