Antique ophthalmic instruments and books: the Royal College Museum.
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History, 19th Century↗
Biomedical subjects
R Keeler
Publications and source records attributed to R Keeler.
Antique ophthalmic instruments and books: the Royal College Museum.
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Books↗
Radioimmunoassay measurement of albumin in urine is a valid method for monitoring analbuminemia in rats.
Plasma and urinary albumin levels, urinary creatinine and urine volumes were measured at two-week intervals in Nagase analbuminemic rats (NAR) of either sex at ages from 42 to 154 days. Age matched Sprague Dawley (SD) rats were used as controls. Plasma concentrations of immunoreactive albumin (iALB) in NAR ranged from 0.007 +/- 0.002 to 0.023 +/- 0.003 mg/ml, and were lower in younger rats. In SD rats, plasma iALB concentrations ranged from 18.9 +/- 1.0 to 46.2 +/- 6.4 mg/ml. Urinary iALB output in NAR was less than 0.05 micrograms/mg creatinine measured over a 24 hr period, whereas it was greater than 20 micrograms/mg creatinine in the SD rats. Measurement of urine iALB concentrations in the NAR colony appears to be a reliable and a non-invasive method for monitoring the persistence of hypoalbuminemia.
Age Factors↗
Big ANF: large-molecular-weight ANF in plasma. I. Gel filtration and affinity chromatography studies.
A large molecular form of immunoreactive atrial natriuretic factor (irANF) was demonstrated in plasma of rabbit and rat on the basis of gel filtration experiments. This big ANF was not retained by octadecylsilane cartridges and cross-reacted with four anti-ANF antisera of different specificities. Gel filtration in acid, but not in 8 M urea, resulted in material with elution characteristics of irANF. Affinity chromatography and gel electrophoresis of big ANF suggested that the material was similar to albumin. However, high concentrations of big ANF were found in analbuminemic rats, with characteristics similar to those seen in rabbit and normal rats (affinity and gel chromatography and gel electrophoresis). We thus conclude that big ANF represents a bound form of ANF in circulation and that the carrier is similar to but not identical with albumin.
Acetates↗
Sodium excretion and renal precession of sodium over inulin.
Renal excretory patterns for inulin and 22Na were measured in rats after simultaneous injection into a renal artery. In normal rats, the excretion of 22Na was much faster than inulin. This is referred to as "precession of sodium" and showed that some of the excreted 22Na had bypassed the intratubular route. During water diuresis, 65% of excreted 22Na was excreted before inulin. The quantity of 22Na preceding inulin (0.10 +/- 0.03% of the amount injected) increased eightfold during infusion of atrial natriuretic peptide (ANP). In saline diuresis, 45% of excreted 22Na (1.47 +/- 0.39% of the amount injected) preceded inulin, but precession was not affected by ANP. In rats with a nephrotic syndrome, 13% of excreted 22Na (0.34 +/- 0.12% of the amount injected) preceded inulin during saline diuresis and increased to 1.66 +/- 0.53% of the amount injected during the infusion of ANP. Precession of sodium was completely abolished in kidneys with papillary necrosis, suggesting that 22Na entered the tubular lumen in the inner medulla. These experiments demonstrate that, in rats, a large fraction of excreted sodium enters the tubules by a route other than filtration. The quantity of sodium entering the tubules by this route shows a 10- to 15-fold variation under conditions that modify the rate of sodium excretion.
Animals↗
Effect of V2 antagonist on clearance of arginine vasopressin by isolated perfused rat kidneys.
