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pubmed:abstractText |
Blood pressure, heart rate and evoked cardiovascular reflexes were examined in cats following chronic treatment with haloperidol, at a dose of 1 mg kg-1 per day, orally for 23 days. Five days after the final dose the animals were anaesthetized and tested for their reaction to various cardiovascular stimuli and to a number of agonist and antagonist drugs, given both intravenously and into the vertebral artery. It was found that treatment with haloperidol caused hypertension in the cats, as well as a potentiation of the pressor response to bilateral carotid occlusion. The response to 30 degrees head-up tilting was also altered so that in treated cats, the blood pressure returned to normal more rapidly during the tilt. There was no difference in the heart rate of the two groups of cats, nor in the pressor response to intravenous noradrenaline or angiotensin II or to afferent brachial nerve stimulation, nor was the depressor action of bradykinin altered. Hexamethonium reduced the blood pressure in both control and treated cats to approximately the same level. Blood O2, CO2, pH and bicarbonate levels were also unaltered by the treatment, as was plasma renin activity. Of the drugs given into the vertebral artery, only noradrenaline, prazosin, ketanserin and haloperidol caused a significantly greater fall in blood pressure in treated than in control cats, while clonidine and St91 were equally effective in both groups. These results suggest that haloperidol treatment has caused a greater modulation of central alpha 1- than of alpha 2-adrenoceptors.
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