Ventricular receptors stimulate vasopressin release during hemorrhage

Abstract

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Evolution of Physiological and Behavioural Mechanisms in Vertebrate Body Fluid Homeostasis

“…However, the increase in vasopressin that occurs in severe haemorrhage may be caused by an increase in the discharge rate of ventricular receptors, not a decrease (Wang et al 1988). Ventricular denervation, but not sinoaortic denervation, markedly attenuated the increase in vasopressin after haemorrhage.…”

Spatially and temporally differentiated patterns ofc‐fosexpression in brainstem catecholamilriergic cell groups induced by cardiovascular challenges in the rat

“…Hypotensive hemorrhage is a broad-spectrum hemodynamic stimulus, eliciting a constellation of compensatory autonomic and humoral responses, in which the renin-angiotensin system, magnocellular neurosecretory system, and the hypothalamopituitary-adrenal axis are actively involved (Gann et al, 1978;Plotsky andvale, 1984;Darlington et al, 1986). Loss of blood results in reduction in blood pressure and volume and unloads the arterial and cardiaclcardiopulmonary mechanoreceptors on the high-and low-pressure sides of the circulatory system, respectively (Hakumaki et al, 1985;Quail et al, 1987;Wang et al, 1988). Information encoded in the discharge pattern of primary afferents (Amdt et al, 1977;Hakumaki et al, 1985) is conveyed to the NTS via the vagus and glossopharyngeal nerves (Contreras et al, 1980;Ciriello, 1983;Donoghue et al, 1984;Housley et al, 1987) for distribution within the central nervous system.…”

Physiology of Kidney Renin

“…It is well known that stimulation of the left atrial receptors leads to a reflex reduction in the RSNA and the inhibition of renin release (298), and a fall in the systemic blood pressure unloads the carotid baroreceptors and leads to the stimulation of renin release (195,868). However, the increased renin secretion in response to hypotensive hypovolemia does not seem to depend on the cardiac or arterial baroreceptors (704,872,873,932).…”