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C Baylis

Publications and source records attributed to C Baylis.

122 records · Page 7Linked to original sources
PubMed1978

Mechanism of the glucocorticoid-induced increase in glomerular filtration rate.

In order to investigate the mechanism(s) by which glucocorticoids increase GFR the determinants of glomerular ultrafiltration were measured in two groups of seven Munich-Wistar rats. Group 1 rats were normal controls and group 2 rats were pretreated with methylprednisolone (MP), 15 mg/kg per day for 4 days prior to study. In rats given MP mean values for SNGFR were about 25% higher than in the control group, averaging 33.6 +/- 1.6 (SE) vs. 27.0 +/- 1.0 nl/min. Mean values for initial glomerular plasma flow rate (QA) were also about 25% higher in MP-treated rats, averaging 83.4 +/- 3.9 vs. 65.9 +/- 1.9 nl/min in controls. Mean values of the transglomerular hydraulic pressure difference (deltaP) as well as afferent (IIA) and efferent (IIE) oncotic pressures were essentially similar between control and MP-treated rats. Filtration pressure equilibrium, i.e., equality between IIE and deltaP, obtained in both groups and the mean minimum estimates of the ultrafiltration coefficient (Kf) were also similar between control and MP-treated rats. Thus, the rise in SNGFR following MP is entirely due to the increase in AQ, rather than to changes in the other determinants of ultrafiltration.

Animals↗
PubMed1978

Modulation by prostaglandin synthesis inhibitors of the action of exogenous angiotensin II on glomerular ultrafiltration in the rat.

We studied the effects of angiotensin II (A II) infusion, with and without inhibition of prostaglandin (PG) synthesis, on the determinants of glomerular ultrafiltration in 27 plasma volume-expanded Munich-Wistar rats. The effects of PG inhibition alone and infusion of vehicle alone also were investigated. With a pressor dose of A II single nephron (SN) GFR and total GFR did not change significantly, despite declines in both glomerular plasma flow rate (QA) and the ultrafiltration coefficient (Kf), due to an offsetting rise in the transcapillary hydraulic pressure difference (deltaP). Afferent and efferent arteriolar resistances (RA and RE) increased by approximately 100% above control during A II infusion. Inhibition of PG synthesis alone and infusion of vehicle alone similarly failed to affect SNGFR and total GFR, and only slight changes occurred in the determinants of glomerular ultrafiltration in these rats. When A II infusion was accompanied by inhibition of PG synthesis, however, profound declines in SNGFR and total GFR were seen, due to further reductions in QA and 2-fold greater increases in RA and RE than occurred with the same dose of A II alone. The A II-induced fall in Kf was not affected by simultaneous PG inhibition. Thus, endogenous PGs attenuate the vasoconstrictor actions of A II on the superficial renal microvasculature and minimize changes in QA, SNGFR, and total GFR. It is likely that an interaction between A II and PG may be important in pathophysiological conditions in which endogenous A II levels are elevated.

Angiotensin II↗
PubMed1978

Permselectivity of the glomerular capillary wall. Facilitated filtration of circulating polycations.

To examine the electrostatic effects of fixed negative charges on the glomerular capillary wall, polydisperse [(3)H]DEAE dextran, a polycationic form of dextran, was infused into 10 Munich-Wistar rats. Fractional clearances of DEAE ranging in radius from 18 to 44A were determined in these rats, together with direct measurements of the forces and flows governing the glomerular filtration rate of water. These results were compared with data previously obtained in Munich-Wistar rats receiving tritiated neutral dextran (D) and polyanionic dextran sulfate (DS). Measured values for the determinants of the glomerular filtration rate of water in rats given DEAE were found to be essentially identical to those in rats given either D or DS. In addition, DEAE was shown to be neither secreted nor reabsorbed. Fractional clearances of polycationic DEAE were increased relative to both D and DS, the increase relative to D being significant for effective molecular radii ranging from 24 to 44A. Fractional DEAE clearances were also measured in a separate group of six Munich-Wistar rats in the early autologous phase of nephrotoxic serum nephritis (NSN). Fractional DEAE clearances in NSN rats were reduced significantly, relative to values measured in normal rats, for effective DEAE radii ranging from 18 to 42A. Moreover, in NSN rats, fixed negative charges on the glomerular capillary wall were greatly reduced, relative to non-NSN rats, as evidenced by a reduction in intensity of colloidal iron staining. Thus, in NSN rats, DEAE clearances were essentially indistinguishable from values obtained with both neutral D and polyanionic DS.

Animals↗
PubMed1977

Mechanisms of the defect in glomerular ultrafiltration associated with gentamicin administration.

