Calcium clearance as a function of sodium clearance in the dog

Walser, Mackenzie

doi:10.1152/ajplegacy.1961.200.5.1099

Cited by 260 publications

(86 citation statements)

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“…For example, in clearance and micropuncture experiments in rabbits by Chonko et al (36), the J, rate in the proximal convoluted tubule was 1.9 nl/mm * min. However, most studies of J, in the proximal tubule in vitro find 50% of this rate, i.e., 0.8-1.0 nl/mm * min (15,18,33,37 The finding of passive calcium transport in the S2 segment of the superficial proximal convoluted tubule of the rabbit is consonant with the published literature that suggests that there is an interdependence of sodium and calcium (38,39). Those maneuvers, which depress proximal tubular reabsorption of sodium and water, such as volume expansion (38), PTH, (40), insulin (41), renal vasodilators (42), and acetazolamide (43), also similarly depress proximal tubular reabsorption of calcium, which results in parallel excretion of sodium and calcium in the final urine.…”

Section: Discussionsupporting

confidence: 77%

Calcium transport in the rabbit superficial proximal convoluted tubule.

Ng¹,

Rouse²,

Suki³

1984

J. Clin. Invest.

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Abstract. Calcium transport was studied in isolated S2 segments of rabbit superficial proximal convoluted tubules. '"Ca was added to the perfusate for measurement of lumen-to-bath flux (JibCa), to the bath for bath-to-lumen flux (JbIc), and to both perfusate and bath for net flux (Jnetc). In these studies, the perfusate consisted of an equilibrium solution that was designed to minimize water flux or electrochemical potential differences (PD). Under these conditions, JibCa (9.1 ± 1.0 peq/mm min) was not different from JblCa (7.3±1.3 peq/mm min), and Jntc1 was not different from zero, which suggests that calcium transport in the superficial proximal convoluted tubule is due primarily to passive transport. The efflux coefficient was 9.5±1.2 X 10-5 cm/ s, which was not significantly different from the influx coefficient, 7.0±1.3 X 10-5 cm/s. When the PD was made positive or negative with use of different perfusates, net calcium absorption or secretion was demonstrated, respectively, which supports a major role for passive transport. These results indicate that in the superficial proximal convoluted tubule ofthe rabbit, passive driving forces are the major determinants of calcium transport.

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Section: Discussionsupporting

confidence: 77%

Calcium transport in the rabbit superficial proximal convoluted tubule.

Ng¹,

Rouse²,

Suki³

1984

J. Clin. Invest.

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“…The renal tubular reabsorption of calcium is closely related to that of sodium (17,18,20,21), and it is likely that certain events promoting sodium transport in the nephron can also augment the reabsorption of calcium. Also, enhanced tubular reabsorption of calcium follows increased action of parathyroid hormone (22,23).…”

Section: Resultsmentioning

confidence: 99%

Changes in Serum and Urinary Calcium during Treatment with Hydrochlorothiazide: Studies on Mechanisms

Brickman¹,

Massry²,

Coburn³

1972

J. Clin. Invest.

218

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A B S T R A C T Studies were undertaken in man to evaluate the roles of volume depletion and of the parathyroid glands in mediating the changes in serum and urinary calcium which follow the administration of hydrochlorothiazide, 100 mg twice daily, for 4 days. 42 studies were carried out in 16 normal subjects, 9 patients with hyperparathyroidism, and 7 vitamin D-treated subjects with hypoparathyroidism. In six studies in normal subjects, daily sodium losses during thiazide administration were quantitatively replaced, and in six other studies the effect of equivalent sodium losses produced by furosemide was evaluated.Although the magnitude of sodium losses was similar in three groups during therapy with thiazides, urinary calcium fell and urinary phosphorus increased significantly only in normal subjects and those with hyperparathyroidism; no change occurred in patients with hypoparathyroidism. With the replacement of the thiazide-induced sodium losses by NaCl in normals, urinary calcium did not change as urinary sodium increased 4-to 5-fold. Furosemide administration produced similar sodium losses while urinary calcium remained at or above control levels. After correction for changes in plasma protein concentration caused by thiazide-induced hemoconcentration, mean levels of serum calcium were significantly increased only in subjects with hyperparathyroidism and vitamin D-treated patients with hypoparathyroidism.

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“…Walser pointed out that the natriuresis induced by mercurial diuretics and acetazoleamide is accompanied by a simultaneous increase in urinary calcium excretion and suggested that the transport of these ions in the kidney is related, with a common transport mechanism possibly being involved. 12 Walser also noted that the diuretics of the benzothiadiazine class have the opposite effect but offered no explanation for this. '3 The reduction in calcium clearance induced by the thiazides could be due to a fall in the filtered calcium load resulting either from diminished glomerular filtration rates, or from increased protein binding of plasma calciumn.…”

Section: Resultsmentioning

confidence: 99%