Hemodynamic activity of
cadralazine (ethyl-2-[6-(2-hydroxypropyl)-ethylaminol-3-pyridazinyl
hydrazine carboxylate), a new, long-acting
antihypertensive agent, was evaluated on systemic and regional circulation in conscious dogs.
Cadralazine given i.v. (1 mg/kg) caused a sustained fall in total peripheral vascular resistances and mean blood pressure (from 103 to 90 mmHg) and an increase in heart rate (from 97 to 161 beats/min). Heart rate variations paralleled the drop in peripheral resistances.
Cadralazine produced a consistent increase in cardiac output, and this effect was related to the increase in heart rate. No significant change in myocardial contractility was observed. Blood flow was increased and vascular resistances decreased in coronary, iliac and mostly in renal vascular beds, whereas the variations in the mesenteric district were not significant. This hemodynamic pattern characterizes
cadralazine as a
vasodilator. Changes in hemodynamic responses to
epinephrine (1 microgram/kg i.v.) after
cadralazine treatment were also evaluated.
Cadralazine reduced
hypertension and
bradycardia effects, increased
hypotension and
tachycardia responses, and caused a further increase in cardiac output and coronary blood flow. These effects of
cadralazine are not due to alpha-blocking or to beta-stimulating properties.