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L Rabinowitz

Publications and source records attributed to L Rabinowitz.

At least 37 records · Page 2Linked to original sources
PubMed1987

Kaliuretic regulatory factors in the rat.

To evaluate the role of aldosterone, plasma potassium, and sodium and urine excretion rates in controlling both total daily potassium excretion and the diurnal cyclic excretion of potassium, we performed experiments on unanesthetized, undisturbed rats kept in a 12-h light/12-h dark environment and fed a liquid diet. Independent variations were imposed on potassium intake, sodium intake, and, in groups of adrenalectomized rats, on aldosterone infusion rates. Potassium intake was 2.6, 10.6, and 18.7 meq/day. Sodium intake was 2.1, 6.7, and 17 meq/day. Aldosterone infusion was 0.1, 0.4, 1, and 10 times a basal rate of 1 microgram.day-1.100 g-1, with constant dexamethasone infusion at 1.43 micrograms.day-1.100 g-1. Twenty-four-hour excretion of potassium and sodium balanced 24-h intake of potassium and sodium regardless of the imposed combination of known regulatory factors. The amplitudes of potassium and sodium excretion during the diurnal cycle were each closely related to the ongoing levels of potassium and sodium intake. Plasma potassium was measured at the peak of the potassium cycle. It is suggested, based on analysis of the results, that when caloric balance was maintained, the amplitude of the diurnal potassium cycle was not importantly influenced by the rates of sodium and urine excretion, and, in addition to effects of aldosterone and plasma potassium concentration, the amplitude was importantly influenced by unspecified, homeostatically effective kaliuretic factors. Adrenalectomized rats receiving subbasal aldosterone replacement rejected the high potassium diet, were anuric, lost weight, and were severely hyperkalemic, observations indicating the necessity of adequate aldosterone for maintenance of potassium homeostasis.

Adrenalectomy↗
PubMed1986

Diurnal potassium excretory cycles in the rat.

Diurnal potassium cycles (DPC) were measured in unanesthetized undisturbed rats fed a liquid diet and maintained in a 12-h light-dark environment. A fourfold step increase in diet potassium content increased DPC amplitude without altering phase. After presentation of the high-potassium diet, the initial adaptive increase in excretion occurred within 1.5 h (diet given during dark phase) and within 6 h (diet given during light phase). On a day when food was withheld (no potassium intake), DPC were present but with a lowered amplitude. The amount of potassium excreted on a fasting day exceeded gut and extracellular fluid potassium content and was only modestly increased when rats were previously fed a high-potassium diet. In adrenalectomized rats that received no steroid replacement or received constant infusions of low levels of aldosterone, dexamethasone, or aldosterone plus dexamethasone, potassium balance and DPC were normal. It is concluded that the amplitude of DPC in the rat is determined in part by the availability of potassium from both intracellular and extracellular potassium pools; mechanisms independent of potassium intake can generate the DPC; and the presence or the cyclic secretion of adrenal steroids is not necessary for the generation of DPC in the rat.

Animals↗
PubMed1985

Intrapulmonary shunting during deliberate hypotension with nifedipine, diltiazem and labetalol in dogs.

Pulmonary shunt (Qs/Qt) was calculated in 49 mongrel dogs weighing 18-20 kg during mechanical ventilation, before and during deliberate hypotension with either nifedipine (group N), diltiazem (group D), labetalol (group L), or ethyl alcohol and polyethylene glycol (group E). A 30 per cent decrease in mean arterial blood pressure occurred after two minutes of nifedipine infusion, two minutes after diltiazem, and three minutes after labetalol; these effects lasted two hours after nifedipine administration, 90 minutes after diltiazem and three hours after labetalol. There was an accompanying significant decrease in systemic and pulmonary vascular resistance. Qs/Qt and cardiac output increased significantly after nifedipine infusion. Shunt increased (mean +/- S.E.) from 9.7 +/- 0.8 to 18.25 +/- 1.05 per cent at two minutes (p less than 0.0005); 19.05 +/- 1.2 per cent at 30 minutes (p less than 0.005); 17.5 +/- 1.6 per cent at two hours (p less than 0.01); and 12 +/- 1.1 per cent at three hours (p less than 0.025). No increase in shunt occurred after the administration of diltiazem, labetalol or polyethylene glycol and ethyl alcohol. Arterial oxygen tension (PaO2) decreased significantly after nifedipine infusion from 146 +/- 11.5 to 105 +/- 3.5 mmHg two minutes after infusion; to 89.5 +/- 3 mmHg 30 minutes after; 115 +/- 4.75 mmHg two hours after; and 130 +/- 10.75 mmHg three hours later. PaO2 was not significantly different after diltiazem, labetalol, or polyethylene glycol and ethyl alcohol administration. With nifedipine cardiac output increased from 2.25 +/- 0.3 to 3.95 +/- 0.25 after two minutes (p less than 0.005) to 3.85 +/- 0.35 after 30 minutes (p less than 0.005), 3.7 +/- 3 after two hours (p less than 0.01) to 2.9 +/- 1.1 after three hours. No significant increase in cardiac output occurred in groups D or L. These results suggest that only nifedipine infusion significantly alters oxygenation in dogs and therefore its use warrants caution in the presence of a preexisting abnormal Qs/Qt.

