Effects of neuropeptides on adaptive autonomic processes
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TL;DR
Examination of the effects of neuropeptides on centrally evoked pressor responses suggests that ACTH4–10 signals intense stress to brain centres which regulate cardiovascular reactions, and DGLVP, on the other hand, may affect both generalized and specific emotional (fear) responses.
Abstract
Neuropeptides related to adrenocorticotrophic hormone (ACTH), vasopressin and oxytocin influence centrally regulated cardiovascular responses. In recent studies ACTH4–10 and lysine8-vasopressin (LVP) were seen to delay the extinction of a classically conditioned cardiac response in the rat. Cardiac response during an emotional behaviour was affected, but differentially, by ACTH4–10 and by des-glycinamide9-lysine8-vasopressin (DGLVP). DGLVP intensified the bradycardia which accompanied passive avoidance behaviour, while ACTH. 4–10 caused tachycardia. The behavioural effect of the two neuropeptides was, however, indistinguishable. In accordance with current psychophysiological views, it is suggested that ACTH4–10 signals intense stress to brain centres which regulate cardiovascular reactions. This signalization may result in a facilitated arousal state which increases the probability of the appropriate behavioural coping. DGLVP, on the other hand, may affect both generalized and specific emotional (fear) responses. This effect of the peptide may be related to an influence on attentional and/or expectancy processes. Observations in rats with hereditary hypothalamic diabetes insipidus indicate that in the genetic absence of vasopressin, behavioural coping is impaired: a specific cardiac response failed to occur but the generalized cardiac reaction was preserved. The likelihood that the autonomic effects of neuropeptides occur as a result of a direct action on cardiovascular control mechanisms rather than as a consequence of their behavioural actions is indicated by an examination of the effects of neuropeptides on centrally evoked pressor responses. Intra-cerebroventricularly administered arginine8-vasopressin and fragments of this peptide have been seen to attenuate blood pressure increase evoked by the electrical stimulation of the mesencephalic reticular formation. The outlined observations indicate neuropeptide influences on adaptive autonomic processes, and suggest that neuropeptide dysfunctions may be involved in psychosomatic disorders.
