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Biomedical subjects

F G Knox

Publications and source records attributed to F G Knox.

At least 145 records · Page 8Linked to original sources
PubMed1982

Restoration of phosphaturic response to parathyroid hormone by glucocorticoid treatment in phosphorus-deprived rats.

In phosphate deprivation, the kidney is resistant to the phosphaturic effects of several well-established phosphaturic stimuli, including PTH. We examined whether a low-phosphate diet would render rats unresponsive to the phosphaturic effects of glucocorticoids in the presence and absence of PTH. Treatment with triamcinolone (1 or 50 mg/kg/day) caused phosphaturia in rats fed a low-phosphate diet and also restored rhe phosphaturic effects of PTH. Plasma phosphate was significantly increased with both doses of glucocorticoid. There were no changes in acid-base parameters with the low dose and a compensated metabolic acidosis with the high dose of glucocorticoid. Renal gluconeogenesis was stimulated at both doses and was further enhanced by PTH at the higher dose. We conclude that glucocorticoids reverse the resistance to the phosphaturic phosphate and/or enhanced renal gluconeogenesis.

Acid-Base Equilibrium↗
PubMed1981

Effect of imidazole on renal function in unilateral ureteral-obstructed rat kidneys.

Imidazole has been proposed to reverse renal vasoconstriction following unilateral obstruction, presumably through blockade of thromboxane A2 (TXA2) synthesis. We examined this hypothesis in rats subjected to unilateral ureteral obstruction for 24 h by 1) performing renal function studies before and during imidazole infusion, and 2) measuring TXB2 and prostaglandin E2 (PGE2) in urine collected before and during imidazole infusion and the profile of products generated by metabolism of arachidonic acid with renal microsomes in vitro. Imidazole infusion was associated with only a bicarbonaturia in the postobstructed kidney; in contrast, clearance of PAH and inulin, fractional sodium excretion, and bicarbonate excretion were all increased in the contralateral kidney. In the postobstructed and contralateral kidneys, TXB2 excretion was diminished and PGE2 excretion was variable not only following imidazole infusion but after saline infusion as well. The profile of products generated by renal microsomal metabolism of arachidonic acid was similar among obstructed, contralateral, and normal kidneys. These results do not support the proposal that TXA2 is the mediator of renal vasoconstriction following unilateral ureteral obstruction.

Animals↗
PubMed1981

Measurement of nephron filtration in the dog: role of proximal intratubular pressure.

Previous studies concerning the measurement of single nephron filtration rate have shown that collections of proximal tubular fluid, in which an oil drop is held in a constant position, do not affect intratubular pressure in the early proximal tubule in the hydropenic rat. Since intratubular pressures are higher in the dog than the rat, we investigated the effect of position-controlled collections on proximal pressure and single nephron filtration rate (SNGFR) in the dog. During position-controlled collections, early proximal pressure fell 5.8 +/- 0.9 mmHg and SNGFR was 76.3 +/- 5.3 nl/min. During proximal re-collections, in which proximal pressure was maintained near the free-flow value using a long immobile oil block, SNGFR was significantly less, 44.4 +/- 5.5 nl/min. For each micropunctured kidney, SNGFR was also estimated by dividing GFR by the number of glomeruli (mean, 5.4 +/- 0.5 X 10(5)). Estimated SNGFR (50.9 +/- 6.3 nl/min) was not significantly different from pressure-controlled SNGFR but was significantly less than position-controlled SNGFR. Accordingly, in the dog, early proximal pressure decreases during position-controlled collection of proximal tubular fluid, resulting in an overestimation of SNGFR. This artifact can be avoided by controlling the intratubular pressure during collection of tubular fluid.

Animals↗
PubMed1981

Nicotinamide adenine dinucleotide and renal response to parathyroid hormone.

We tested the hypothesis that NAD plays a role in the cellular mechanism of action of parathyroid hormone (PTH) on phosphate transport. PTH significantly increased urinary cyclic AMP and phosphate excretions in thyroparathyroidectomized rats. The NAD+/NADH ratio, but not total NAD content, in renal cortical tissue was significantly higher in rats infused with PTH than in controls. The results demonstrate that the phosphaturic effect of PTH is associated with a shift in the renal cortical NADH to NAD+ and provides evidence for a role for NAD+ in the cellular regulation of phosphate transport.