Anesthesia↗
PubMed1985

Effect of aldosterone on potassium excretion during potassium chloride infusion in sheep.

Experiments were performed on normal mature ewes to quantitate the effect of acute variations in aldosterone activity on renal K excretion. Six-hour clearance studies were performed on three sheep. Treatments were control (no infusion), infusion of KCl (140 meq in 2 h) alone or with superimposed infusions of aldosterone (20 micrograms/h), or infusion of aldosterone antagonist potassium canrenoate (100 mg/h). During KCl infusion there were simultaneous increases in plasma K, K excretion, and Na excretion. Aldosterone treatment diminished the increase in plasma K and in Na excretion but increased the rate of K excretion. Canrenoate had opposite effects. The rate of change of K excretion relative to the change in plasma K was 417 for aldosterone and 102 microeq/min per meq/l for canrenoate treatments, P less than 0.05. Before KCl infusion aldosterone decreased the rate of Na excretion and the salivary Na-to-K ratio but did not alter plasma K or K excretion. Aldosterone has a potent kaliuretic action in sheep when plasma K is elevated.

Aldosterone↗
PubMed1985

Effects of KCl infusion on potassium excretion in sheep.

To determine the quantitative relation of K excretion (UKV) to plasma K concentration (PK), three fasted, conscious, mature ewes were infused intravenously with 50 mmol KCl over 15, 30, and 60 min. Control experiments were without infusion. During KCl infusion PK was increased to 7.26 +/- 0.40 (15 min), 6.68 +/- 0.48 (30 min), and 5.59 +/- 0.3 meq/liter (60 min). During all three infusions the increase in UKV relative to the increase in PK was similar. The mean delta UKV/delta PK ratio was 160 +/- 30 (SD) mueq/min per meq/liter (range 102-203). On termination of each infusion PK decreased to control values, but UKV either remained elevated (60-min infusion) or first decreased and then increased (15- and 30-min infusions). The second, delayed kaliuresis began 30-45 min after initiation of KCl infusion and accelerated a return to the level of K balance of the control experiments. A plot of UKV against the corresponding period PK showed that, at a common value of PK, UKV was higher following KCl infusion when PK was dropping than during KCl infusion when PK was rising. The mechanisms responsible for this hysteresis phenomenon are not identified.

Aldosterone↗
PubMed1984

Hyperglycaemia in infantile gastroenteritis.

The prevalence and pathogenesis of hyperglycaemia were investigated in a consecutive series of 27 black infants admitted to hospital with gastroenteritis over a period of three months. Hyperglycaemia (plasma glucose concentration greater than 10 mmol/l) occurred in 15 (55%) of these patients. The pathogenesis was not clear but possible contributory factors included raised concentrations of the stress hormones pancreatic glucagon, growth hormone, and cortisol; hypokalaemia; and peripheral insulin resistance. Intravenous rehydration, without insulin, corrected the plasma glucose concentrations and restored the hormonal profile towards normal within 36 to 48 hours.

Child, Preschool↗
PubMed1984

Effects of glucagon, insulin, propionate, acetate, and HCO3 on K excretion in sheep.

The effects on renal K excretion of 1 h intravenous infusion of glucagon, insulin, Na propionate, Na acetate, or NaHCO3 were studied in mature, conscious fasted ewes. These treatments were compared with the fasted state without treatment (control) and with feeding a single daily meal. Renal K excretion was increased by feeding and by Na propionate and Na acetate treatments but not by infusion of glucagon, insulin, and NaHCO3. Since hormone levels were elevated more by specific hormone infusions than by feeding or Na propionate infusions, these results do not support a role for glucagon and insulin in mediating the increases in renal K excretion that occurred after meals or during acetate and propionate infusions. The mechanisms responsible for the acetate- and propionate-induced kaliuresis are not clear but do not appear to include changes in plasma K (PK), glucagon, and insulin (Pinsulin) or in urine flow and urine Na excretion. However, a relation between insulin and K was observed during infusion of KCl in fasting sheep. Above a PK threshold of 4 meq/l, Pinsulin (ng/ml) = 1.52 PK (meq/l) - 5.89. In other experiments, K excretion increased after an intravenous bolus injection of 1 mg of glucagon, indicating that sheep, like humans and dogs, respond to pharmacologic doses of glucagon with kaliuresis.

