The present study examined the hypothesis that
hypovolemia stimulates
vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial
hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to
hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After
subcutaneous injection of 30%
polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in
alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral
vagotomy had minimal effects on basal VP levels, and
vagotomy in chronic NTS-lesioned rats did not prevent
hemorrhage-evoked increases in VP secretion. These results do not support the idea that
hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for
hypovolemia-induced VP secretion in rats.