Isolated rat kidneys were perfused with Krebs-Henseleit-bovine serum albumin solution at a mean pressure of 99 +/- 2.6 mmHg. After control periods, arginine vasopressin (AVP) was added to the perfusate at a final calculated concentration of 25 pg/ml (2.5 x 10(-11) M). Urine and perfusate samples were collected at 15-min intervals for the following 60 min to measure kidney function and the renal clearance of immunoreactive AVP (irAVP). At 15-30 min after the addition of AVP, total renal clearance of irAVP was 1,623 +/- 190 microliters.min-1.g kidney wt-1. Glomerular filtration accounted for 35 +/- 3.0% of the total clearance, and 65 +/- 10.3% was cleared by peritubular pathways. Of the filtered irAVP, 48 +/- 4.8% was recovered in the urine. To investigate the importance of V2 receptors in the metabolism of AVP, clearance measurements were made in the presence of the V2 antagonist [d(CH2)5,D-Ile2,Ile4,Arg8]AVP (5 x 10(-9) M). Total renal clearance of irAVP was reduced by 48% to 848 +/- 79 microliters.min-1.g-1. This reduction was entirely accounted for by the complete inhibition of peritubular clearance of irAVP. In the presence of the V2 antagonist, irAVP was cleared only by filtration. The proportion of filtered AVP recovered in the urine (53 +/- 8.7%) was not significantly altered by the presence of the V2 antagonist. We conclude that a major component of the renal clearance of AVP depends on receptor-mediated uptake of AVP in the kidney cells.
Animals↗
Abnormal renal response to twenty-four-hour dehydration and fasting in Nagase analbuminemic rats.
We assessed renal function in fasting adult Nagase analbuminemic rats (NAR). Sodium output in male and female NAR was 68% and 46%, respectively, of the output of age- and sex-matched normal Sprague-Dawley (SD) rats. Potassium excretion was significantly greater in female NAR but there was no difference between male NAR and SD rats. The renal clearances of urea and creatinine were reduced in NAR with corresponding increases in plasma concentrations; however, the urea and creatinine concentrations were not different in plasma samples taken from normally fed and hydrated SD and NAR rats. Exchangeable body sodium and sodium space was significantly larger in normally fed and hydrated NAR than in SD but there were no differences in plasma sodium concentrations or plasma volumes. Although plasma concentrations of albumin in NAR were only about 0.07% of the concentration in SD rats, the renal clearance of albumin in NAR was threefold greater. Kidney weights in NAR were 10 to 16% less than in SD rats but liver weights were 22 to 42% greater. Clearly, renal function was markedly abnormal in Nagase rats during a 24-hour fast.
Animals↗
Natriuretic response to hypervolemia is absent in rats with papillary necrosis.
The renal responses to acute expansion of the blood volume (20%), acute saline loading (5% body wt), or administration of atrial natriuretic peptide (ANP) were investigated in rats 7-10 days after inducing experimental renal papillary necrosis by the injection of bromoethylamine hydrobromide. In normal rats, urinary Na output (UNaV) increased from 1 +/- 0.4 to 16.6 +/- 1.7 mumol/min. In rats with papillary necrosis, UNaV only increased from 1.1 +/- 0.2 to 2.5 +/- 0.5 mumol/min. In contrast, the natriuretic responses to saline loading in normal rats (from 1.7 +/- 0.2 to 21.6 +/- 2.4 mumol/min) and to the infusion of ANP (from 0.8 +/- 0.1 to 7.6 +/- 0.8 mumol/min) were not significantly attenuated in rats with papillary necrosis. The absence of a natriuretic response to hypervolemia in rats with papillary necrosis was not a result of failure to secrete ANP, because plasma levels of immunoreactive ANP increased three- to four-fold in rats with papillary necrosis and in untreated rats. It is concluded that the mechanisms mediating the natriuretic and diuretic responses to acute expansion of the blood volume mainly involve alterations in inner medullary function. In contrast, natriuretic responses to saline loading and pharmacological doses of ANP are apparently mediated by more superficial cortical nephrons.
Animals↗
Chemical medullectomy does not prevent sodium retention in nephrotic rats.
Experiments were performed to study the effect of chemical medullectomy on the renal retention of sodium in rats with an experimental nephrotic syndrome. Nephrosis was induced in rats by a single injection of puromycin aminonucleoside (PAN) and the renal excretion of water and electrolytes was monitored for 11 days. Sodium output in nephrotic rats fell to approximately 10% of control levels and exchangeable body sodium increased to 54.6 +/- 2.7 mM/kg compared with 41.5 +/- 0.8 mM/kg in controls. The animals had edema and ascites and there was a 35% increase in plasma volume and a corresponding fall in hematocrit. Severe structural and functional damage to the inner renal medulla induced by the injection of bromoethylamine hydrobromide (BEA) resulted in little change in the pattern of sodium and water retention caused by PAN alone. Exchangeable body sodium in rats treated with PAN and BEA was 51.5 +/- 3.8 mM/kg. It is concluded that an intact inner renal medulla is not necessary for sodium retention to occur in PAN nephrosis in rats.
