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Usually the V1 receptor is present in the platelets, liver, vascular smooth muscle and also in the various regions of CNS.
At the time when the ADH is binds to the V1 receptor, it leads to the Gq/11-mediated Phospholipase C activation and further it leads to the enhancement in the intracellular calcium.
The vasopressin - mediated vasoconstriction is normally much seen in the renal and hepatic artery beds.
Most important vasopressin outcomes of enhanced plasma concentration of the ADH are having great clinical importance in clinical settings, this pressor effect is really useful in controlling the bleeding esophageal varicies .
An thoroughly selective V1 vasopressin analogue have shown to have a much same consequence in the individuals with sepsis.
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