Interaction between the Hypothalamic Defence Reaction and Cardiac Ventricular Receptor Reflexes

Abstract

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.

Role of cardiac vagal c-fibers in cardiovascular control

“…The interaction between the cardiovascular effects induced by stimulation in the hypothalamic defense area and the cardiac C-fiber reflexes has been studied in the cat by Wennergren et al (1976b).…”

“…The marked poststimulatory bradycardia seen immediately upon release of defense area stimulation is probably triggered in part from these left ventricular C-fibers because bradycardia can be observed after complete baroreceptor denervation (Lisander et al, 1975). During the defense area stimulation the reflex bradycardia response is, however, centrally suppressed (Wennergren et al, 1976b) and can first be observed in the poststimulatory period. Sinoaortic denervation in dogs will induce an acute and marked elevation of blood pressure.…”

“…During the period of exercise the reflex vagal bradycardia from the ventricular C-fibers will be blocked by central influencies (Wennergren et al, 1976b), but the sharp fall in heart rate after cessation of exercise might be a reflex effect via arterial baroreceptors and cardiac receptors.…”

“…Ventricular pressure receptors with medullated afferents (Kolatat et al, 1967), atrial receptors with medullated afferents (Recordati et al, 1971;Zucker and Gilmore, 1974), and ventricular nonmedullated endings (Thordn, 1972a;1976b are activated within 1 rain after onset of an experimental coronary artery occlusion. However, the left ventricular receptors with nonmedullated afferents are likely to be the receptor station responsible, for the same reasons as discussed earlier in connection with the receptor group responsible for the reflex response to aortic occlusion.…”

Interaction between “mental stress” and baroreceptor reflexes concerning effects on heart rate, mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats

“…This dissociation with a reduced reflex control of heart rate but a normal or even augmented reflex control of renal sympathetic activity when arterial baroreceptors and cardiac mechanoreceptors are activated in SHR, suggest that central mechanisms are involved as earlier discussed by Ricksten & Thortn (1981). It has been shown that stimulation of the hypothalamic defence area can strongly suppress the efferent vagal component of the reflex bradycardia during baroreceptor or cardiac volume receptor activation, while the concomitant reflex inhibition of vasoconstrictor fibre activity baroreceptor stimulation remain largely unaffected by the hypothalamic stimulation (Gebber & Snyder 1970, Djojosugito et al 1970, Wennergren et al 1976, Wilson et al 1971. This seems to be due to a selective central suppression of the reflex arch involving the efferent vagal fibres to the heart.…”