Animals↗
Comparative effects of retinoic acid and jervine on chondrocyte differentiation.
Jervine and retinoic acid are both teratogenic to structures which are initially modelled in cartilage. Differences in periods of maximal sensitivity, as well as in certain aspects of the morphological manifestations of exposure, indicate that these two teratogens act via different molecular mechanisms. Here we compare the effects of jervine and retinoic acid in three culture systems which represent sequential stages of the chondrocyte lineage. Proliferation of pluripotent C3H 10T 1/2 cells was decreased by exposure to jervine but was not affected by retinoic acid. Differentiation of high-density "spot" cultures of embryonic limb bud mesenchyme were sensitive to both compounds. Mature chondrocytes were resistant to jervine but "dedifferentiated" after 48-hour exposure to retinoic acid. We conclude that jervine compromises rapidly dividing chondrogenic precursors, whereas retinoic acid has little effect prior to the expression of cartilage-specific proteins.
Animals↗
Atrial peptides and the renal response to hypervolemia in nephrotic rats.
Immunoreactive atrial natriuretic peptide (iANP) levels in plasma of edematous rats with an experimental nephrotic syndrome produced by the injection of puromycin aminonucleoside (PAN) were not different from those in untreated rats. To test the ability of nephrotic rats to secrete iANP in response to a volume stress, the rats were subjected to 20% expansion of their estimated blood volumes using blood from donor rats. PAN-treated rats had very small natriuretic and diuretic responses compared with untreated rats; however, there was no difference in the secretory response of iANP, which increased approximately threefold in each group. There were highly significant correlations between changes in plasma iANP and changes in right atrial pressure in both normal and nephrotic rats. Nephrotic rats that were infused with synthetic ANP showed only a very small natriuretic and diuretic response compared with normal rats, and no change in glomerular filtration rate. The hypotensive response was still present, however. Urine concentration in nephrotic rats was much lower than in controls and was not increased by exogenous arginine vasopressin. It is concluded that the absence of a normal natriuretic and diuretic response to hypervolemia in PAN-treated rats is not caused by a failure to secrete ANP but might be a result of an intrarenal defect that makes their kidneys unresponsive.
Animals↗
Extracted and nonextracted atrial natriuretic peptide in rabbits during tachycardia.
The time course of changes in the plasma concentration of immunoreactive atrial natriuretic peptide (iANP) accompanying tachycardia was measured in anesthetized rabbits. In contrast to the hemodynamic changes, which occurred within the 1st min of tachycardia, the plasma iANP increased gradually and did not reach significantly elevated levels until 10 min into the stimulation period. After 20 min of tachycardia iANP was almost 200 pg/ml. Immunoreactive ANP was measured prior to and following extraction. Although the basal levels of iANP were higher in the unextracted than in extracted plasma (62 vs. 22 pg/ml), the time course of changes in iANP was identical in both. The gradual increase in iANP suggests that the release of iANP in this model may not simply be a consequence of the increase in atrial pressure.
Animals↗
Lesions of potato sprout and extracted potato sprout alkaloid toxicity in Syrian hamsters.
Hamsters were gavaged either dried potato sprout material, alkaloid extract of potato sprouts, or the marc from which the alkaloid fraction was extracted and then were examined for gross and microscopic lesions. Nine of 10 hamsters receiving dried potato sprout material and 3 of 5 hamsters receiving alkaloid extract had severe gastric and intestinal mucosal necrosis which was most severe in the glandular stomach, duodenum and proximal jejunum. All control hamsters gavaged with water and all hamsters gavaged with the potato sprout marc survived to the time of euthanasia and did not have gross or microscopic lesions.
Alkaloids↗
Heterologous radioimmunoassay of atrial natriuretic polypeptide in dog and rabbit plasma.
