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Baroreceptor input regulates osmotic control of central vasopressin secretion
M F Callahan1, M Ludwig, K P Tsai
1Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston Salem, N.C. 27157-1083, USA. mcallahan@medcenter.wpmail.wfu.edu
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.
Insights
Sinoaortic baroreceptor denervation (SAD) heightens the osmotic sensitivity of vasopressin (VP) neurons. This leads to increased VP release and greater cardiovascular responses to osmotic challenges, both direct and peripheral.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Endocrinology
Background:
- Sinoaortic baroreceptor denervation (SAD) alters cardiovascular and endocrine responses.
- Previous studies indicate SAD increases vasopressin (VP) and oxytocin (OT) secretion and pressor agent responses.
Purpose of the Study:
- To investigate if SAD enhances cardiovascular and endocrine responses to direct and peripheral osmotic stimulation of the supraoptic nucleus (SON).
Main Methods:
- Rats underwent sinoaortic baroreceptor denervation (SAD) or sham operation.
- Supraoptic nucleus (SON) microdialysis measured peptide release (VP, OT) and mean arterial pressure (MAP).
- Direct SON and peripheral osmotic stimulation with hypertonic NaCl were employed.
Main Results:
- SAD rats exhibited significantly greater osmotically induced VP release in the SON compared to controls.
- Cardiovascular pressor responses to osmotic stimulation were significantly enhanced in SAD rats.
- SAD rats showed a markedly increased central VP response to peripheral osmotic stimulation.
Conclusions:
- Baroreceptor denervation induces heightened osmotic sensitivity in VP neurons.
- Increased central VP release occurs in response to both direct and peripheral hypertonic NaCl stimulation following SAD.
- SAD leads to augmented cardiovascular and endocrine responses to osmotic stimuli.