Micropuncture Study of Inorganic Phosphate Excretion in the Rat *

Strickler, James C.; Thompson, David D.; Klose, Ruth M.; Giebisch, Gerhard; Gluck, Judith N.; Vaughan, Judith B.

doi:10.1172/jci105035

Cited by 152 publications

(62 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The tubular PO 4 load of 18.45 ^moles/min/ kg, corresponds to a fractional reabsorption of 73%; i.e., in normal animals 73% of the filtrated phosphate is reabsorbed after passage through the first two-thirds of the proximal tubule. This reabsorption corresponds to the values which have been reported by Strickler et al [31]. He found, also in micropuncture studies, a phosphate reabsorption of 10.10 ^moles/min/kg and a fractional reabsorption of 76%.…”

Section: Discussionsupporting

confidence: 88%

The Effect of Vitamin D on Renal Inorganic Phosphate Reabsorption of Normal Rats, Parathyroidectomized Rats, and Rats with Rickets

1971

View full text Add to dashboard Cite

ExtractIn order to determine the effect of vitamin D on tubular reabsorption of phosphate, micropuncture studies were performed in the proximal convolution of normal rats, of parathyroidectomized rats, and of rats with rickets. The studies showed that vitamin D exerted a direct effect on transtubular reabsorption of phosphate that was independent of parathyroid function. The glomerular filtration rate was not affected by vitamin D. The reabsorption of phosphate of normal rats was 13.51 yumoles/min per kg. This corresponds to a fractional reabsorption of 73%. With vitamin D the fractional reabsorption increased to 86%. Despite continuous infusion of vitamin D, the phosphate reabsorption decreased to 13.95 /^moles/min/kg (fractional reabsorption 74%) after 180-240 min. Parathyroidectomized rats also showed a decreased transtubular reabsorption of phosphate during vitamin D infusion. In animals under a phosphate load who suffered from rickets, it was possible to normalize the decreased rate of reabsorption of phosphate (fractional reabsorption 59%) by the administration of vitamin D (fractional reabsorption 78%). SpeculationWe were unable to determine why, despite continuous infusion of vitamin D and independent of the dosage, a decrease occurred in the increased reabsorption after 90-120 min and why after 180-240 min this function returned to the starting value. Since at this latter time toxic renal damage is unlikely and renal function was controlled during the whole experiment, the question arises whether inadequate activation, reactive breakdown of vitamin D, or development of resistance to the physiological activity of the vitamin is involved.

show abstract

Section: Discussionsupporting

confidence: 88%

The Effect of Vitamin D on Renal Inorganic Phosphate Reabsorption of Normal Rats, Parathyroidectomized Rats, and Rats with Rickets

1971

View full text Add to dashboard Cite

show abstract

“…It therefore seemed pertinent to investigate the interactions of other agents which are important in controlling renal phosphate (as well as calcium and sodium) transport with regard to their capacity to influence the renal effects of vitamin D. Accordingly, the relationships between TCT, cAMP, 25HCC, and serum calcium concentration on ionic excretion were explored, a mechanism which might explain their individual and combined effects was proposed, and an attempt was made to evaluate this proposal. Major emphasis has been placed on the study of alterations in the excretion of the phosphate ion, not only because of the predominant effect of PTH on its renal reabsorption, but also because, unlike sodium and calcium, the bulk of its tubular transfer appears to be accomplished in the proximal nephron (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Study of the Renal Tubular Interactions of Thyrocalcitonin, Cyclic Adenosine 3′, 5′ -Monophosphate, 25-Hydroxycholecalciferol, and Calcium Ion

