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Biomedical subjects

L E Earley

Publications and source records attributed to L E Earley.

At least 37 records · Page 2Linked to original sources
PubMed1971

Demonstration of independent roles of proximal tubular reabsorption and intratubular load in the phenomenon of glomerulotubular balance during aortic constriction in the rat.

The mechanism of glomerulotubular balance was investigated by microperfusion of the rat proximal tubule at two different rates before and after contriction of the aorta sufficient to produce a 50% reduction in whole kidney filtration rate and plasma flow. At a perfusion rate of 28 nl/min the absolute rate of proximal tubular reabsorption averaged 4.80+/-0.28 nl/mm.min in the absence of aortic constriction. Reducing the perfusion rate by one-half resulted in only a 22% decrease in the absolute rate of reabsorption, and imbalance between load and reabsorption resulted as fractional reabsorption of the perfused volume increased from 0.56 to 0.83 at 3 mm length of perfused tubule. These observations support other studies indicating that changing the load presented to the individual proximal tubule does not change reabsorptive rate sufficiently to result in glomerulotubular balance. Aortic constriction decreased the absolute rate of proximal tubular reabsorption approximately 50%, resulting in imbalance between load and reabsorption at the higher perfusion rate (fractional reabsorption of the perfused volume fell to 0.23 at 3 mm). Thus, the decrease in proximal tubular reabsorption necessary for glomerulotubular balance will occur independent of a change in the load presented for reabsorption. Balance between load and reabsorption was produced artificially by combining aortic constriction and a reduction in perfusion rate proportional to the reduction in whole kidney filtration rate. Mathematical analysis of the data suggests that the absolute rate of reabsorption along the accessible length of the proximal tubule is constant and is not proportional to the volume of fluid reaching a given site. Thus, there appears to be no contribution to glomerulotubular balance of any intra- or extratubular mechanism directly coupling load and the rate of proximal tubular reabsorption. It is concluded that glomerulotubular balance during aortic constriction is a consequence of hemodynamic effects of the maneuver to decrease filtration rate and the rate of proximal tubular reabsorption independently but in an approximately proportional manner.

Animals↗
PubMed1971

The relative contributions of reabsorptive rate and redistributed nephron filtration rate to changes in proximal tubular fractional reabsorption during acute saline infusion and aortic constriction in the rat.

The absolute rate of reabsorption by superficial rat proximal tubules was measured by the in situ microperfusion technique under conditions of hydropenia, infusion of saline, and infusion of saline plus aortic constriction sufficient to decrease whole kidney filtration rate below hydropenic levels. Fractional reabsorption was measured in adjacent filtering nephrons by collecting and recollecting tubular fluid from late proximal convolutions during each experimental condition. During hydropenia, the absolute rate of proximal tubular reabsorption averaged 3.56 +/-0.60 nl/min per mm and late proximal tubular fractional reabsorption averaged 0.56 +/-0.10. From these two measurements and measurements of tubule length to the site of micropuncture, a value for filtration rate was calculated for filtering nephrons. During hydropenia this value averaged 32.9 +/-7.1 nl/min. Saline infusion increased sodium excretion to 5.5% of the filtered load as the absolute rate of proximal tubular reabsorption decreased 38% and fractional reabsorption decreased 45%. Calculated superficial nephron filtration rate increased 21% which on the average was identical with the simultaneously measured increase in whole kidney filtration rate. Similar results were obtained in a separate group of animals by the technique of total collection of late proximal tubular fluid. Aortic constriction during saline infusion decreased whole kidney and calculated nephron filtration rate to the same degree and to values lower than those during hydropenia. Fractional reabsorption increased but not to hydropenic values. The persistent natriuresis during aortic constriction was associated with a continued depression of the absolute rate of proximal tubular reabsorption which was sufficient to maintain an increased delivery of filtrate out of the proximal tubule despite the fall in nephron filtration rate. These results indicate that depressed fractional reabsorption in the proximal tubule during acute saline infusion is due predominantly to a decrease in absolute reabsorptive rate and to a lesser extent to an increase in superficial nephron filtration rate which is proportional to the increase in whole kidney filtration. Continued natriuresis when filtration rate is decreased during saline infusion can be accounted for entirely by the persistent large reduction in the absolute rate of proximal tubular reabsorption.

