Centrally-induced vasopressor responses to ouabain are augmented in spontaneously hypertensive rats.

Dihydroxyouabain (ouabain), 1.0-10 micrograms, per rat, injected intracerebroventricularly, produced dose-related vasopressor responses accompanied by corresponding increases in abdominal sympathetic nerve activity in 16 weeks old Wistar (NT) rats anesthetized with urethane. The heart rate then also increased, dose-dependently, to ouabain injected in doses up to 10 micrograms. However, 100 micrograms produced arrhythmia resulting in bradycardia. Pressor effects were appreciable within one minute after the ouabain injection, but did not become maximal until between 7-10 min later. Either the removal of sympathetic vasomotor tone by surgical section of the spinal cord or intravenous pretreatment with a vasopressin antagonist significantly reduced the vasopressor responses in the NT rat. Ouabain, 10 micrograms, injected intraventricularly in 16 weeks old Kyoto Wistar rats produced similar cardiovascular responses to those in the NT rat, but the magnitude of the blood pressure responses, along with the heart rate and sympathetic responses, was larger in SHR than in WKY. These results suggest that dihydroxyouabain acts centrally to elevate the blood pressure by increasing not only the sympathetic discharge but also, perhaps, the secretion of vasopressin. In light of previous studies showing that SHRs exhibit both sympathetic hyperactivity and hypersecretion of vasopressin, the present results suggest that their enhanced responsiveness to ouabain could result from both the sympathetic hyperactivity and an enhanced vasopressin release as a result of the centrally injected ouabain.