Acetates↗
PubMed1984

Sheep renal potassium excretion: efferent kaliuretic regulatory factors.

The possibility that efferent factors in addition to aldosterone and plasma K may mediate the renal response to large variations in K intake in sheep was explored in experiments on four mature ewes. K supplementation of a normal diet provided a total K intake of 1,300-1,500 meq/day for 3 days and produced a high K excretion (737 +/- 34 mu eq/min) with plasma K 4.67 +/- 0.07 meq/liter. K deprivation by 83 h of fasting produced low K excretion (48 +/- 10 mu eq/min) with plasma K 3.60 +/- 0.14 meq/liter. Additional treatments during both K-supplemented and K-deprived states included: raising plasma K through the range 4-7 meq/liter by intravenous infusion of 45 meq KCl in 30 min; intravenous infusion of aldosterone (20 micrograms/h) or of an aldosterone antagonist, potassium canrenoate (100 mg/h). Na supplementation during fasting was by rumen infusion of Na acetate-Na propionate (1,000 meq Na/day). Results showed that the increase in plasma K during intravenous K infusion directly elevated K excretion, that aldosterone enhanced and canrenoate depressed the kaliuretic effect of K infusion, and that Na loading during fasting enhanced the kaliuretic effect of aldosterone. Comparisons, made at the same level of plasma K, indicated that differences in plasma K, aldosterone, or Na excretion were not sufficient individually or in combination to account for the large differences of 350-1,150 mu eq/min in K excretion that existed between K-supplemented and K-deprived states. Unidentified kaliuretic regulatory factors appear to play a major role in the homeostatic control of K excretion in sheep under the circumstances of these experiments.

Aldosterone↗
PubMed1984

Time course of adaptation to altered K intake in rats and sheep.

The early time course of adaptation to large step increases in K intake was examined in sheep and rats. Fifteen 3-day experiments were performed on four mature ewes. They received on each day a single meal (730-930 meq K/day) and on days 2 and 3 a rumen KCl supplement (600 mM/day). Adaptation to the changed intake occurred within 47 h and was defined by the ratio of urinary K/K intake approximating normal preloading ratios. K excretion did not correlate significantly with plasma K or with Na excretion. Three groups of four rats, body wt 210 g, were studied over 19 days. Four rats fed a basal diet excreted 1.96 +/- 0.04 (n = 19) meq/day K. For four rats, the basal diet was supplemented with KCl on days 5-15, during which time K excretion was 9.34 +/- 0.36 (n = 11) meq/day; four rats with a higher KCl supplement on days 5-15 excreted 15.37 +/- 0.69 (n = 11) meq/day K. For rats, adaptation to increased and decreased intake was rapid, occurring on the first day of changed intake when urinary K excretion approximated intake. The rapid K adaptation was contrary to the generally accepted, but experimentally unverified, view that adaptation is a chronic process requiring 1 or more weeks to develop.

Acclimatization↗
PubMed1980

Urea and renal concentrating ability in the rabbit.

The hypotheses of passive salt accumulation predict an enhancement of renal concentrating ability by urea. We tested this prediction in rabbits, a species whose nephons when studied in vitro show tansport properties that support these hypotheses. We used calm, unanesthetized, hydropenic, vasopressin-treated rabbits with intact kidneys fed a 16% protein diet, and we observed the effect of urea administration at two rates of solute excretion (60 and 190 microOsm/min . kg body wt; N = 10 and 5, respectively). After an i.v. mannitol infusion, when urea was infused, the i.v. solute excretion rate was unchanged, the changes in urine urea concentration were large (a change of 767 and 408 mumoles/ml), but only small and variable changes in urine osmolality occured (a change of 78 +/- 146, and 36 +/- 50 microOsm/g H20). In additional experiments, we removed the kidneys from antidiuretic, or urea- or mannitol-infused rabbits and measured the intrarenal distribution of sodium, potassium, urea, and chloride. When the urine urea level was greater than 400 mmoles, the urine-to-papilla ratios for urea were 1.6 to 3.6. This suggested that a low collecting duct permeability to urea could explain the absence of a marked enhancement of concentrating ability during urea administration. Further analysis, based on a model of inner medullary solute compartments, indicated that sodium chloride was the major (86%) osmotically active solute in the medullary central core of these rabbits and that it was not influenced by changes in urinary urea concentration. The results of tissue analysis were consonant with either active or passive sodium chloride reabsorption from the thin ascending limb of Henle's loop in these rabbits.

