Intravenous infusion of clonidine causes an acute rise in blood pressure due to activation of post-synaptic a2 receptors in vascular smooth muscle. The affinity of clonidine for these receptors is high, although the drug is a partial agonist with relatively low efficacy at these sites. The hypertensive response that follows parenteral administration of clonidine generally is not seen when the drug is given orally. After either oral or parenteral administration, the transient vasoconstriction is followed by a more prolonged hypotensive response that results from decreased sympathetic outflow from the CNS, apparently from activation of a2 receptors in the lower brainstem region. Clonidine also stimulates parasympathetic outflow, which may contribute to the slowing of heart rate. in addition, some of the antihypertensive effects of clonidine may be mediated by activation of presynaptic a2 receptors that suppress the release of NE, ATP, and NPY from postganglionic sympathetic nerves. Clonidine decreases the plasma concentration of NE and reduces its excretion in the urine.

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