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Biomedical subjects

A Haramati

Publications and source records attributed to A Haramati.

46 records · Page 3Linked to original sources
PubMed1984

Adenosine-induced decrease in renin release: dissociation from hemodynamic effects.

Adenosine has been reported to produce a biphasic renal blood flow (RBF) response (vasoconstriction followed by a return of flow to control level) and a decrease in glomerular filtration rate (GFR) when infused into the kidney. Intrarenal adenosine infusion also leads to a decrease in renin release. By altering the hemodynamic response to adenosine, we sought to determine whether the decrease in renin release depends on vascular or filtration-induced events. In nine dogs with nonfiltering kidneys, adenosine infusion (3 X 10(-7) mol/min) resulted in a biphasic RBF response and an inhibition of renin release (309 +/- 53 vs. 71 +/- 26 ng ANG I/min). In 11 dogs treated with verapamil (10 micrograms X kg-1 X min-1) no vasoconstriction or decrease in GFR occurred; however, renin release was inhibited by adenosine (1,300 +/- 159 vs. 534 +/- 225 ng ANG I/min). In a third group of nine dogs whose ureteral pressure was raised to 80 cmH2O, adenosine infusion produced a sustained vasoconstriction and an inhibition of renin release (3,086 +/- 1,144 vs. 328 +/- 130 ng ANG I/min). These experiments, in which the renin release effects of adenosine are dissociated from the hemodynamic effects, lead us to conclude that the inhibition of renin release produced by adenosine does not depend either on the vascular or filtration-induced effects of adenosine.

Adenosine↗
PubMed1984

Renal handling of phosphate during acute respiratory acidosis and alkalosis in the rat.

Clearance experiments were performed in acutely thyroparathyroidectomized rats to evaluate the renal handling of phosphate during respiratory acidosis (R ACID) and alkalosis (R ALK) in rats fed either a normal (0.7%) or low (0.07%) phosphate diet for 4 days. Different acid-base states were achieved by varying the mixture of carbon dioxide in the inspired air. Each group received graded infusions of phosphate to control for differences in plasma phosphate (PPi) and to determine the maximum transport capacity of phosphate reabsorption (TmPi/GFR). In rats fed a normal phosphate diet, PPi and the fractional excretion of phosphate (FEPi) were significantly greater in R ACID than in R ALK. However, there were no differences between R ACID and R ALK when FEPi was evaluated as a function of the PPi, and values for TmPi/GFR during R ACID were not different from those during R ALK. In rats fed low phosphate diet, PPi during R ACID was significantly greater than during R ALK, yet FEPi was less than 1% in all groups due to an adaptive increase in TmPi/GFR. Further, the TmPi/GFR was similar irrespective of the acid-base state. We conclude that acute respiratory acid-base changes do not alter the intrinsic capacity of the kidney to reabsorb phosphate.

Acidosis, Respiratory↗
PubMed1983

Tubular capacity of phosphate transport in phosphate-deprived rats: effects of nicotinamide and PTH.

The present study tested the hypothesis that nicotinamide and/or parathyroid hormone (PTH) would reverse the resistance of phosphate-deprived rats to the phosphaturic effects of phosphate infusions by reducing the tubular capacity for phosphate transport. The response to progressively increasing rates of phosphate infusion (1, 2, and 3 mumol/min) was evaluated in thyroparathyroidectomized (TPTX) rats fed low phosphate diet (0.07%) for 4 days and treated with either vehicle or nicotinamide 2 h before the experiment. Following phosphate infusions, phosphate excretion was unchanged in vehicle-treated rats but increased progressively in nicotinamide-treated rats to 60% of the final rate of infusion. In a second series conducted in the presence of exogenous PTH, vehicle-treated rats responded to phosphate infusions by increasing phosphate excretion to 80-90% of the rate of infusion. In the presence of both nicotinamide and PTH, the rate of phosphate excretion matched the rate of infusion. Vehicle-treated rats displayed the highest reabsorptive rates without reaching a transport maximum, whereas a lower maximum reabsorptive rate was evident in nicotinamide-treated rats. However, in both groups given PTH, not only was the transport maximum lower but it declined with further increases in filtered load. We conclude that nicotinamide and PTH reverse the effects of dietary phosphate deprivation by decreasing the tubular capacity for phosphate transport.

Animals↗
PubMed1983

Adaptation of deep and superficial nephrons to changes in dietary phosphate intake.

