Glomerular filtration during furosemide diuresis in the dog.

Simultaneous clearance and micropuncture experiments were performed in pentobarbital-anesthetized dogs to determine the effect of furosemide (F; 5 mg/kg) on some of the determinants of GFR during replacement of urine losses. Glomerular capillary pressure (PG) was estimated from stop flow pressure (SFP) plus systemic colloid osmotic pressure (pi alpha). Because renal vasodilation during F administration occurs more often when blood pressure is elevated, two groups of dogs were studied. At endogenous renal perfusion pressure (RPP) of 130 mm Hg, one group responded to F with a 28% increase in renal blood flow (RBF). PG rose (a rise of 18 mm Hg) in proportion to the rise in proximal tubule pressure (PT) (a rise of 20 mm Hg). Thus, the difference in pressures (PG - PT) was unchanged, as was GFR. The second group had RPP lowered by renal artery constriction to a point near the lower limit of autoregulation (104 mm Hg). These dogs responded to F with no increase in RBF; PG was lower and remained constant during F, PT, however, increased (a rise of 10 mm Hg). The difference in pressures (delta P) decreased by 30%, and GFR decreased by 40%. Single nephron glomerular filtration rate (SNGFR) also decreased, and estimated Kf, the ultrafiltration coefficient, actually rose slightly. The major reason for the fall in GFR and SNGFR was due to a decrease in delta P rather than a decrease in Kf. The decrease in delta P can be attributed to failure of the renal vasculature to dilate because PG and RBF remained constant. It is likely that these events will be observed less often at hypertensive BP than at normal BP where renal vascular resistence is already close to a minimum value.