Puschett¹,

Beck²,

Jelonek³

et al. 1974

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T Acute clearance studies were performed in thyroparathyroidectomized animals to determine the actions and interactions of thyrocalcitonin (TCT), cyclic adenosine 3'5'-monophosphate (cAMP), 25-hydroxycholecalciferol (25HCC), and calcium ion on the reabsorption of phosphate, calcium, sodium, and potassium by the kidney. The infusion of 25HCC in a dosage of 60 U/h to moderately saline-expanded animals (2.5% body weight) induced a fall in the excretion of all of the ions under study after 90-120 min similar to that observed in previous experiments from this laboratory. Mean decrements in fractional excretion were: phosphate, 42.0% (P < 0.005); calcium, 25.0% (P < 0.005); sodium, 23.4% (P < 0.001); and potassium, 14.7% (P < 0.005). The superimposition of either porcine or salmon TCT (1-100 MRC U/h for 2 h) resulted in no further alterations in electrolyte excretion. However, the infusion of TCT during steady-state saline expansion, before the administration of 25HCC, obviated the renal transport effects of the vitamin D metabolite. Both in the latter studies, as well as those in whiicl similar doses of TCT were given to hydropenic animnals, the hormone itself failed to induce any consistent alteration in electrolyte excretion. Cyclic AMP (50 mg/h) caused an increase in the excretion of phosphate, sodium, and potassium and no change in calcium excretion. Like TCT, the nucleotide blocked the action of 25HCC on the kidney. Raising the mean level of serum ultrafilterable calcium to 3.02±0.25 mEq/liter from 1.62±0

show abstract

“…5C) rather than direct secretion of P i . In mammals (Strickler et al, 1964;Agus et al, 1971), changes in P i reabsorption similarly regulate the degree of urinary P i excretion. The decline of plasma Na + and Cl − in acid-exposed goldfish (Table 1) has been seen previously in other acid-exposed teleosts (McDonald et al, 1980;McDonald and Wood, 1981;Ultsch et al, 1981;Fugelli and Vislie, 1982;Wright et al, 2014).…”

Section: General Acid-base and Ion Responsesmentioning

confidence: 99%

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

Lawrence

Wright

Wood

2015

Journal of Experimental Biology

View full text Add to dashboard Cite

Relative to the gills, the mechanisms by which the kidney contributes to ammonia and acid-base homeostasis in fish are poorly understood. Goldfish were exposed to a low pH environment (pH 4.0, 48 h), which induced a characteristic metabolic acidosis and an increase in total plasma [ammonia] but reduced plasma ammonia partial pressure (P NH3 ). In the kidney tissue, total ammonia, lactate and intracellular pH remained unchanged. The urinary excretion rate of net base under control conditions changed to net acid excretion under low pH, with contributions from both the NH 4 + (∼30%) and titratable acidity minus bicarbonate (∼70%; TA-HCO 3 − ) components. Inorganic phosphate (P i ), urea and Na + excretion rates were also elevated while Cl − excretion rates were unchanged. Renal alanine aminotransferase activity increased under acidosis. The increase in renal ammonia excretion was due to significant increases in both the glomerular filtration and the tubular secretion rates of ammonia, with the latter accounting for ∼75% of the increase. There was also a 3.5-fold increase in the mRNA expression of renal Rhcg-b (Rhcg1) mRNA. There was no relationship between ammonia secretion and Na + reabsorption. These data indicate that increased renal ammonia secretion during acidosis is probably mediated through Rhesus (Rh) glycoproteins and occurs independently of Na + transport, in contrast to branchial and epidermal models of Na + -dependent ammonia transport in freshwater fish. Rather, we propose a model of parallel H + /NH 3 transport as the primary mechanism of renal tubular ammonia secretion that is dependent on renal amino acid catabolism.

show abstract

Micropuncture Study of Inorganic Phosphate Excretion in the Rat *

Cited by 152 publications

References 27 publications

The Effect of Vitamin D on Renal Inorganic Phosphate Reabsorption of Normal Rats, Parathyroidectomized Rats, and Rats with Rickets

The Effect of Vitamin D on Renal Inorganic Phosphate Reabsorption of Normal Rats, Parathyroidectomized Rats, and Rats with Rickets

Study of the Renal Tubular Interactions of Thyrocalcitonin, Cyclic Adenosine 3′, 5′ -Monophosphate, 25-Hydroxycholecalciferol, and Calcium Ion

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

Contact Info

Product

Resources

About