Lichardus B

Regulation of the sympathetic nervous system by circulating vasopressin.

Neural regulation of the sympathoadrenal system (SAS) is not yet fully understood. It has been shown that various areas within the brain interact with sympathetic preganglionic neurons in the thoracic cord (1,2). Secretion of epinephrine (EPI) or norepinephrine (NE) into the blood of rats was found to be changed after electrical stimulation of certain areas in the medulla oblongata (3), the pons, and the midbrain (4), as well as in different parts of the hypothalamus (5,6). Plasma catecholamines were shown to be modulated also by the action of brain catecholamines (7).

The Anterior Third Ventricle Region is a Receptor Site for Composition Rather than Volume of Body Fluids

The first International Symposium on natriuretic hormones took place in 1969 at Smolenice Castle. At that time, the prevailing evidence pointed to the existence of only one specific natriuretic hormone: a small peptide. This hormone was postulated to inhibit the activity of the transporting enzyme, Na,K-ATPase, and was later classified as an endogenous inhibitor of the sodium pump—a digoxin-like substance. At a subsequent meeting in 1980 in Bratislava, it was decided to change the title to natriuretic hormones. The reason for the change was that in addition to the suggested, but still unidentified, natriuretic, hormone a number of well known hormones had been described that promoted renal sodium excretion (certain prostaglandins, kinins, dopamine, vasopressin, oxytocin, substance P, etc.) (1).

Circulating Vasopressin Attenuates the Increased Activity of the Sympathetic Nervous System Induced by Anterolateral Deafferentation of the Hypothalamus

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.