Abstract

Increases in plasma VP in response to osmotic stimulation are critical for water conservation, while VP released into the pituitary portal circulation is an important regulator of ACTH secretion and does not contribute to plasma VP levels. The role of the adrenal medulla in the specificity of these responses was studied in rats subjected to osmotic and non-osmotic stress two months following adrenal demedullation or sham operation. Basal and stimulated plasma corticosterone, aldosterone, ACTH and PRA levels in adrenal demedullated rats were similar to those in the sham operated groups indicating recovery of adrenocortical function. Basal plasma VP level were similar in sham operated controls and adrenal demedullated rats (0.93 +/- 0.13 and 1.0 +/- 0.1 pg/ml, respectively) and rose to comparable levels in both groups following 48 h osmotic stimulation by water deprivation (14.4 +/- 1.3 and 20.7 +/- 3.4, respectively). On the other hand, while in sham operated rats, immobilization for 15 min, a non-osmotic stress, had no effect on plasma VP levels in control or water deprived (2.0 +/- 0.9 and 15.0 +/- 2.7 pg/ml), in adrenal demedullated rats, caused dramatic increases in plasma VP from 1.0+/-0.1 to 126.0+/029.9 pg/ml in controls, and from 20.7 +/- 3.4 to 155 +/- 37 pg/ml in water deprived rats. Intraperitoneal hypertonic saline injection, a combination of osmotic and painful stress, caused much higher increases in plasma VP in adrenal demedullated rats (138.0 +/- 22.1 compared with 34.7 +/- 3.7 pg/ml in sham operated rats). Water deprivation potentiated this response to 70.0 +/- 8.3 and 295 +/- 24 pg/ml in sham operated and adrenal demedullated rats, respectively. VP mRNA measured by in situ hybridization, and irVP measured by immunohistochemistry, were elevated in magnocellular neurones in the hypothalamus of adrenal demedullated rats. The demonstration of marked plasma VP responses to non-osmotic stimuli in adrenal demedullated rats, suggests a modulatory role for the adrenal medulla in the specificity of the secretory responses of the magnocellular and parvicellular vasopressinergic systems.

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