1 Department of Physiology and Biophysics, University of Mississippi School of Medicine Jackson, Mississippi 39216
Experimental hypertension was produced in dogs by salt loading after renal mass had been surgically reduced to an estimated one-third normal. Salt loading was accomplished in one group of five dogs by administering isotonic saline in lieu of drinking water and in another group of six dogs by continuously infusing isotonic saline. Arterial pressure, cardiac output, heart rate, stroke volume, and total peripheral resistance were determined at frequent intervals during a 1-week control period and a 2-week salt-loading period in both groups. In addition, right atrial pressure, blood urea nitrogen, serum sodium, and serum potassium were determined in the group that was continuously infused. Both groups demonstrated an increase in mean arterial pressure to hypertensive levels, transiently increased cardiac output and stroke volume, initially depressed then subsequently increased total peripheral resistance, and initially depressed and variable heart rate. It is concluded that salt loading in a partially nephrectomized dog causes elevated arterial pressure that is initially induced by increased cardiac output but that is eventually sustained by increased peripheral resistance. Possible mechanisms are discussed.
Accepted on June 16, 1969
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