An acute intravenous injection of clonidine may produce a transient pressor response that apparently is due to stimulation of peripheral vascular a-receptors. The pressor response does not occur after oral administration, because the drug's centrally mediated depressor action overrides it.
The decrease in blood pressure produced by cloni-dine correlates better with a decreased cardiac output than with a reduction in peripheral vascular resistance. The reduction in cardiac output is the result of both a decreased heart rate and reduced stroke work; the latter effect is probably caused by a diminished venous return.
Renal blood flow and glomerular filtration are not decreased, although renal resistance is diminished. Like a-methyldopa, it is a useful agent for hypertension complicated by renal disease. Plasma renin activity is reduced by clonidine, presumably as a result of a centrally mediated decrease in sympathetic stimulation of the juxtaglomerular cells of the kidney.
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