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Recent case reports suggest that pulmonary hypertension could be caused by minoxidil, a new potent vasodilating antihypertensive drug. Therefore, we evaluated the incidence and severity of pulmonary hypertension in 110 patients with systemic hypertension. Fourteen patients were treated with minoxidil for 2 to 35 months (mean 19.9 months), 15 were treated with no drugs, and the remaining 81 patients received conventional antihypertensive agents of several types. Pulmonary vascular resistance correlated positively (P is less than 0.05) with systemic vascular resistance. Minoxidil-treated patients with hypertension previously refractory to conventional therapy had slightly lower pulmonary vascular resistance than other hypertensive subjects. There was no correlation between pulmonary vascular resistance and duration of minoxidil therapy or other types of antihypertensive regimens. The positive correlation between pulmonary and systemic vascular resistance suggests the possibility of a causal hypertension relation in the two vascular beds.

The antihypertensive mechanisms of single and combined therapy with a beta-adrenergic antagonist (propranolol) and a vasodilator (hydralazine) were investigated in 9 patients with moderately severe hypertension, who were receiving maintenance diuretic (hydrochlorothiazide) treatment. Hemodynamic and neuroendocrine responses were determined at rest and during lower body negative pressure, and dynamic and static exercise stress after the chronic administration of propranolol and hydralazine, given alone or in combination. All 3 drug regimens, each administered for at least 10 weeks, reduced blood pressure (p less than 0.05) compared with diuretic-only therapy in patients at rest, in both the supine and standing position, and during lower body negative pressure and dynamic exercise. There was a significant additive antihypertensive effect when propranolol and hydralazine were combined. Only combination therapy effectively lowered pressure during static exercise. The regimens produced divergent effects on the supine cardiac output: a decrease with propranolol (p less than 0.05), no change with combination therapy and an increase with hydralazine (p less than 0.05). Both hydralazine and combination therapy significantly reduced supine total peripheral resistance (p less than 0.05), whereas propranolol produced no change. All 3 drug treatments significantly reduced total peripheral resistance during upright rest and dynamic exercise (p less than 0.05), without changing cardiac output or maximal exercise capacity. During exercise, cardiac output was maintained in patients treated with propranolol and in those treated with combined therapy by increases in stroke volume (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The beneficial effects of acute prazosin therapy in patients with congestive heart failure (CHF) have been well documented; however, its chronic efficacy over several months has not previously been evaluated in a placebo-controlled manner. Therefore, an assessment was made by radionuclide ventriculography of the effect of prazosin, 20 mg/day, on left ventricular ejection fraction and end-systolic and end-diastolic volumes at rest and on peak upright bicycle exercise, as well as its effect on right ventricular ejection fraction at rest, exercise time and work load, and standard clinical variables in 23 patients with stable class III symptoms of CHF. The study consisted of a 6-month randomized, double-blind, controlled evaluation of prazosin versus placebo in patients receiving a stable dose of digitalis and diuretics for at least 1 month. At entry, the prazosin and placebo groups did not differ in any respect. Prazosin caused no demonstrable effect on clinical variables such as status of symptoms, heart rate, mean arterial pressure, and cardiothoracic ratio when compared with placebo. Prazosin also caused no demonstrable effect compared with placebo on absolute or percent changes in radionuclide variables at rest or on peak exercise, or on exercise time or exercise work load. In addition, prazosin had no consistent effect compared with placebo on plasma renin activity or plasma catecholamine levels. However, there was a slight but significant increase in weight (p less than 0.0001) and in plasma renin activity in the upright position (p less than 0.002) with time, as well as a tendency for the diuretic dose to increase with time in both groups. Thus, long-term prazosin therapy generally produces no demonstrable subjective or objective improvement in patients with stable, chronic class III CHF receiving digitalis and diuretic therapy.