Micropuncture studies were performed in three groups of Munich-Wistar rats: eight normal hydropenic controls (group I) and two groups (eight rats each) which were treated with gentamicin in doses of either 4 or 40 mg/kg/day for ten days (groups II and III, respectively). Following gentamicin administration, values for single nephron (SN) GFR were reduced markedly, from the control mean of 31 +/- 0.7 (SEM) nl/min to 22.4 +/- 1.5 and 20.5 +/- 0.9 for groups II and III, respectively. Declines in whole kidney GFR paralleled these falls in SNGFR. The primary cause of the reduction in SNGFR was a marked decline in glomerular capillary ultrafiltration coefficient, Kf, in both gentamicin treatment groups. None of the other determinants of glomerular ultrafiltration were significantly affected in the low dose group (group II). In the high dose group (group III), however, mean values for initial glomerular plasma flow rate and mean transglomerular hydraulic pressure difference were significantly lower than in the control group, accounting for the somewhat greater decline in SNGFR observed in group III. Electron microscopic examination of kidney tissue from rats treated with both doses of gentamicin revealed no obvious abnormalities of the glomerular capillary wall, whereas the previously described morphologic aberrations of proximal convoluted tubule cells were readily demonstrable.

Animals↗
PubMed1977

Dynamics of glomerular ultrafiltration. IX. Effects of plasma protein concentration.

Experiments were carried out on 42 Munich-Wistar rats with surface glomeruli accessible to micropuncture to investigate the effects of reduction in systemic plasma protein concentration. CA, and thus afferent oncotic pressure, IIA, on the determinants of glomerular ultrafiltration. In animals in which CA was reduced by a variety of maneuvers, observed values for single-nephron GFR were lower than values predicted by the Starling relation, when the latter were calculated assuming that the observed increase in the net driving pressure for ultrafiltration (due to the reduction in IIA) was the only factor perturbed. In all experimental conditions where CA was reduced, rats were invariably observed to be at filtration pressure disequilibrium, permitting calculation of unique values of the ultrafiltration coefficient, Kt. In all low-CA groups, mean values of Kf were uniformly lower than values obtainedin normoproteinemic control animals. The failure of SNGFR to rise to predicted values when CA is reduced is therefore due to the concomitant reduction in Kf. No morphological basis for this reduction in Kf was discerned.

Animals↗
PubMed1977

Mechanisms of the puromycin-induced defects in the transglomerular passage of water and macromolecules.

To investigate the mechanism(s) of increased filtration of serum proteins after glomerular injury, polydisperse samples of uncharged [(3)H]dextran (D) or anionic [(3)H]dextran sulfate (DS) were infused into 14 control and 16 puromycin aminonucleoside- (PAN) treated Munich-Wistar rats. Fractional clearances of D or DS ranging in radius from 18 to 42A were determined in these rats, together with direct measurements of the forces governing the glomerular filtration rate of water. Whole kidney and single nephron glomerular filtration rates were approximately 40% lower in PAN-treated rats, relative to controls, due mainly to a marked reduction in the glomerular capillary ultrafiltration coefficient and, to a lesser extent, to a small reduction in glomerular plasma flow rate as well. In PAN-treated rats, as in normal controls, inulin was found to permeate the glomerular capillary wall without measurable restriction, and both D and DS were shown to be neither secreted nor reabsorbed. Fractional clearances of uncharged D were reduced after PAN administration, falling significantly for effective D radii from 22 to 38A. Utilizing a theory based on macromolecular transport through pores, these results indicate that in PAN-treated rats, effective pore radius is the same as in controls, approximately 44A. In PAN nephrosis, however, the ratio of total pore surface area/pore length, a measure of pore density, is reduced to approximately one-third that of control, due very likely to a reduction in filtration surface area. In contrast to the results with uncharged D, fractional clearances of DS were found to increase after PAN administration for all DS radii studied. These results with D and DS suggest that proteinuria in PAN nephrosis is due, not to an increase in effective pore radius or number of pores, but rather to a diminution of the electrostatic barrier function of the glomerular capillary wall, thereby allowing increased passage of polyanions such as DS and albumin.

Animals↗
PubMed1976

The effect of plasma potassium in determining normal rates of excretion of potassium in dogs.

Doses of 5-15 mmol KCl or KHCO3 (less than the daily intake in food) given by stomach tube or intravenous infusion, produced increases in plasma K and in K excretion, the time delay between change in plasma K and rate of excretion being minimal. Without doses of K salts in control experiments, plasma K concentration was about 4 mmol/1 and K excretion about 5 mumol/min. After doses of KCl or KHCO3, plasma K and rate of excretion of K both increased, increase of 0-5 mmol/1 in plasma K being associated with an increase of about 35 mumo1/min in K excretion. Increased excretion of K was accompanied by a small increase in Na excretion. Excretion of both C1 and HCO3 increased, C1 more after HCO3 more after KHCO3. The results indicate that within normal ranges, plasma K is an important factor determining the rate of excretion of K.

