Baroreceptor Input Regulates Osmotic Control of Central Vasopressin Secretion

Abstract

Sinoaortic baroreceptor denervation (SAD) results in increased osmotically induced secretion of vasopressin (VP) and oxytocin (OT) and increased cardiovascular responses to many centrally acting pressor agents. Studies were conducted to determine whether SAD increases the cardiovascular and endocrine responses to direct and peripheral osmotic stimulation of the supraoptic nucleus (SON). SON microdialysis was performed in urethane-anesthetized male rats with measurement of dialysate peptides, mean arterial pressure (MAP) and heart rate. Experiment 1 tested the effect of direct stimulation of the SON with hypertonic NaCl in SAD, sham-operated (control) and intake-matched (matched) rats. Osmotically induced VP release into the SON was significantly greater in SAD than in control or matched groups. VP release peaked at 36 ± 13 and 15 ± 7 pg in SAD and controls, respectively, with no increase observed in the matched group. Plasma VP was significantly elevated after SON osmotic stimulation with no differences observed among the groups. The pressor response to osmotic stimulation was greater in SAD (29 ± 4 mm Hg) than in control (20 ± 3 mm Hg) and matched animals (15 ± 3 mm Hg). Experiment 2 tested the effect of intraperitoneal injection of hypertonic NaCl on SON VP and OT release. SAD rats showed an increased central VP response to peripheral osmotic stimulation, a 64-fold increase in SAD as compared to a 4-fold one in controls. Central OT release was not significantly altered (peak of 22 ± 6 vs. 11 ± 4 pg, SAD vs. control). A direct SON osmotic challenge given 3.5 h after the intraperitoneal test confirmed an increased VP responsiveness in the SAD group. Plasma VP and OT were significantly increased after intraperitoneal hypertonic saline with no difference observed between groups. The MAP response to intraperitoneal hypertonic saline was greater in the SAD group with an elevation of 37 ± 4 versus 18 ± 3 mm Hg observed in SAD versus control subjects. These results demonstrate that baroreceptor denervation produces a state of heightened osmotic sensitivity for VP neurons, with evidence for increased central VP release to both direct and peripheral hypertonic NaCl stimulation.

Antagonistic Oxytocin/α2‐Adrenoreceptor Interactions in the Nucleus Tractus Solitarii: Relevance for Central Cardiovascular Control

“…In fact, the role of oxytocin in heart rate control seems to be more pronounced than its role in blood pressure regulation. Oxytocin secretion is strongly influenced by sinoaortic denervation (37, 38) and oxytocin mediates stress‐induced tachycardia without affecting blood pressure (9).…”

Dendritic Release of Neurotransmitters

“…That oxytocin, but not vasopressin, is released within the SON and PVN in response to suckling has been demonstrated in push-pull perfusion studies in anaesthetized lactating rats (19) and microdialysis studies in conscious parturient and lactating animals (22). Somatodendritic suckling- or parturition-induced oxytocin release is inhibited by oxytocin antagonists infused into the SON, suggesting the receptor-mediated autoregulation of oxytocin release (163, 164).…”

“…The control of central peptide release by volume and pressor stimuli is also revealed by studies of hemorrhage and baroreceptor denervation; concentrations of vasopressin both in the plasma and in the PVN increase markedly in response to hemorrhage (179). Hemorrhage-induced decrease of arterial blood pressure stimulates vasopressin secretion through inhibition of baroreceptors and activation of chemoreceptors in the aortic arch and carotid body, while sinoaortic baroreceptor denervation increases the osmotically induced release of vasopressin and oxytocin from the posterior pituitary (159) and also increases somatodendritic vasopressin release stimulated by direct or peripheral hypertonic saline stimulation (22). …”

Vasopressin During Cardiopulmonary Resuscitation and Different Shock States

“…Howevduces little elevation in vasopressin plasma levels until blood er, in a similar manner to oxytocin-mediated paradoxical vasodilavolume decreases by >10%. [6] tation of vascular smooth muscle, vasodilatation after vasopressin has been described, not only in the pulmonary, coronary, and However, vasopressin secretion can also be directly stimulated vertebrobasilar circulation, but, interestingly, also in the mesenterby hypoxia, endotoxin, low levels of norepinephrine (noraic vascular bed. In a porcine cardiopulmonary resuscitation (CPR) drenaline) and angiotensin, and hypoglycemia.…”