Why the study?
Does renal denervation and angiotensin II inhibition alter nephron filtration rate and glomerular hemodynamics in hydropenic rats?
Does renal denervation and angiotensin II inhibition alter nephron filtration rate and glomerular hemodynamics in hydropenic rats?
Renal denervation in hydropenic rats enhances endogenous angiotensin II activity, which reduces the glomerular ultrafiltration coefficient and modulates renal vascular resistance.
Does not support clinical translation from rat models; leaves open whether denervation-angiotensin interactions alter human glomerular hemodynamics.
Nephron filtration rate (SNGFR), its determinants, and proximal tubular reabsorption were measured in hydropenic Munich-Wistar rats with sham-operated (sham) or denervated (DNx) kidneys before and during the administration of [Sar1, Ala8]angiotensin II or SQ 14225. The glomerular ultrafiltration coefficient (LpA) was significantly lower in DNx than in sham rats (P less than 0.025). However, SNGFR was not altered due to an offsetting increment in transcapillary glomerular hydrostatic pressure (delta P) in DNx (P less than 0.005). The marked increment of delta P in DNx was due to an increase in the glomerular capillary hydrostatic pressure, secondary to decreased afferent arteriolar resistance. The infusion of angiotensin II inhibitors to denervated kidneys completely normalized LpA but did not alter sham values. SQ 14225 but not [Sar1, Ala8]angiotensin II infusion provided a nephron plasma flow-dependent increase in SNGFR, secondary to a striking reduction in both glomerular vascular resistances. Endogenous angiotensin II activity may be enhanced by renal denervation, and angiotensin II acts to reduce LpA in this condition and may modulate the final level of renal vascular resistances after acute renal denervation.
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Pelayo et al. (1984) studied this question.
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