Clonidine vascular effects

The decrease in blood pressure produced by clonidine 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. 

Reduction in arterial blood pressure by clonidine is accompanied by decreased renal vascular resistance and maintenance of renal blood flow. As with methyldopa, clonidine reduces blood pressure in the supine position and only rarely causes postural hypotension. Pressor effects of clonidine are not observed after ingestion of therapeutic doses of clonidine, but severe hypertension can complicate a massive overdose. 

Clonidine (Fig. 10.11) is another imidazoline compound but, unlike xylometazoline, it is not an agonist for vascular Ml receptors. It is a weaker base (pKfl 8.25) than xylometazoline and it appears to he selective for pres)maptic receptors which inhihit the release of noradrenaline. Presynaptic a.2 receptors essentially funrtion as a feedback mechanism where the noradrenaline, released into the synaptic cleft, itself inhibits further release. Thus noradrenaline release is inhibited and the blood vessels are dilated. It is less often prescribed than many hypertensive agents because of its potential to produce a rebound effect when it is withdrawn, resulting in a hypertensive crisis. 

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