Why the study?
Do anteroventral third ventricle (AV3V) lesions prevent increases in blood pressure and vascular Na+-pump activity in rats with two-kidney Goldblatt hypertension?
Do anteroventral third ventricle (AV3V) lesions prevent increases in blood pressure and vascular Na+-pump activity in rats with two-kidney Goldblatt hypertension?
AV3V lesions prevent the development of hypertension and increased vascular Na+-pump activity in a rat model of renovascular hypertension, suggesting a central nervous system role in regulating vascular sodium pump function.
AV3V lesions may implicate central regulation of vascular Na+-pump in rat renovascular hypertension; leaves open translation to human disease and should not change practice.
We studied the effects of anteroventral third ventricle (AV3V) lesions on the vascular Na+-pump activity and blood pressure of rats prepared by the two-kidney Goldblatt procedure. Blood pressures and Na+-pump activity of the isolated tail arteries, measured as ouabain-sensitive 86Rb+-uptake were determined in rats with renal artery clips, rats with AV3V lesions, and rats with AV3V lesions. Rats with renal artery clips developed higher blood pressures (40%) and higher vascular Na+-pump activity (20%-35%) than rats with no renal clips. Placement of AV3V lesions prior to the placement of renal clips prevented the increase in blood pressure and the increase in vascular Na+-pump activity. Plasma potassium and creatinine concentrations, nonspecific 86Rb+-uptake, and hematocrit were not different among these groups. Plasma sodium concentration was elevated in the AV3V lesioned control group. These experiments suggest a possible role of this CNS region in the regulation of vascular Na+-pump function during hypertensive states.
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Songu‐Mize et al. (1983) studied this question.
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