Aminohippuric Acids↗
PubMed1971

The mechanism of decreased intestinal sodium and water absorption after acute volume expansion in the rat.

Studies were performed in rat small intestine in vivo to determine the effect of saline infusion on intestinal transport of Na(+) and H(2)O. Saline infusion decreased net Na(+) flux (J(n) (Na)) from 12.7 +/-0.8 to 6.4 +/-1.5 muEq/hr per cm in the jejunum when the intestinal perfusate contained both Na(+) and glucose. A similar fall in J(n) (Na) occurred in ileum. When mannitol was substituted for glucose in the perfusate, control absorption decreased 29% in jejunum and 18% in ileum, but saline infusion still caused a decrease in J(n) (Na) quantitatively similar to that seen when glucose was present. When choline was substituted for Na(+) in the perfusate, there was net movement of Na(+) from blood to lumen during control and this net secretion was increased further after saline infusion. These observations suggest that saline infusion has a similar effect to decrease intestinal J(n) (Na) under three widely different conditions of basal sodium transport. Permeability of intestinal mucosa to inulin was very low under basal conditions but increased fivefold after saline infusion, and the unidirectional flux of Na(+) from blood to lumen doubled. This increase in unidirectional flux of Na(+) was greater than the observed decrease in J(n) (Na).Thus, saline infusion decreased net absorption of Na(+) and H(2)O from small intestine through mechanisms which did not appear to be dependent upon the rate of Na(+) flux from lumen to blood, and in association with an increased flux of inulin and Na(+) into the intestinal lumen. The data suggest that the effect of saline infusion to decrease net absorption from the intestine could be due either to an increase in passive permeability of the epithelium which could disrupt solute gradients within the membrane or to an increase in flow of solution into the intestinal lumen.

Animals↗
PubMed1970

Effects of hematocrit on renal hemodynamics and sodium excretion in hydropenic and volume-expanded dogs.

The effects of hematocrit on renal hemodynamics and sodium excretion were studied in anesthetized dogs during both hydropenia and volume expansion. The hematocrit was decreased by isovolemic exchange with the animal's own previously harvested plasma and increased by isovolemic exchange with fresh, washed red blood cells. Renal perfusion pressure was maintained constant throughout the experiments by the adjustment of a suprarenal aortic clamp. During hydropenia, a decrease in hematocrit was associated with an increase in sodium and potassium excretion and solutefree water reabsorption. These changes were accompained by an increase in renal plasma flow and renal blood flow and a decrease in renal vascular resistance. Glomerular filtration rate was unchanged and filtration fraction was significantly decreased as hematocrit was lowered. Increasing hematocrit during hydropenia had the opposite effects on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics. In another group of animals, hematocrit was lowered during volume expansion with either saline or plasma, then returned to the control level by isovolemic exchange with washed red blood cells. This increase in hematocrit during volume expansion had a similar effect on electrolyte excretion, solute-free water reabsorption, and renal hemodynamics as during hydropenia. These results therefore suggest that acute changes in hematocrit may significantly affect sodium excretion and renal hemodynamics during both hydropenia and volume expansion. The changes in solute-free water reabsorption and potassium excretion suggest that the alterations in hematocrit may affect primarily the reabsorption of sodium in the proximal tubule. The concommitant effects of hematocrit on renal vascular resistance and filtration fraction may mediate this change in sodium reabsorption by altering hydrostatic and oncotic pressures in the peritubular circulation.

Animals↗
PubMed1969

Sodium metabolism.

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Adrenal Cortex Hormones↗