Animals↗
PubMed1980

Renal brush border membrane adaptation to phosphorus deprivation: effects of fasting versus low-phosphorus diet.

Alimentary phosphorus deprivation due to a low-phosphorus diet (LPD) elicits a profound antiphosphaturia and an increase in sodium-dependent inorganic phosphate (Pi) uptake by renal cortical brush border membrane (BBM) vesicles. But, in alimentary phosphorus deprivation due to total fasting, high urinary excretion of Pi persists. In the present study, we determined whether low tubular reabsorption of Pi in fasting is due to a diminished capacity of the specific Pi transport system with the renal cortical luminal BBM or whether it is due to a reduced transepithelial reabsorption of Pi because of metabolic conditions occurring in proximal tubule cells during fasting. Sodium-dependent Pi transport in compared with fasted rats or rats fed a normal phosphorus diet. Sodium-dependent uptake of D-glucose was significantly lower in LPD rats, compared with fast animals or animals fed a normal diet. Thus, in contrast to LPD, fasting does nt elicit an increase in Pi transport and a decrease in D-glucose transport across the isolated renal BBM. The same differences in BBM transport of Pi were present also in thyroparathyroidectomized rats. Further experiments demonstrated that the adaptation of renal function and the renal BBM transport to LPD are overridden by a subsequent period of total fasting. Results of the present study show that fasting both prevents and reverses the renal response of rats to alimentary phosphorus deprivation. The differences in Pi excretion between fasted rats, LPD rats, and LPD rats subsequently fasted are attributed, at least in part, to specific adaptive changes in sodium-dependent Pi transport across the luminal BBM, rather than to alterations in other cellular (metabolic) components of transepithelial Pi reabsorption in the proximal tubule.

Animals↗
PubMed1980

Effect of NH4Cl on phosphaturic response to PTH in the hamster: dissociation from acidemia.

Previous studies indicate that the hamster fasted for 16 h fails to demonstrate a significant phosphaturic response to parathyroid hormone (PTH). However, when hamsters were infused with ammonium chloride, a phosphaturic response to PTH was observed. The present studies evaluate the respective roles of acidemia and the ammonium ion in this response. As in previous studies, fasted thyroparathyroidectomized (TPTX) hamsters infused with PTH showed no significant increase in the fractional excretion of phosphate (FE rho), from 19 +/- 2 to 22 +/- 1%. Neither respiratory acidosis (hypercapnia) nor metabolic acidosis (HCl infusion) enhanced the phosphaturic effect of PTH, FE rho 21 +/- 4 to 20 +/- 6 and 15 +/- 2 to 16 +/- 3%, respectively. Both ammonium chloride and ammonium bicarbonate infusions enhanced the phosphaturic response; FE rho increased from 15 +/- 5 to 27 +/- 5% (P < 0.02) and 17 +/- 3 to 25 +/- 3% (P < 0.05), respectively. We conclude that the enhancement of the phosphaturic effect of PTH in the fasted hamster by ammonium chloride infusions can be dissociated from acidemia.

Acidosis↗
PubMed1980

Renal interstitial pressure and sodium excretion during renal vein constriction.

Studies were performed on anesthetized dogs to determine the relationship of interstitial pressure to sodium excretion during renal vein constriction in the presence and absence of volume expansion. Renal interstitial pressure was measured from implanted capsules during basal renal venous pressure and increased pressures of 10, 20, 30, and 40 mmHg. A positive relationship between renal venous pressure and interstitial pressure was demonstrated in hydropenia and in volume expansion, with markedly higher interstitial pressures obtained in volume expansion. A positive correlation was demonstrated between fractional sodium excretion and renal interstitial pressure in hydropenia as compared to a significant negative correlation in volume expansion. Negative correlations were demonstrated in volume expansion between renal interstitial pressure and glomerular filtration rate and renal blood flow as compared to no significant change in these parameters in hydropenia. Accordingly, a positive correlation was demonstrated between renal interstitial pressure and sodium excretion in hydropenia but not in volume expansion. Volume expansion was characterized by higher interstitial pressure and decreased sodium excretion in association with decreased renal blood flow and glomerular filtration rate.

