The primary hemodynamic alteration responsible for the hypotensive effects of a-methyldopa remains in dispute. When the patient is supine, the reduction in blood pressure produced by a-methyldopa correlates best with a decrease in peripheral vascular resistance, cardiac output being only slightly reduced. When the patient is upright, the fall in blood pressure corresponds more closely with a reduced cardiac output.
An important aspect of a-methyldopa's hemodynamic effects is that renal blood flow and glomerular filtration rate are not reduced. As occurs with most sympathetic depressant drugs and vasodilators, long-term therapy with a-methyldopa leads to fluid retention, edema formation, and plasma volume expansion. While data conflict somewhat, it is generally thought that a-methyldopa suppresses plasma renin activity.
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