CHRONIC NUCLEUS-TRACTUS-SOLITARIUS LESIONS DO NOT PREVENT HYPOVOLEMIA-INDUCED VASOPRESSIN SECRETION IN RATS

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor i nput. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 1 0 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral le sions of nucleus tractus solitarius (NTS). The VP response to hemorrha ge was similar to that seen in control rats and chronic sinoaortic-den ervated (SAD) rats. After subcutaneous injection of 30% polyethylene g lycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP l evels that correlated with the induced depletion of plasma volume. Add itionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal ef fects on basal VP levels, and vagotomy in chronic NTS-lesioned rats di d not prevent hemorrhage-evoked increases in VP secretion. These resul ts do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, ne ither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.