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T H Steele

Publications and source records attributed to T H Steele.

At least 37 records · Page 2Linked to original sources
PubMed1982

Pressure-dependent action of angiotensin II on glomerular filtration in the isolated rat kidney.

We examined the action of angiotensin II (AII) on isolated rat kidney perfused with a recirculating cell-free solution at either 12 pKa (90 mmHg) or 17 kPa (128 mmHg). The renal perfusion pressure was maintained constant while sufficient AII was added to increase the renal vascular resistance by 50%. In the low-pressure kidneys. AII increased the glomerular filtration rate (GFR) by 155%, increased sodium reabsorption by 157%, and decreased the urine sodium concentration by 34% without affecting sodium excretion. In the high-pressure kidneys, GFR initially was significantly greater but was not affected by AII. In these experiments, AII had no effect on sodium reabsorption or excretion and decreased the urine sodium concentration by 7%. The data suggest that AII could be involved in autoregulation of the GFR without producing large changes in sodium excretion.

Angiotensin II↗
PubMed1982

Interactions of starvation and selective phosphorus depletion on renal phosphate reabsorption.

Renal phosphate (Pi) wastage following 7 days of starvation was investigated in normal rats (HI-P) and others previously stabilized on a low phosphorus (LO-P)diet. In LO-P animals, Pi excretion increased after starvation, but was significantly less than in starved HI-P rats. After thyroparathyroidectomy, the increase in Pi excretion after parathyroid hormone (PTH) was significantly greater in nonacidotic starved HI-P rats than in LO-P animals. However, PTH elicited a 31-fold increase in Pi excretion in both of these groups. Starved LO-P and HI-P rats responded equivalently to dibutyryl cyclic AMP. The renal response to phosphate depletion normally promotes Pi conservation, but is attenuated markedly by 7 days of subsequent starvation. This results from at least partial restoration of phosphaturic responsiveness to PTH during starvation.

Animals↗
PubMed1982

Simultaneous medullary sponge and adult polycystic kidney disease: the need for accurate diagnosis.

Two cases of simultaneous medullary sponge and adult polycystic kidney disease developed in siblings. The diagnoses of polycystic kidneys were made by renal ultrasonography and medullary sponge kidney was diagnosed roentgenographically. The family history was markedly positive for "cystic" disease. Medullary sponge kidney might be a precursor of polycystic kidney disease in some instances, or, more likely, this represents two separate afflictions occurring in the same individuals. When large medullary sponge kidneys are encountered, the possibility of concomitant polycystic kidney disease should be entertained and investigated with a sonogram. While the prognosis of isolated sponge kidney is excellent, polycystic kidney disease eventually leads to hypertension and renal failure.

Adult↗
PubMed1981

Acid-base maneuvers and phosphate transport in the isolated rat kidney.

The influence of bicarbonate (HCO3-), the carbon dioxide tension (PCO2), and pH on phosphate (Pi) excretion were assessed in isolated rat kidneys, perfused in vitro with recirculating synthetic solutions. After establishing control values, the perfusate HCO3- or PCO2 was altered separately. When the perfusate pH was decreased, either by increasing PCO2 or decreasing HCO3-, the absolute and fractional Pi excretions increased. Perfusate alkalinization by slightly decreasing the PCO2 did not affect Pi excretion, but increasing the perfusate pH with addition of HCO3- elicited phosphaturia. Other kidneys were perfused with a solution from which the CO2/HCO3- buffer system was nominally absent. Alkalinization of HCO3--free perfusate had no effect upon Pi excretion, but acidification resulted in marked phosphaturia. Perfusate acidification, whether achieved by decreasing HCO3-, increasing PCO2, or by adding hydrogen ions, uniformly elicited phosphaturia. The data indicate that either decreasing the extracellular pH or increasing the extracellular HCO3- inhibits renal Pi reabsorption.

Acid-Base Equilibrium↗
PubMed1979

Hypouricemia.

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Body Water↗
PubMed1979

Mechanism of the uricosuric activity of ticrynafen.

Studies employing pyrazinamide, which have included the measurements of clearances of pyrazinamide and pyrazinoate, as well as of ticrynafen itself and its principal metabolite, have lent support to the hypothesis that ticrynafen inhibits the tubular reabsorption of both filtered and secreted urate by nephrons of the human kidney. The inhibition of the reabsorption of secreted urate by ticrynafen appears to be quantitatively important for eliciting its uricosuric and hypouricemic responses. Because the uricosuric and natriuretic responses correlate with urinary ticrynafen concentrations, the drug appears to inhibit tubular reabsorption after gaining access to tubule fluid. As a consequence of its extensive binding to plasma proteins, clearance data suggest that tubular secretion of ticrynafen is necessary for its action.

Diuretics↗
PubMed1979

Renal handling of urate: application to the action of tienilic acid.

The renal handling of urate is complex, involving its filtration by glomeruli, partial tubular reabsorption, tubular secretion and also the reabsorption of a portion of the secreted urate. Studies employing tienilic acid, both acutely and chronically, have suggested that this compound exerts its uricosuric action and decreases the plasma urate by inhibiting renal urate reabsorption. The magnitude of the natriuretic and uricosuric actions of tienilic acid are correlated with the concentration of drug in the urine. Crystal equilibration studies have suggested that tienilic acid should not predispose to crystalluria with either uric acid or monosodium urate.

Animals↗
PubMed1978

Renal response to phosphorus deprivation in the isolated rat kidney.

