Circulating Vasopressin Attenuates the Increased Activity of the Sympathetic Nervous System Induced by Anterolateral Deafferentation of the Hypothalamus
Autor: | Gábor B. Makara, O. Földes, Oprsalová Z, Daniela Jezova, Lichardus B, R. Kvetnansky, N. Michajlovskij |
---|---|
Rok vydání: | 1988 |
Předmět: |
Nervous system
Agonist medicine.medical_specialty Sympathetic nervous system Vasopressin Chemistry medicine.drug_class Baroreflex medicine.anatomical_structure Endocrinology Posterior pituitary Hypothalamus Arginine vasopressin receptor 2 Internal medicine medicine hormones hormone substitutes and hormone antagonists |
Zdroj: | Progress in Neuropeptide Research ISBN: 9783764322687 |
DOI: | 10.1007/978-3-0348-5692-8_11 |
Popis: | Circulating vasopressin facilitates baroreflex function and, thus, controls the activity of the symphathetic nervous system. In the present work elevation of plasma norepinephrine (NE) levels was induced in rats by anterolateral cut (ALC) of the medial basal hypothalamus (MB). The intervention interrupted the vasopressinergic pathways from supraoptic and paraventricular nuclei to the posterior pituitary. The plasma NE response to immobilization stress was further potentiated in rats with ALC as compared to sham operated animals. The administration of Pitressin Tannat, a V 1 /V 2 -receptor agonist (1 IU per rat i.m. on 7 consecutive days) or dDAVP a V2 receptor agonist and non-pressoric synthetic analog of vasopressin, (approx. 100 μg per rat in drinking water on 7 consecutive days) reduced plasma NE levels in unstressed rats. However, the stress-induced potentiation of plasma NE elevation in rats with ALC was not significantly influenced by the apparently non-pressoric doses of exogenous vasopressin. It thus seems that vasopressin regulation of resting sympathetic activity is mediated predominantly by V2 subtype receptors. On the other hand, additional regulatory mechanisms seem to be involved in immobilization stress-induced potentiation of plasma NE evelation. |
Databáze: | OpenAIRE |
Externí odkaz: |