Excitation of the cardiac vagus by vasopressin in mammals.

Abstract

SUMMARY1. In unanaesthetized sheep, the sensitivity of the baroreceptor-cardio-inhibitory reflex was greater when intravenous vasopressin was used to raise blood pressure, than when intravenous phenylephrine was used to raise blood pressure. This difference was still evident in animals in which fl-adrenergic blockade had been carried out using propranolol.2. In the presence of combined f-adrenergic and muscarinic blockade, a direct negative chronotropic effect of intravenous vasopressin could not be demonstrated. It was concluded, therefore, that intravenous vasopressin enhanced cardiac vagal tone.3. This effect of vasopressin on efferent cardiac vagal tone was confirmed directly in anaesthetized dogs by recording from single cardiac vagal efferent fibres. Furthermore, recordings from single carotid sinus baroreceptor fibres did not demonstrate a direct action of vasopressin on the sensitivity of the baroreceptors. However, the pressor effect of vasopressin is associated with a greater increase in efferent cardiac vagal discharge than that seen when equipressor doses of phenylephrine are given, or when blood pressure is raised by a similar amount by inflation of an intra-aortic balloon.4. Studies in isolated guinea-pig atrial preparations and in anaesthetized rabbits and dogs, revealed no consistent peripheral action of vasopressin on the action of the vagus at the heart.

The cardiovascular effects of vasopressin after haemorrhage in anaesthetized rats.

“…Alternatively the reduced heart rate in both groups of l.e. rats may result from a central effect of vasopressin such as the inhibition of central sympathetic activity (Gardiner & Bennett, 1982) or central stimulation of cardiac vagal tone (Courtice et al 1984). Vasopressinergic fibres project from the paraventricular nuclei to the dorsal motor nucleus of the vagus (Safroniew, 1980) and also to sympathetic preganglionic neurones in the thoracic spinal cord (Yamashita, Kannan, Inenaga & Koizumi, 1983).…”

“…Vasopressin may directly influence cardiac function (Pullan, Johnston, Anderson & Korner, 1980). Alternatively release of the polypeptide within the central nervous system may modulate the activity of neurones that are implicated in the regulation of the cardiovascular system (Gardiner & Bennett, 1982;Courtice, Kwong, Lumbers & Potter, 1984).…”

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

“…AVP facilitates efferent cardiac vagal activity, reflex bradyeardia and reflex inhibition of sympathetic nerve activity, whereas All attenuates all of these (Lumbers, McCloskey & Potter, 1979;Courtice, Kwong, Lumbers & Potter, 1984;Schmid, Guo & Abboud, 1985;Peuler, Edwards, Schmid & Johnson, 1990). Interaction between the effects of the two peptides has also been reported; All attenuates the cardio-inhibitory effects of AVP (Caine, Lumbers & Reid, 1985).…”

Cerebellar Afferents to Neuroendocrine Cells: Implications for Adaptive Responses to Simulated Weightlessness.

“…Circulating vasopressin inhibits the sympathetic outflow [36] but accelerates the efferent vagal tone [37]. It is therefore reasonable to assume that in reactions, such as the defense or fastigial pressor response, neurally mediated inhibition of the baroreflex is also accompanied by inhibition of the vasopressin release by the hypothalamo-neurohypophyseal system.…”