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PubMed1979

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.

Animals↗
PubMed1981

Mechanism of osmotic diuresis.

Mannitol might inhibit paracellular reabsorption of water and sodium chloride in the proximal tubules by reducing the osmotic driving force. We examined this hypothesis in anesthetized dogs. Bicarbonate reabsorption was kept constant by sodium bicarbonate infusion, and transcellular sodium chloride reabsorption was inhibited by ethacrynic acid. The glomerular filtration rate (GFR) was varied by altering renal perfusion pressure. Mannitol infusion reduced sodium chloride reabsorption from 62 +/- 5% to 33 +/- 5% of the filtered load. The calculated increase in reabsorbate osmolality, averaging 82 +/- 6 mOsm/kg H2O, was due to sodium bicarbonate and equalled the increase in plasma osmolality. Mannitol concentration averaged 81 +/- 7 mM in plasma and 101 +/- 12 mM in urine. A linear relationship between reabsorption and GFR (glomerulo-tubular balance) was maintained over the same range of GFR before and after mannitol infusion. Mannitol infusion reduced sodium chloride reabsorption from 2.6 to 1.4 moles for each mole of sodium bicarbonate reabsorbed. During mannitol infusion, acetazolamide inhibited sodium bicarbonate reabsorption as in control experiments, but reduced sodium chloride reabsorption less. We conclude that reduced water reabsorption increases sodium bicarbonate concentration in the paracellular fluid as much as mannitol concentration is raised in the plasma and glomerular filtrate. Along the proximal tubules, net osmotic force is progressively reduced as mannitol concentration rises, accounting for reduced water and sodium chloride reabsorption.

Acetazolamide↗
PubMed1997

Inhibition of angiotensin-converting enzyme modulates structural and functional adaptation to loop diuretic-induced diuresis.

The roles of elevated cell sodium concentrations and the angiotensin-aldosterone system (AAS) in the structural and functional adaptation of the distal tubule and collecting duct system to a chronic increase of sodium delivery were examined using electron microprobe and quantitative morphologic/stereologic analyses. Studies were performed on rats given the loop diuretic torasemide acutely (20 min) or chronically (12 days), either alone or in combination with the angiotensin-converting enzyme (ACE) inhibitor, enalapril. In the sodium-absorbing cells of the distal tubule and cortical collecting duct-that is, in distal convoluted tubule (DCT), connecting tubule (CNT) and principal cells-an acute increase in sodium delivery caused a significant rise in intracellular sodium concentration and rubidium uptake, the latter an index of in vivo Na,K(Rb)-ATPase activity. The elevated cell sodium concentrations returned to, or close to, control values during chronic torasemide treatment. Intracellular rubidium concentrations, measured after a 30-second rubidium exposure, were not different from controls in DCT and CNT cells but were still higher in principal cells. Since, however, the distribution space for rubidium was significantly increased in chronic torasemide animals, rubidium uptake, and hence Na,K-ATPase activity, must have increased in proportion to cell volume in DCT and CNT cells, but more than proportionately in principal cells. When ACE was inhibited during chronic torasemide, the epithelial volume of DCT and cortical collecting duct (CCD) was increased mainly by lengthening and not, as was the case in rats given torasemide alone, by thickening of the tubule wall. Adaptation of the proximal tubule exclusively by lengthening was not affected by inhibition of the ACE. These data indicate that changes in cell ion composition may participate in initiating cell processes leading to adaptation of distal nephron segments to chronically increased salt delivery. Inhibition of the ACE reverses the torasemide-induced increase in apparent Na pump density in principal cells and seems to shift the relationship between hypertrophy and hyperplasia noted in DCT and CCD after chronic torasemide in favor of hyperplasia.

Aldosterone↗