尾仲 達史

Effects of a dopamine D1 receptor antagonist, SCH 23390, were investigated on plasma level of vasopressin after stressful stimuli in rats. The antagonist markedly attenuated the increase in plasma level of vasopressin after electric footshocks but not after s.c. injected hypertonic saline. The antagonist, however, did not significantly change the suppressive vasopressin response to fear-related emotional stress, though the drug suppressed motor behavior of the rat during testing period. These data suggest that dopamine D1 receptors play an important role selectively in the facilitatory vasopressin response to noxious stimuli in rats.

The possibility that arterial baroreceptors may be involved in the potentiation of vasopressin or oxytocin secretion observed after noxious stimuli was tested in male rats after sino-aortic denervation (SAD). There was no significant difference in plasma level of vasopressin or oxytocin between the SAD and the corresponding sham-operation control (SHAM) groups with or without electric shocks. An i.p. injected alpha-1-adrenergic receptor antagonist, prazosin, decreased arterial blood pressure both in the SAD and in the SHAM groups. However, the increased levels of these hormones after prazosin were significantly lower in the SAD than in the SHAM groups. Reflexly evoked tachycardia after prazosin occurred in the SHAM but not in the SAD groups. These results suggest that afferent neural signals originating from arterial baroreceptors are not involved in potentiation of vasopressin and oxytocin secretion after noxious stimuli in the rat.

Interactions between emotional stress due to fear and hypovolemic stimuli on vasopressin secretion were studied in rats. Intraperitoneally injected dextran did not significantly change plasma osmolality osmolality and arterial blood pressure but increased blood hemoglobin and plasma vasopressin level. An i.v. infused physiological solution reversed these changes. Emotional stress due to fear acquired by learning suppressed plasma vasopressin level in dextran-injected rats. Emotional stress due to fear produced by low-frequency footshocks also suppressed the increased plasma vasopressin level. These results suggest that emotional stress due to fear interacts with afferent neural signals originating from cardio-vascular volume receptors in the control of vasopressin secretion.