Dietary phosphate intake is now recognized to be a primary regulator of renal phosphate excretion. However, the nephron sites involved in the adaptation to changes in dietary phosphate are unclear. We tested the hypothesis that deep and superficial nephrons respond differently to changes in dietary phosphate by comparing fractional phosphate delivery (FDP%) from proximal tubules of both nephron populations. Because phosphate reabsorption is not detectable in the ascending loop of Henle, FDP% to the superficial early distal tubule and papillary loop of Henle reflect delivery from superficial and deep nephron proximal tubules, respectively. Micropuncture experiments were performed in 17 acutely TPTX rats fed either a low (0.07%) or a high (1.8%) phosphate diet for 4 days prior to the experiment. In low phosphate diet, fractional phosphate excretion was 0.93 +/- 0.26%. FDP% was 7.5 +/- 0.5 and 9.1 +/- 2.2% from superficial and deep nephron proximal tubules, respectively (P greater than 0.05). In high phosphate diet, fractional phosphate excretion was 29.6 +/- 5.0%. FDP% was significantly greater from superficial proximal tubules, 33.9 +/- 4.6%, compared with that from deep nephron proximal tubules, 14.0 +/- 2.7% (P less than 0.05). We conclude that significant adaptation of phosphate reabsorption in response to changes in dietary phosphate intake occurs in the superficial but not in the deep nephron proximal tubule in acutely TPTX volume-expanded rats. In addition, the presence of distal phosphate reabsorption was not evident in high phosphate diet but must occur in low phosphate diet.

Animals↗
PubMed1983

Role of hydrostatic and oncotic pressures in renal sodium reabsorption.

Physical factors, and renal interstitial hydrostatic pressure in particular, have an important effect on sodium excretion by the kidney. Changes in hydrostatic and oncotic pressures in the peritubular microcirculation may have effects on proximal tubule reabsorption under some, but not all, circumstances. In regard to control of sodium excretion, the loop of Henle may be a particularly important segment which is sensitive to transepithelial hydrostatic pressure changes. There is little evidence to support an effect of physical factors on sodium reabsorption by the distal tubule. The collecting tubule may be another pressure-sensitive site; however, changes in sodium reabsorption by deep nephrons in the kidney may account for changes that have been attributed to the collecting duct. Changes in intrarenal pressure may be an important link in the regulation of sodium excretion, particularly in pathological circumstances, such as the exaggerated natriuresis of hypertension and the sodium retention seen in congestive heart failure.

Absorption↗
PubMed1983

Restoration of phosphaturia in phosphate-deprived rats in the presence of both parathyroid hormone and phosphate infusion.

The present study tested the hypothesis that the combination of parathyroid hormone and phosphate infusion would be phosphaturic in phosphate-deprived rats. Clearance experiments were performed in Sprague-Dawley rats fed a low-phosphate diet for 4 days. The animals were first given a phosphate infusion and then administered parathyroid hormone. The reverse experiment was also performed in a second group of rats by giving the hormone first followed by a phosphate infusion. There was no increase in phosphate excretion in response to phosphate infusion or parathyroid hormone given alone. However, the combination of parathyroid hormone and phosphate infusions, given in either order, was phosphaturic in phosphate-deprived rats.

Animals↗
PubMed1980

Chloride concentration gradient in newborn dogs in the presence of distal nephron blockade.

Renal tubular Na+, Cl-, and H2O reabsorption was determined in 14 newborn dogs, 3--29 days of age, and in three adult dogs. In all animals NaCl reabsorption beyond the proximal tubule was blocked with ethacrynic acid (2 mg/kg) and amiloride (2.4 mg/kg). During distal blockade, fractional reabsorption of NaCl and water in both newborns and adults was approximately 70%, and there was a urine-to-plasma chloride gradient equal to 1.34 +/- 0.01, indicating that the proximal tubules of the newborn as well as those of the adult can generate a transtubular Cl- gradient. Upon administration of acetazolamide (50 mg/kg), there was a dramatic increase in excretion of Na+, Cl-, HCO3-, and water, and a decrease in the transtubular chloride gradient. After acetazolamide, the degree of inhibition of HCO3 reabsorption was well correlated with that of Na+, (r = 0.77) or Cl- (r = 0.74), and Na+ or Cl- inhibition exceeded that of HCO3-. In the newborn animal, the ratio of inner-to outer cortical nephron function is high at birth and declines rapidly during the first few weeks of life. However, there was no correlation between age and changes in either electrolyte excretion or in the transtubular chloride gradient. Therefore, the newborn dog possesses Cl- permselective tubules in the inner cortex that, in the presence of intact HCO3- reabsorption, are capable of establishing a functional transtubular Cl- gradient contributing to NaCl reabsorption.

Aging↗