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D L Maude

Publications and source records attributed to D L Maude.

13 recordsLinked to original sources
PubMed1984

Pressure natriuresis and prostaglandin secretion by perfused rat kidney.

Isolated rat kidneys respond to elevations of perfusion pressure with an increase in glomerular filtration rate (GFR), filtration fraction (FF), and sodium excretion (UNaV) and a fall in fractional sodium reabsorption (FRNa). Significant linear correlations exist between each of these dependent variables and the renal artery pressure (P). In control kidneys, pressure natriuresis is seen to result both from an increase in filtered sodium load and a decrease in FRNa. In kidneys treated with indomethacin in doses which curtail the release into the perfusate of prostaglandin E2 (PGE2) and the prostacyclin metabolite, 6-keto-PGF1 alpha, the regression lines relating GFR, FF, and UNaV to P are shifted to the right. Thus, prostaglandin-inhibited kidneys require higher pressures than control kidneys to maintain comparable rates of filtration and sodium excretion. Total renal vascular resistance (RVR) is also higher in inhibited kidneys. These findings suggest that in the isolated perfused rat kidney, prostaglandins promote pressure natriuresis by maintaining afferent arteriolar dilation. Their inhibition leads to afferent constriction, which raises RVR, lowers FF and GFR, and reduces sodium excretion.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Handling of insulin by the isolated perfused rat kidney.

The organ clearance of insulin calculated from the rate of disappearance of immunoreactive insulin from the perfusate averages 0.76 ml.min-1.g kidneys wt-1, a value greater than the simultaneously measured glomerular filtration rate. Clearance does not fall when hormone concentration is as high as 7 X 10(-8) M (10,000 microunits/ml). Fifteen percent of the cleared insulin is excreted in the urine; the remainder is chemically modified and appears in the perfusate both as low molecular weight fragments and as high molecular weight species. In the process of clearing the hormone, kidney tissue accumulates both intact insulin and 125I-labeled insulin degradation products. the organ clearance of insulin is not curtailed when the glomerular filtration rate is sufficiently reduced (by lowering perfusate pressure) to cause urine flow to cease. Studies using hyperglycemic perfusates and kidneys taken from starving or streptozotocin-diabetic animals provided no evidence that the kidney plays a role in the regulation of plasma glucose by modulating the rate of insulin degradation.

Animals↗
PubMed1981

Acid excretion by bicarbonate-free perfused rat kidney.

We measured titratable acid (TA) and NH4 excretion by isolated rat kidneys perfused either with conventional bicarbonate-containing solutions or with solutions in which bicarbonate was replaced by propionate. Rates of TA excretion by bicarbonate-perfused kidneys were similar to in vivo values, 0.27 +/- 0.04 mueq.ml GF-1 (0.21 mueq.min-1.g-1), and increased significantly under bicarbonate-free conditions to 0.70 +/- 0.12 mueq.ml GF-1 (0.42 mueq.min-1.g-1). At the same time the perfusate/urine pH difference (delta pH) increased significantly, from 0.63 +/- 0.06 to 0.92 +/- 0.06. Carbonic anhydrase inhibition by 5 X 10(-4) M acetazolamide alkalinized the urine of bicarbonate-perfused kidneys, while in the bicarbonate-free preparation the urine remained acid (delta pH = 0.27 +/- 0.04) and titratable acid continued to be excreted, though at a reduced rate, 0.19 +/- 0.04 mueq.ml GF-1. Under these same bicarbonate-free carbonic anhydrase-inhibited conditions, lowering the perfusate pH from 7.4 to 7.1 increased delta pH to 0.36 +/- 0.02 and caused total acid excretion (TA + NH4) to rise from 0.29 +/- 0.04 to 0.45 +/- 0.06 mueq.ml GF-1, and increasing the perfusate [HPO4] from 2.4 to 9.6 mM increased TA to 0.80 +/- 0.09 mueq.ml GF-1.

Acetazolamide↗
PubMedDate not supplied

Salt excretion and vascular resistance of perfused kidneys of Dahl rats.

We used a cell-free, 5% albumin-containing bicarbonate saline solution to perfuse kidneys of salt-sensitive (S) and salt resistant (R) rats derived from Dahl's original strains. The animals had been maintained on diets whose salt content was either 8% ((+)Na) or 0.4% ((-)Na). On these regimens only S(+)Na rats become hypertensive. Glomerular filtration rate (GFR), urinary sodium excretion (NaE), renal vascular resistance (RVR), and filtration fraction were measured as perfusate pressure (P) was increased in stepwise fashion from the 80-100 to the 140-160 mm Hg range. Pressure-GFR and pressure-natriuresis curves for the S(-)Na kidneys were displaced to the right of R, so that for any given value of P both GFR and NaE were significantly less for S(-)Na than for R kidneys. Kidneys from hypertensive (S(+)Na) animals had even more markedly impaired filtration and salt excretion. Although R and S(-)Na kidneys had nearly the same RVR at the lowest perfusate pressures, only the S kidney showed an autoregulatory rise in RVR as perfusate pressure was increased. Filtration fraction did not change, so the rise in resistance probably reflects chiefly afferent arteriolar constriction. Thus, in comparison with R, perfused S kidneys show an intrinsic defect in salt excretion ascribable to a reduced filtered sodium load. The rightward shift of their pressure-GFR curves may be due to an exaggerated afferent arteriolar vasoconstrictor response to increase in perfusion pressure.

Animals↗