Animals↗
PubMed1976

The effect of the anions, phosphate and sulphate, on normal rates of excretion of potassium in dogs.

Small doses of (NH4)2HPO4 or KH2PO4 by stomach tube caused increase in plasma PO4 and PO4 excretion. Above a threshold of 0-8 mmol. 1(-1), increase of plasma PO4 by 0-5 mmol. 1(-1) caused PO4 excretion to increase by about 35 mumol. min.-1 After KH2PO4 this relationship was not altered by the concurrent increases in plasma K and K excretion. After doses of (NH4)2SO4 or K2SO4, excretion of SO4 was similarly related to plasma SO4 and was independent of plasma K and K excretion. An effect of PO4 on K excretion was observed after doses of (NH4)2HPO4, when increased excretion of PO4 was accompanied by increased excretion of K without change in plasma K. There was also increased excretion of NH4 and a small increase in Na excretion. The changes were similar to those produced by (NH4)2SO4 [O'Connor and Summerill, 1976]. KH2PO4 and K2SO4 produced increase in plasma K and increased excretion of K not significantly different from the changes produced by KCl or KHCO3 [Baylis and O'Connor, 1976]. After KH2PO2 or K2SO4, the urinary anion was PO4 or SO4, instead of Cl and HCO3. Any effect of anions on K excretion was much less than the effect of increase in plasma K. At low rates of excretion of K, increased urinary excretion of impermeant anion can determine increased excretion of K. However, the effect of anion is small in comparison with the effect of increase in plasma K.

Animals↗
PubMed1976

Effects of some vasodilator drugs on transcapillary fluid exchange in renal cortex.

In 23 Munich-Wistar rats with surface glomeruli, the determinants of glomerular ultrafiltration and peritubular capillary uptake of proximal reabsorbate were studied before and during intra-arterial infusions of mildly vasodepressor doses of prostaglandin E1,acetylcholine, and bradykinin. For each drug single-nephron glomerular filtration rate remained unchanged from normal hydropenic values while glomerular plasma flow rate increased, resulting in declines in single-nephron filtration fraction (SNFF). Mean glomerular transcapillary hydraulic pressure difference (delta P) increased or remained unchanged on average. Declines in SNFF were accompanied by reductions in efferent arteriolar oncotic pressure (piE). Filtration pressure equilibrium, equality between pi E and delta P, obtained before but not during drug infusions. In the latter situation values for the glomerular capillary ultrafiltration coefficient were calculated and found to be significantly reduced from published control values. Despite marked falls in pi E during drug infusion, absolute proximal reabsorption was not reduced significantly, due, it is suggested, to the opposing effects of increases in efferent arteriolar plasma flow and interstitial hydraulic pressure.

Acetylcholine↗
PubMed1976

Transport of molecules across renal glomerular capillaries.

Direct measurements of the pressures and flows governing the formation of glomerular ultrafiltrate have been made possible in recent years by virtue of 1) the discovery of rats and monkeys possessing glomerular capillaries on the renal cortical surface, accessible to micropuncture, and 2) technological advances that permit measurement of intracapillary hydraulic pressure and assessment of the change in colloid osmotic pressure along the glomerular capillary network. Based on these direct measurements, evidence has been obtained to indicate that glomerular capillary hydraulic pressure and hence the net driving force for ultrafiltration are lower than previously believed. By the efferent end of the glomerular capillary network, net filtration of fluid ceases, owing to a reduction in the net driving force to zero. Evidence in the rat indicates that the process of ultrafiltration is highly dependent on glomerular plasma flow rate. Studies in rats with surface glomeruli have also made possible an assessment of the factors that govern the transport of macromolecules across the highly specialized capillary network. In addition to molecular size, transcapillary movement of macromolecules is influenced by the glomerular filtration rate, since total transport reflects the combined contributions of convection as well as diffusion. Molecular charge has also been found to be an important determinant of the transport of macromolecules, very likely contributing to the marked restriction to the transcapillary movement of albumin. This electrostatic restriction to the transport of polyanions such as albumin, by some fixed, negatively charged component(s) of the glomerular capillary wall, is markedly reduced in primary glomerular injury. Evidence indicates that glomerular injury results in loss of these fixed negative charges from the capillary walls, providing an attractive explanation for the enhanced filtration of albumin, and hence the proteinuria, observed in a variety of glomerulopathic states.

Albumins↗