Animals↗
PubMed1980

Localization of the nephron sites responsible for mineralocorticoid escape in rats.

Fractional delivery of sodium (FDNA) from the superficial late distal tubule is increased in deoxycorticosterone acetate-(DOCA) treated rats, which may compensate for a presumed mineralocorticoid-stimulated sodium reabsorption in the cortical collecting tubule. In the present study, late proximal (LPT) and early distal tubules (EDT) were micropunctured during volume expansion in control and DOCA-treated rats. Whereas FDNa to the LPT was similar in the two groups, FDNa to the EDT was greater in DOCA-treated than in control rats. Additionally, LPT and deep loop of Henle (LH) were micropunctured in volume-expanded control and DOCA-treated rats. FDNa to the bend of the LH was increased in DOCA-treated rats compared to controls. These findings indicate that in DOCA escape sodium reabsorption is diminished in the pars recta and/or loop of Henle of superficial nephrons and there is increased delivery to the bend of the loop of deep nephrons. We conclude that mineralocorticoid escape is most likely due to increased sodium delivery to the cortical collecting tubule from both deep and superficial nephrons.

Absorption↗
PubMed1980

Phosphorus excretion in tumoral calcinosis: response to parathyroid hormone and acetazolamide.

The cause of hyperphosphatemia in patients with tumoral calcinosis never been explained. We studied two related patients who had tumoral calcinosis and hyperphosphatemia and two normal controls to determine their renal tubular response to parathyroid hormone (PTH) and acetazolamide (ACZ). During baseline periods, the patients had abnormally low fractional excretion of phosphorus (FEP) despite their hyperphosphatemia. Values for patients were 0.114 and 0.128; for controls, values were 0.193 and 0.165. PTH caused an increase in FEP and urinary cAMP in both patients and controls. ACZ also increased FEP in both groups, and the effects of PTH and ACZ were additive, suggesting that patients with tumoral calcinosis have normal sensitivities to PTH and normal responses to ACZ. Levels of vitamin D metabolites in the patients were normal. We conclude that patients with tumoral calcinosis have a reduced ability to excrete phosphorus. This defect does not seem to be due to impaired PTH secretion, an abnormal phosphaturic response to this hormone, or a disturbance of vitamin D metabolism.

Acetazolamide↗
PubMed1980

Failure of high doses of Sar1-lle8-angiotensin II to abolish autoregulation of renal blood flow.

We used very high doses of a competitive inhibitor of angiotensin II to investigate the role of the intrarenal renin-angiotensin system in the autoregulation of renal blood flow. Studies were carried out in dogs in which the renin and prostaglandin systems were suppressed. The results of our studies indicate that angiotensin II is not a prime mediator of the autoregulation of renal blood flow in response to reduced perfusion pressure.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1980

Diuretics: role of sodium balance.

Diuretics are commonly prescribed for a wide variety of clinical problems, including hypertension, extracellular volume excess, and disorders of calcium metabolism. Although natriuresis with altered sodium balance is not always the therapeutic goal, this feature of the diuretics is essential for optimal results, irrespective of the clinical problem.

Acute Kidney Injury↗
PubMed1979

Alkaline phosphatase in adaptation to low dietary phosphate intake.

Previous findings suggest that alkaline phosphatase (Alk Pase) may be involved in phosphate transport. Since phosphate reabsorption is enhanced in the kidney and duodenum of animals stabilized on a low-phosphorus diet (LPD), Alk Pase was measured in the kidney, small intestine, and other tissues in LPD rats. In particulate fractions from the renal cortex, intestine, renal medulla, liver, and heart ventricle from LPD rats the activity of Alk Pase was significantly increased but the activities of other plasma membrane enzymes were not different between control and LPD groups. The increased Alk Pase in the renal cortex was localized to the brush border of the proximal tubule histochemically and by measurement of Alk Pase in brush-border preparations. Also in the renal cortex, typical enzymes associated with mitochondria, lysosomes, and cytosol were unchanged with the exception of cytosolic adenosine 3',5' cyclic-monophosphate phosphodiesterase, which was increased in LPD rats. Alk Pase in the renal cortex and intestine may play a role in the enhanced phosphate reabsorption in LPD animals.

Alkaline Phosphatase↗