Absorption↗
PubMed1979

Renal sodium and potassium excretion in sheep given amiloride.

When amiloride was given (IV) to unanesthetized ewes, potassium excretion decreased to one-third of baseline values, and sodium excretion increased 6- to 180-fold. Potassium excretion during amiloride administration was relatively invariant with respect to duration (0 to 270 minutes) or rate of amiloride administration (0.125 to 2.0 mg/minute), but sodium excretion clearly increased with both duration and dose rate in individual experiments. This increase was independent of the rate of concomitant saline administration. Thus, sheep fed a normal ration (about 600 mEq of potassium per day) respond to amiloride as do man, dogs, and rats. The relationship of sodium excretion to rate and duration of amiloride administration is not unique to sheep, but has not been stressed in previous studies on other species.

Amiloride↗
PubMed1978

Epidemic listeriosis. Report of 14 cases detected in 9 months.

During the period August 1977 to April 1978, 14 Black patients in Johannesburg area had systemic infections caused by Listeria monocytogenes. Nine of these patients were neonates who presented with septicaemia (5 cases) or septicaemia and meningitis (4 cases) and 5 were adults, all of whom had meningitis. The mortality rate was 43% (6/14), with 4 neonatal and 2 adult deaths. All isolates of L. monocytogenes were type 4b. Only sporadic cases of human listeriosis have previously been reported in South Africa, and the cases reported here constitute the first epidemic in this country.

Adult↗
PubMed1978

Renal potassium excretion in sheep during sodium sulfate, phosphate, and chloride infusion.

The renal excretion of potassium by unanesthetized sheep was studied in clearance studies in which water and sodium excretion were elevated by intravenous infusion of isotonic sodium chloride, hypertonic sodium phosphate, or hypertonic sodium sulfate. Aldosterone was infused at 10 microgram/h in some experiments with sodium sulfate. Sodium excretion increased in all experiments, rising at times to equal 25% of the filtered load. Urine flow increased in most experiments. Glomerular filtration rate increased only with infusion of isotonic saline. No consistent change in potassium excretion occurred under any of these loading conditions. This finding contrasts with the increase in potassium excretion commonly seen in man, dogs, and rats intravenously loaded with sodium salts.

Aldosterone↗
PubMed1977

Aldosterone and postprandial renal excretion of sodium and potassium in sheep.

When sheep rapidly eat a meal of dry feed a period of antinatriuresis and antidiuresis is rapidly initiated and lasts for 2-3 hrs. This is followed by a postprandial period of natriuresis and diuresis. This study tested the hypothesis that the postprandial natriuresis was due to a reduction in the secretion of aldosterone. In unanesthetized ewes of about 50 kg body wt, measurements were made of sodium and potassium excretion beginning in the terminal phase of the feed-induced antinatriuresis and continuing through the period of postprandial natriuresis. Aldosterone, given by constant infusion at a physiological dose (10 microgram/h), inhibited the natriuresis. Spironolactone, a competitive inhibitor of aldosterone given as a single intravenous injection of 5 mg/kg body wt, did not significantly increase the natriuresis. These results support the stated hypothesis. Neither aldosterone nor spironolactone had a significant effect on potassium excretion. This finding supports earlier view that aldosterone has only a small role in the homeostatic control of potassium excretion in sheep.

Aldosterone↗
PubMed1977

Renal concentrating ability in the uninephrectomized rat.

To investigate the effects of uninephrectomy on renal concentrating ability, studies were performed on unanesthetized rats 5-11 days after uninephrectomy (UN) or a sham operation (SO). Female rats were deprived of water for 27 h prior to the infusion of inulin and para-aminohippurate and urine collection. They were also preconditioned to being handled and to the experimental locale. During a nondiuretic state urine osmolality was the same for all UN and SO groups (mean about 1,700 micro osmol/g H2O), whereas the mean solute excretion rate (micro osmol/min per kg body wt per kidney) was 74 in the UN and 35 in the SO rats. When SO rats were infused with mannitol or isotonic saline to increase their solute excretion rate per kidney to the level of the UN rats, urine osmolality dropped 200-1,000 micro osmol/g H2O; when urea was infused, urine osmolality did not drop. Thus, after uninephrectomy and a consequent doubling of the solute excretion rate per kidney, renal concentrating ability was higher than predicted on the basis of a comparable but acute elevation of the solute excretion rate. The glomerular filtration rate was about 17 ml/min per kg body wt in the SO rats and was 1.2 times greater (on a per kidney basis) in the UN rats. These exceptionally high glomerular filtration rats are attributed to preexperimental conditioning of the rats and the absence of stress during urine collection.

Animals↗