ACUTE NA-ATPASE INHIBITION WITH BUFALIN IMPAIRS PRESSURE NATRIURESIS IN THE RAT(,K+)

Although it has been reported that Na+,K+-ATPase inhibition with bufal in induces acute and chronic hypertension in the rat, the mechanisms m ediating this response are unclear. To examine the role of the kidney in this process, glomerular filtration rate, renal blood flow, and pre ssure natriuresis were determined in rats treated with bufalin or vehi cle during changes in renal perfusion pressure. Mean arterial pressure increased from 123+/-4 to 149+/-3 mm Hg (P<.05) after 40 minutes of i ntravenous bufalin and remained at this level. In control rats, glomer ular filtration rate was well autoregulated. In bufalin-treated rats, glomerular filtration rate fell with decreasing renal perfusion pressu re. Glomerular filtration rate autoregulatory index was greater in buf alin-treated than control rats (P<.05). Renal blood flow showed a simi lar pattern. Urine flow and sodium excretion were less in bufalin-trea ted than control rats at equivalent renal perfusion pressures. The slo pe of the line describing the relation between urine flow and renal pe rfusion pressure was greater (P<.05) in control than bufalin-treated r ats. Similarly, the slope of the line relating sodium excretion to ren al perfusion pressure was greater (P<.05) in control than bufalin-trea ted rats. Thus, acute increases in blood pressure during Na+,K+-ATPase inhibition are associated with impaired renal autoregulation and pres sure natriuresis. This effect may be important in chronic hypertension associated with Na+,K+-ATPase inhibition in the rat.