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C J Lote

Publications and source records attributed to C J Lote.

At least 55 records · Page 3Linked to original sources
PubMed1985

Renal extraction and clearance of p-aminohippurate during saline and dextrose infusion in the rat.

The reliability of the use of p-aminohippurate (PAH) as a clearance marker for the determination of renal plasma flow during saline or dextrose infusion was investigated in conscious and anaesthetized rats. In the conscious rat (wt. 350-400 g) infused for 4 h with 0.85% saline followed by 3 h of 2.5% dextrose, PAH clearance averaged 11.50 +/- 1.45 ml/min during saline infusion and 7.83 +/- 0.82 ml/min during dextrose infusion. The difference was significant (P less than 0.02). Inulin clearance, however, was unchanged. With dextrose as the initial infusate, PAH clearance averaged 5.86 +/- 0.65 ml/min and increased (P less than 0.01) to 8.74 +/- 0.71 ml/min following a change of infusate to saline, although inulin clearance was again unchanged. In separate groups of rats anaesthetized with sodium pentobarbitone, a comparison was made between renal blood flow values calculated from PAH clearance and haematocrit, and those determined simultaneously using an electromagnetic flow probe placed on the left renal artery. During 0.85% saline infusion, the calculated value was 88.1 +/- 8.4% of that measured using the flow probe. During 2.5% dextrose infusion the value determined from PAH clearance was only 47.3 +/- 4.2% of that obtained using the flow probe, and this is significantly (P less than 0.01) lower than the ratio found during saline infusion. In another study, renal venous blood samples were obtained from sodium-pentobarbitone-anaesthetized rats during 0.85% saline or 2.5% dextrose infusions, for calculation of the renal PAH extraction ratio. During saline infusion, PAH extraction averaged 68.3 +/- 2.5%, whereas during dextrose infusion PAH extraction was lower (P less than 0.001) and averaged only 48.8 +/- 3.2%. It is concluded that PAH clearance grossly underestimates renal plasma flow during 2.5% dextrose infusion in the rat.

Aminohippuric Acids↗
PubMed1985

Does cyclosporine inhibit renal prostaglandin synthesis?

Urinary PGE2 excretion was measured in female renal allograft recipients being treated either with prednisolone and cyclosporine (Cys) or with prednisolone and azathioprine. The mean urinary PGE2 excretion in patients on Cys of 940 pmol/4 hr was lower than in patients on prednisolone and azathioprine (2033 pmol/4 hr) although the difference did not achieve statistical significance. These data are consistent with the hypothesis that Cys inhibits renal prostaglandin synthesis.

Cyclosporins↗
PubMed1984

The effect of urine pH on the reduction of urinary PGE2 excretion by indomethacin.

Urinary PGE2 excretion is influenced by urinary pH, being higher at high pH values. Indomethacin (10 mg/kg body wt, i.p.) was found to reduce urinary PGE2 excretion to the same absolute value irrespective of the initial PGE2 output. It is concluded that measurements of 'percentage inhibition' of urinary PGE2 excretion by non-steroidal anti-inflammatory agents must be interpreted with caution.

Animals↗
PubMed1984

Urinary pH as a determinant of prostaglandin E2 excretion by the conscious rat.

The urinary excretion of prostaglandin E2 (PGE2) was measured in conscious rats under conditions which produced either acid or alkaline urine, but a similar change in fluid and solute excretion. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE2 was approximately 3-fold greater (P less than 0.001) than the control (pH 6.2). The urine flow and sodium output were also increased. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE2 excretion was reduced (P less than 0.01) to approximately half the control output. The urine flow and sodium output increased. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P less than 0.002) was established between urine pH and PGE2 excretion. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE2 in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.

Ammonium Chloride↗
PubMed1983

The influence of renal prostaglandins on urinary calcium excretion in idiopathic urolithiasis.