Atrial natriuretic peptide (ANP) was measured in plasma of dogs and rabbits by radioimmunoassay (RIA) using a commercially available anti alpha-ANP serum and compared to our measurements of ANP in rats and humans. Plasma concentration of ANP in dog coronary sinus (234.9 +/- 41.0 pg/ml) was significantly greater than in systemic arterial blood (81.2 +/- 8.4 pg/ml). Gel filtration of dog coronary sinus plasma resulted in an ANP peak with the elution volume (Ve) of synthetic atriopeptin III (AIII) and a minor peak eluting with the void volume (Vo). Rabbit systemic arterial plasma ANP was 53.3 +/- 4.3 pg/ml and yielded one peak, with a Ve of AIII. Ion exchange chromatography of dog and rabbit atrial extracts (AE) resulted in a major ANP region which resembled AIII. Gel filtration of AE showed larger molecular species as well as AIII. Dilutions of dog and rabbit plasma and AE were parallel with the AIII standard in radioimmunoassay.
Animals↗
Evidence that prostaglandin E2 stimulates chloride secretion in cultured A6 renal epithelial cells.
The effects of prostaglandin E2 (PGE2) on the transport of sodium and chloride were studied in cultured A6 renal epithelial cells. PGE2 on the basolateral but not the apical surface increased transmonolayer short-circuit current (Isc) and conductance. These changes could not be inhibited with amiloride or furosemide in the apical medium. Flux measurements showed that although Isc and net flux of sodium were equal in unstimulated cells, after addition of PGE2 the current increased with no corresponding changes in bidirectional or net flux of sodium. Immersing the cells in sodium-free or chloride-free media inhibited the effects of PGE2. Measurements of the simultaneous fluxes of sodium and chloride showed that after PGE2 was added there was a net flux of chloride from the basal to the apical side (secretion) that was equal to the change in Isc. The effects of PGE2 were inhibited by furosemide in the basal medium. We conclude that PGE2 stimulates a process of chloride secretion in A6 cells.
Amiloride↗
The effects of "dead space" and urine flow changes on measurements of glomerular filtration rate by clearance methods.
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Animals↗
Effects of atrial natriuretic factor on renal handling of water and electrolytes in rats.
The intravenous injection of an extract of atrial myocardium into anesthetized rats during a hypotonic diuresis resulted in an increase in the renal excretion of water, sodium, potassium, calcium, magnesium, and phosphate. There was an increase in urine concentration which was probably a result of the secretion of vasopressin since it did not occur in Brattleboro (di/di) rats. A transient increase in glomerular filtration rate and renal plasma flow occurred during the first five minutes with a more sustained rise in filtration fraction. Injection of atrial extract also caused a partial inhibition of solute-free water formation in Brattleboro rats subjected to water diuresis and a partial inhibition of solute-free water reabsorption in rats subjected to maximal antidiuresis by infusing vasopressin. In neither case was the degree of inhibition as profound as that observed after injecting furosemide in a dose which caused a comparable natriuretic response. A large dose of furosemide blocked the natriuretic response to atrial extracts whereas, when a comparable level of sodium and water output was produced by massive infusions of saline, the natriuretic response to atrial extract was increased. It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Furosemide might also act at the same tubular site or inhibit tubular secretion of the atrial natriuretic factor.
Animals↗
Atrial natriuretic factor has a direct, prostaglandin-independent action on kidneys.
Intravenous injection of a saline extract of lyophilized rat atrial myocardium into anesthetized rats caused a massive diuresis and natriuresis of short duration. There was also a significant increase in potassium excretion and a fall in urine osmolality. There were no significant changes in solute-free water reabsorption, glomerular filtration rate, renal plasma flow, or filtration fraction as measured by conventional clearance methods. Mean arterial pressure was significantly reduced during the natriuretic response. The natriuretic and diuretic response was not blocked by inhibition of prostaglandin synthesis with aspirin and indomethacin. Infusion of a small amount of atrial extract directly into the left kidney resulted in a natriuretic and diuretic response which was predominantly localized to the left kidney. It is concluded that saline extracts of rat atrial myocardium contain a potent natriuretic substance which acts directly on kidneys by a mechanism which does not depend upon increased synthesis of prostaglandins.
Animals↗