Release of Antidiuretic Hormone from Neurohypophysis in Response to Hypotension in Dogs

MURASE Toshio

doi:10.1507/endocrine1927.46.12_1161

It has been postulated that the release of antidiuretic hormone (ADH) is regulated by the changes of plasma tonicity and blood volume. But, in addition to these factors, the changes of arterial blood pressure may participate in the control of its secretion.In order to clarify the role of arterial baroreceptors on the release of ADH, the following experiments were performed on dogs. In the first series of experiments, splectomized dogs were used under chloralose-urethane anesthesia. The animals were bled gradedly from a femoral artery, and the amount of each bleeding was 0.5% body weight. Arterial blood was collected and ADH concentrations in plasma were assayed with Yoshida's method. In these experiments, it was observed that the rises of ADH titers in plasma were highly correlated to the reduction of mean arterial blood pressure. On the besis of these results, eight of the dogs under nembutal anesthesia were used for the next experiment in order to observe the effect of acutely induced hypotension on the ADH release. Sodium nitroprusside with 300 μg/ml concentration was infused intravenously at a rate of 13.8-14.7 μg/kg/min over 0.9-3.0 minutes until a mean arterial blood pressure fell to the 51% initial value. Timed samples of arterial blood were collected and ADH concentrations were also determined. Hypotension induced by infusion of sodium nitroprusside resulted in an increse in plasma ADH concentrations from 18.6±4.7 to 52.71±8.7μU/ml. These rises are statistically highly significant (p<0.005). Four minutes later, the mean arterial blood pressure recovered to almost control levels and the elevated plasma ADH titers decreased significantly to 27.2±9.6 μU/ml (p<0.02). But twelve minutes later, striking rises of plasma ADH concentrations were observed in six of the eight dogs (299±121 μU/ml). The rises were variable in amounts, and so these are statistically not significant (0.05<p<0.1). Compared with the results of the following experiments of hemorrhagic hypotension, it cannot be considered that these rises occurred as a delayed response to hypotension. It was reported that sodium nitroprusside may act directly on vascular smooth muscles and depresses blood pressure. It decomposes gradually in the blood with liberation of cyanogen which inhibit cell respiration. Although there is no direct evidence relevant to this point, massive amounts of ADH released may be stimulated by sodium nitroprusside itself and/or its metabolites. In the third series, the experiments of hemorrhagic hypotension were undertaken under nembutal anesthesia in eight dogs. Animals were bled from a femoral ertery at a speed of 6.7±14.7 ml/kg/min for 1.6-3.8 minutes until a mean arterial blood pressure fell to the same order of magnitude that was induced by sodium nitroprusside infusion. Timed arterial blood samples were drawn and ADH concentrations were also measured. The shed blood was returned immediately via an antecubital vein within four minutes. Hemorrhagic hypotension caused significant increase in plasma ADH concentrations from 19.4±7.9 to 110.3±237.7 μU/ml (p<0.05). Four minutes later, when a mean arterial blood pressure elevated markedly to the level of 146% initial value in response to prompt transfusion of the shed blood, ADH titers in plasma fell significantly to 36.8±8.5 μU/ml (p<0.05) and thereafter progressively returned to the control level. The increment of ADH titers in plasma in response to hemorrhagic hypotension seemed to be somewhat higher than those in response to hypotension induced by sodium nitroprusside infusion (0.1<p<0.2). This tendency can possibly be accounted for by considering that in hemorrhagic hypotension, besides the hypotensive effect, reduction of blood volume additively stimulated the release of ADH.

Release of Antidiuretic Hormone from Neurohypophysis in Response to Hypotension in Dogs

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