Vasopressin causes endothelium-independent contractions of the rat arteries being a potent full agonist in the aorta and renal artery, but a weak partial agonist in the common carotid artery. The contractile effect in the aorta and renal artery was observed with concentrations similar to those detected in circulating blood during hemorrhage, septic shock, increased intracranial pressure and hypoxia. On the contrary, in that concentration range vasopressin did not produce any change in tension of the common carotid artery. These results are consistent with the hypothesis that increased levels of circulating vasopressin may contribute to redistribution of blood from the peripheral to the cerebral circulation.
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