Vasopressin release induced by hemorrhage in the goat.

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AbstractEffects of moderate hemorrhage were studied in normovolemic and hydrated conscious goats. Plasma arginine vasopressin (AVP) in jugular vein blood did not rise in response to bleeding of 8 and 12 ml/kg b.wt. After a blood loss of 16 ml/kg an abrupt and conspicuous rise in plasma AVP (to > 10 times basic level) was seen in 50% of the experiments, whereas no rise in AVP occurred in the remaining experiments. Bleeding at 20 and 24 ml/kg gave a more consistent AVP response. Hydration did apparently not reduce the AVP‐responsiveness to bleeding. The plasma vasopressin concentration returned to pre‐hemorrhage level about 3 h after bleeding, i.e. before the blood was re‐transfused. A minor, and inconsistent rise in plasma renin activity occurred in response to bleeding. Central venous pressure fell during hemorrhage and stayed depressed until the blood was re‐transfused. Since the depression was of the same order in all experiments, and was still present when plasma AVP had returned to pre‐hemorrhage level, the fall in venous pressure was obviously not the main cause of the AVP‐response. However, the pronounced rise in plasma vasopressin was correlated to a fall in the arterial pressure and to hyperventilation. No urge to drink developed during any of the hemorrhage experiments. It is concluded that the goat does not readily respond to hemorrhage with vasopressin liberation. When it happens, pressor amounts of the hormone are released, and a fall in arterial pressure and/or increased stimulation of respiratory chemoreceptors (hypoxia?) appear(s) to be the ultimate cause(s) of the release. This thirst‐independent regulation of vasopressin secretion is obviously of no importance in day to day control of water balance, but may help to maintain the arterial blood pressure in emergency situations.