In order to study further the adaptation of inorganic phsophate (Pi) reabsorption during phosphorus depletion, Pi transport was measured at three perfusate Pi concentrations in isolated perfused rat kidney preparations, utilizing synthetic albumin-containing cell-free perfusate. With elevation of the perfusate Pi, phosphaturia was significantly less, and absolute Pi reabsorption was significantly greater in kidneys derived from phosphorus-deprived rats than in organs from nondeprived counterparts. Prior parathyroidectomy did not affect the transport of Pi by the isolated kidney preparation. Increasing the perfusate Pi did not diminish hypercalciuria in kidneys from phosphorus-deprived rats. The results indicate that the adaptive response in Pi reabsorption during phosphorus deprivation can be demonstrated independently of the composition of fluid perfusing the kidney. The mechanism underlying the adaptation, however, remains unclarified.

Animals↗
PubMed1978

Blunted norepinephrine natriuresis in the isolated spontaneously hypertensive rat kidney.

In order to characterize the relationship between blood pressure and renal sodium handling in the Kyoto spontaneously hypertensive rat (SHR), we did renal clearance and isolated perfusion studies in SHR and Wistar-Kyoto controls (WKY). Clearance studies revealed no differences in renal function between SHR and WKY. Isolated perfused kidneys from SHR demonstrated a diminished glomerular filtration rate (GFR) compared to WKY kidneys when both were perfused at normotensive pressures. Increasing the perfusion pressures to hypertensive levels by adjusting the perfusate flow rate increased both the GFR and sodium excretion to equivalent values. However, the addition of norepinephrine 15 ng/ml, to the perfusate resulted in a far greater natriuretic response in WKY kidneys than in SHR, despite equivalent increases in perfusion pressures, renal resistances, GFR, and filtration fractions. These results suggest that norepinephrine exerts a direct or indirect inhibitory action on renal sodium transport, and this effect is diminished in SHR kidneys. Additionally, abnormalities in renal sodium transport may play a role in the pathogenesis of hypertension in the SHR.

Animals↗
PubMed1978

Supersaturation of urine with uric acid and urate: response to a uricosuric diuretic.

In order to assess the possibility that treatment with the uricosuric diuretic ticrynafen (tienilic acid) could lead to UA or MSU crystalluria, the degree of urinary supersaturation with respect to these crystalloids was assessed in persons receiving the diuretic for 1 week, and the results were compared with similar data generated from the use of probenecid. Initially, only probenecid significantly increased the degree of urinary suspersaturation with respect to MSU, and after adjustment of urine pH values to 5.5, probenecid also increased the degree of urinary supersaturation with respect to nonionized UA. At a pH of 5.5, the urine was significantly more supersaturated with nonionized UA after a single dose of probenecid than after ticrynafen (tienilic acid). Ticrynafen never significantly affected the degree of urinary supersaturation with respect to UA or MSU. Neither agent affected small amounts of "colloidal" or "bound" urinary urate. Insofar as the degree of urinary supersaturation with these crystalloids predisposes to crystalluria and calculus formation, ticrynafen (tienilic acid) appears to present no increased risk.

Crystallization↗
PubMed1977

Bicarbonate-induced phosphaturia: Dependence upon the magnitude of phosphate reabsorption.

The acute effect of bicarbonate infusion on inorganic phsophate (Pi) reabsorption was determined in thyroparathyroidectomized (TPTX) rats stabilized on a high phsophorus diet. In the normophosphatemic state, bicarbonate did not affect Pi reabsorption significantly. On the other hand, after hyperphosphatemia was induced by phosphate loading, bicarbonate inhibited Pi reabsorption. In order to determin if eht aboslute level of plasma or filtered Pi was an improtant determinant of this phosphaturic action of bicarbonate during hyperphosphatemia, equivalent rates of Pi reabsorption were achieved after phosphate infusion in TPTX rats previously stabilized on a low dietary phosphorus intake, but at significantly lower plasma Pi concentrations and filtered Pi loads than in their high dietary phosphorus counterparts. Bicarbonate inhibited Pi reabsorption equivalently in both hyperphosphatemic groups, indicating that the magnitude of Pi transport itself was of importance in determining the inhibitory response to bicarbonate. In addition, the results suggest that transport mechanisms for bicarbonate and Pi may interact competitively.

Animals↗
PubMed1977

Renal response to phosphorus deprivation: effect of the parathyroids and bicarbonate.

Plasma inorganic phosphate (Pi) and Pi reabsorption were compared in intact and chronically thyroparathyroidectomized (TPTX) rats stabilized on a high or low-phosphorus diet after volume expansion with equivalent sodium bicarbonate or sodium chloride. Phosphate infusion after sodium chloride-loading resulted in greater hyperphosphatemia and diminished phosphaturia in TPTX rats than intact high-phosphorus rats. After sodium bicarbonate-loading, however, there was no difference between intact and TPTX high-phosphorus animals because bicarbonate inhibited Pi reabsorption extensively in both. In contrast, phosphate infusion after sodium chloride-loading in phosphorus-deprived rats elicited greater degrees of hyperphosphatemia and increased Pi reabsorption, irrespective of the presence or absence of the parathyroids. Sodium bicarbonate-loading inhibited Pi reabsorption significantly less in phosphorus-deprived rats than in high-phosphorus animals. Paradoxically, this inhibitory effect of bicarbonate in phosphorus depletion was greater in TPTX rats than in intact animals. Therefore, the presence of the parathyroids did not interfere with Pi reabsorption during phosphate infusion in sodium bicarbonate-loaded phosphorus-deprived rats. Sodium bicarbonate-loading interfered with Pi reabsorption most prominently in phosphorus-deprived rats when the parathyroids were absent.

Animals↗