Dynamics of the pulmonary circulation in systemic hypertension.

Pulmonary and systemic hemodynamics in 28 mild to moderate hypertensive patients (group II) with left ventricular (LV) hypertrophy (ECG and echo criteria) and 22 severe hypertensive patients with LV hypertrophy (group III) were compared with 20 patients with mild-to-moderate hypertension in WHO stage I (group I). Mean right atrial pressure was equivalent in groups II and III and significantly higher in the last group than in group I. An increased pulmonary arterial resistance (PAR) in group II and, to a large extent, in group III accounted for the elevation of diastolic and mean pulmonary arterial pressure in both groups in comparison with group I. Cardiac index (CI) was lower and systemic vascular resistance (SVR) higher in group III than in group I. Pulmonary capillary wedge pressure (PCWP) values were within the normal range and equivalent between groups II and III, and both significantly higher than in group I. PAR showed a positive relation with SVR (r = 0.30, P less than 0.01) and an inverse relation with CI (r = -0.561, P less than 0.001). Findings indicate that in systemic hypertension with LV hypertrophy there is an elevation of the right ventricular filling pressure and the pulmonary arterial pressure whose degree is even higher in severe hypertension. This increase is not necessarily a consequence of impairment of LV function as suggested by the normal range of PCWP values.

Comparison between the effects of urapidil and methyldopa on left ventricular hypertrophy and haemodynamics in humans.

In a randomised double-blind study the effects on left ventricular mass (LV mass) and cardiac haemodynamics of urapidil, an antihypertensive agent with a vascular postsynaptic alpha 1-blocking action and a central antihypertensive effect, were compared with those of methyldopa in 29 patients with essential hypertension. During a 3-month period, urapidil was initially given at 120 mg/day and increased to 180 mg/day if a satisfactory antihypertensive response was not achieved. Methyldopa was started at 100 mg/day and increased to 1500 mg/day if an adequate blood pressure response was not achieved. Echocardiographic measurements were obtained at baseline and after 12 weeks' active treatment. The frequency rates of responders (DBP less than 95 mm Hg) on urapidil and methyldopa were 54% and 62%, respectively, after 12 weeks. In the group as a whole there was a nonsignificant tendency for decreased LV mass on both active drugs. However, the haemodynamic changes were difficult to interpret because of baseline differences between the 2 treatment groups.

Hemodynamic effects of guanfacine in essential hypertension.

Hemodynamic evaluation of three men and eight women aged 20 to 58 years (mean, 44 years) with essential hypertension was performed before and after a single dose of guanfacine and before and after long-term administration of the drug, which is a stimulant of central alpha-adrenergic receptors. Mean (+/- SE) recordings of blood pressure before catheterization were 168/115 +/- 6/3 mmHg when supine and 168/112 +/- 8/4 mmHg when standing. Within two hours of oral administration of 3 mg of guanfacine, the heart rate decreased from a mean of 77 +/- 2 to 69 +/- 3 beats/min (P less than 0.05), and the pulmonary capillary wedge pressure (PCWP) decreased from a mean of 9 +/- 1 to 6 +/- 1 mmHg (P less than 0.02). The mean readings of pulmonary arterial pressure also decreased, as follows: systolic, from 22 +/- 2 to 18 +/- 0.14 mmHg (P less than 0.05); diastolic, from 9 +/- 1 to 7 +/- 1 mmHg (P less than 0.05); and mean, from 15 +/- 1 to 12 +/- 2 mmHg (P less than 0.05). No changes were observed in systemic blood pressure, the cardiac index, systemic vascular resistance, or total pulmonary vascular resistance. After a six-week course (mean dosage, 3.9 +/- 0.57 mg/day), the following variables decreased significantly: systemic blood pressure--systolic, diastolic, and mean, both supine and standing (P less than 0.001); heart rate (P less than 0.001); and systemic vascular resistance (P less than 0.01). The PCWP reached values similar to those measured during the control phase. Increases were noted in pulmonary artery systolic pressure (P less than 0.05), mean right atrial pressure (P less than 0.01), and in the stroke volume index (P less than 0.05). It is likely that the main hemodynamic mechanism underlying the long-term antihypertensive effect of guanfacine is a decrease in systemic vascular resistance.