Abstract
Effects of renal artery infusion of hypertonic solutions of glucose, mannitol, Na2SO4, NaCl and urea on renal blood flow (RBF) and renal handling of PAH were studied in anesthetized dogs. RBF was determined by continuous venous outflow recording and glomerular filtration rate as renal plasma flow times creatinine extraction ratio. Glucose solution increased, mannitol and Na2SO4 did not significantly alter while urea and NaCl depressed RBF. Only for NaCl RBF depression became greater with increasing solute loads applied. Spontaneous renal vasoconstriction and ureteral occlusion prevented RBF fall during urea and NaCl infusions. It is proposed that renal vascular reponse to local elevation of plasma osmolality is a resultant of two opposed effects: nonspecific vasodilatation as described for other vascular beds and vasoconstriction characteristic for renal vasculature and demonstrable only in normally functioning kidney. The extraction ratio of PAH (E PAH) was not altered by hypertonic urea but decreased with the four remaining infusates. The net tubular transport of PAH fell with NaCl infusion but was not changed with glucose, Na2SO4, mannitol and urea. It is concluded thatE PAH depression during NaCl infusion was due to inhibition of cellular PAH transport while that observed with glucose, Na2SO4 and mannitol reflected increased fraction of RBF perfusing nonsecretory renal medullary tissue.
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