Hypercalciuria is well recognized as an important factor in the cause of idiopathic calcium stone disease. Identification of the exact mechanism for the renal tubular handling of calcium has proved elusive, hence, treatment methods to alter the concentration of urine calcium in hypercalciuric stone formers have hitherto been non-specific. It is now well established that renal prostaglandins influence intrarenal hemodynamics and tubular electrolyte excretion. As the renal handling of sodium and calcium is intimately related, the possibility that the mechanism underlying hypercalciuria may be prostaglandin mediated was considered. Experiments were performed in conscious Sprague-Dawley rats (n = 10) to determine the changes in calcium excretion following prostaglandin synthetase inhibition with indomethacin. Calcium excretion was significantly reduced (p less than 0.01), compared with control animals (n = 10). Further experiments were performed in anesthetized monkeys (Macaca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in glomerular filtration rate or blood pressure. Forty-three hypercalciuric patients were treated with a prostaglandin inhibitor for periods ranging from 2 to 4 weeks, and all showed a significant fall in urinary calcium excretion to within the normal range. This clinical and experimental study suggests that prostaglandin (PGE2) is a hormone which determines the renal handling of calcium by influencing renal tubular function.

Animals↗
PubMed1983

The influence of prostaglandin E2 and indomethacin on the renal corticomedullary solute gradient in the rat.

The renal corticomedullary solute gradient and the urinary excretion of fluid and solute were determined during a saline infusion in anaesthetized and conscious rats. In the anaesthetized group the influence of PGE2 (100 ng min-1) given by a local renal infusion was investigated. In the conscious group (where prostaglandin synthesis does not contribute to renal blood flow) the effect of indomethacin (i.v. 10 mg kg-1) was determined. Following PGE2 infusion the corticomedullary gradient for sodium was depressed, equalizing the sodium concentration between the papilla tip and the final urine. Sodium output and urine flow were elevated, but both urinary and gradient changes could be dissociated from any increase in renal blood flow, assessed by PAH clearance. Following treatment with the prostaglandin synthetase inhibitor indomethacin in the conscious rat, the corticomedullary osmotic gradient was elevated while the urine flow was reduced. This increase in the gradient produced by indomethacin was, however, found to be independent of the decrease in urine flow. The results of the present experiments are consistent with the hypothesis that prostaglandin synthesis helps to determine the renal corticomedullary osmotic gradient, and does so by a mechanism unlikely to involve changes in renal blood flow or tubular flow rate: a permeability hypothesis is proposed.

Animals↗
PubMed1983

Prostaglandin E2 excretion, urine flow and papillary osmolality during saline or dextrose infusion in the conscious rat.

Conscious rats received infusions at 5.8 ml./hr of either 0.9% NaCl or 5% dextrose, via a tail vein, for 6 hr. During this infusion period, urine was collected from the animals, and the urine volume, sodium concentration and immunoreactive PGE2 were determined. Urine flow in both groups was stable during the 2-6 hr period of the infusion and was not significantly different between the two groups. Sodium output was also stable over the 2-6 hr infusion period but obviously the output of the saline-infused group was higher than that of the dextrose-infused group. Urinary PGE2 output was not significantly different between the groups in the 2-4 hr period (79.4 +/- 8.6 p-mole/2 hr in the saline-infused group, 82.1 +/- 5.7 p-mole/2 hr in the dextrose-infused group). In the 4-6 hr period, PGE2 output remained at this level (82.0 +/- 7.8 p-mole/2 hr) in the dextrose-infused group, but fell significantly (to 53.7 +/- 5.0 p-mole/2 hr) in the saline-infused group. In separate groups of animals which received saline or dextrose infusions as above, renal papillary osmolality was determined. The osmolality was significantly (P less than 0.001) higher in the saline-infused group. It is concluded that renal PGE2 synthesis is unlikely to be directly involved in sodium homeostasis and that PGE2 synthesis as measured by urinary PGE2 excretion is not controlled by the papillary osmolality.

