Effects of acute renal denervation on kidney function in deoxycorticosterone acetate-hypertensive swine

Abstract

Deoxycorticosterone acetate-induced hypertension in Yucatan miniature swine appears to involve elevated peripheral sympathetic activity. Abnormalities in renal function in these hypertensive animals are also apparent. To determine the extent to which renal nerve activity controls kidney function in animals with established deoxycorticosterone acetate hypertension, the effects of acute renal surgical denervation were assessed in five normal and 10 deoxycorticosterone acetate-treated swine. After 12 to 16 weeks of treatment, mean arterial pressure rose from the normal level of 110 to 120 to 164 ± 4 mm Hg but was decreased to 131 ± 4 mm Hg by anesthesia. In the normal animals, blood pressure under anesthesia was 114 ± 9 mm Hg. Acute left kidney surgical denervation significantly decreased renal vascular resistance and increased renal blood flow, glomerular filtration rate, urine flow, and sodium excretion only in the treated animals. In an additional group of six normal and eight deoxycorticosterone acetate-treated swine, the responses to renal pharmacological denervation with intrarenal guanethidine were evaluated. Guanethidine had no significant effect on renal blood flow, vascular resistance, glomerular filtration rate, urine flow, or sodium excretion in the normal animals. In contrast, in the mineralocorticoid-hypertensive animals, guanethidine significantly decreased renal vascular resistance and caused a diuresis and natriuresis with no change in glomerular filtration rate. We conclude that, in deoxycorticosterone acetate-treated miniature swine with established hypertension, renal nerve activity appears to be elevated and important in determining renal hemodynamics and sodium and water excretion.