Hemodynamic and neurohumoral effects of moxonidine in patients with essential hypertension
- Cite this article as:
- Mitrovic, V., Patyna, W., Hüting, J. et al. Cardiovasc Drug Ther (1991) 5: 967. doi:10.1007/BF00143521
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The hemodynamic and neurohumoral effects of a single oral dose (0.4 mg) of the novel centrally acting antihypertensive agent moxonidine were investigated over 4 hours in ten patients with essential hypertension (WHO I-II). Pulmonary pressure indices and cardiac output were determined both at rest and during ergometric exercise by means of Swan-Ganz catheterization. Blood pressure was measured by sphygmomanometry and in the brachial artery. Moxonidine induced a significant fall in blood pressure over the 4-hour observation period from 176/105 mmHg to 158/95 mmHg (p<0.01), accompanied by a decrease in systemic vascular resistance from 1695 to 1427 dyn.sec/cm5 (p<0.01). Cardiac output remained unchanged, while heart rate increased slightly from 69 to 75 beats/min (p<0.01). No significant changes were recorded for either pulmonary artery pressure or pulmonary vascular resistance. Plasma levels of noradrenaline (337 vs. 224 pg/ml) and renin (2.6 vs 2.0 ng/ml/hr) activity fell significantly after moxonidine (p<0.05), both at rest and during exercise. Although aldosterone plasma levels fell slightly, levels of angiotensin II and ANF remained unchanged.
Moxonidine has favorable effects on hemodynamics and the neurohumoral system in patients with essential hypertension and is well tolerated at the dose administered.