Animals↗
PubMed1982

Effect of prolactin on urinary excretion and renal haemodynamics in conscious rats.

1. Conscious rats received a saline infusion (5.8 ml . hr-1) via a tail vein, for a 6 hr period. For the final 2 hr of this infusion period, prolactin (7.1 microgram (100 g body wt.)-1 . hr-1) was incorporated in the infusate. A control group of animals continued to receive saline alone. 2. In the first hour of prolactin administration (in comparison with the control group), urine flow, sodium output and osmolal output were all significantly reduced (P less than 0.02); there was also a reduction (P less than 0.05) in renal plasma flow (p-amino-hippurate clearance), but the filtration fraction did not alter. The changes in urinary excretion, and in renal haemodynamics, did not persist for the second hour of prolactin administration, but there was a sustained increase in body fluid volume. 3. It is possible that altered renal haemodynamics are responsible for the reduced urinary water and solute excretion which occurs during acute prolactin administration.

Animals↗
PubMed1982

Prolactin release in response to infusion of isotonic or hypertonic saline.

In ketamine-anaesthetized rats, the infusion of 10 ml either isotonic (0.9%) or hypertonic (3.0%) saline over a 30-min period was associated with a decrease in the secretory activity of the anterior pituitary prolactin cells (assessed morphologically by electron microscopy), and a decrease in the serum prolactin concentration (determined by radioimmunoassay). The hypertonic saline infusion significantly (P less than 0.01) increased the serum osmolality whereas the isotonic infusion did not. The results indicated that prolactin release is reduced in response to volume expansion regardless of whether the fluid load is isotonic or hypertonic, and suggested that, in the rat, the hormone may play a role in volume regulation rather than osmoregulation.

Animals↗
PubMed1981

The influence of renal prostaglandins on glomerular filtration rate (GFR) and calcium excretion in urolithiasis.

In a clinical study of 275 idiopathic stone formers the GFR was significantly raised in hypercalciuric patients compared with normal controls P less than 0.001). The possibility that the mechanism underlying hypercalciuria and raised GFR may be prostaglandin-mediated was considered because it is now well established that prostaglandins regulate intra-renal haemodynamics and influence tubular electrolyte excretion. Experiments were performed in conscious Sprague Dawley rats to determine the changes in calcium and sodium excretion following prostaglandin synthetase inhibition with indomethacin. Both calcium and sodium excretion together with urine flow were significantly reduced (P less than 0.002). Further experiments were performed in anaesthetised monkeys (Macacca fascicularis) to see if the inhibitory effect of indomethacin was reversible. Exogenous prostaglandin (PGE2) infusion resulted in a marked calciuretic response without producing changes in GFR or blood pressure. Selected hypercalciuric patients were treated with indomethacin, which resulted in a significant fall in urinary calcium excretion (P less than 0.001). This clinical and experimental study suggests that PGE2 is the hormone which determines the renal handling of calcium by controlling renal tubular function.

Adolescent↗
PubMed1980

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

1. Conscious rats, with implanted carotid arterial cannulae, received a saline infusion (5.8 ml./hr) via a tail vein for a 6 hr period. The urinary excretion of water, sodium, potassium, urea and the osmolal output were monitored, together with the systemic blood pressure. Glomerular filtration rate (inulin clearance) and effective renal plasma flow (p-aminohippurate clearance) were also measured. Four hours after the start of the infusion, indomethacin (10 mg/kg body weight) in buffered saline, or buffered saline alone, was administered via the tail vein. 2. Following indomethacin administration, urine flow, sodium output and osmolal output were markedly reduced (P less than 0.01). However, there were no measurable changes in the systemic blood pressure, glomerular filtration rate, or effective renal plasma flow. 3. It is concluded that the changes in urinary excretion observed after indomethacin are not dependent on changes in effective renal plasma flow or glomerular filtration, and it is suggested that indomethacin inhibits the synthesis of endogenous prostaglandins which directly influence renal tubular function.

Animals↗