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  • Title: Hemodynamic effects of guanfacine in essential hypertension.
    Author: Feldstein CA, Cohen AA, Sabaris RP, Burucúa JE.
    Journal: Clin Ther; 1984; 6(3):325-34. PubMed ID: 6373009.
    Abstract:
    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.
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