Effects of Colchicine and Vinblastine on the Cellular Action of Vasopressin in Mammalian Kidney A POSSIBLE ROLE OF MICROTUBULES

Douša, Thomas P.; Barnes, Larry D.

doi:10.1172/jci107760

Cited by 50 publications

(16 citation statements)

References 33 publications

(49 reference statements)

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“…The striking increase in acid excretion was associated with a significant increase in plasma bicarbonate concentration, from 22.2±0.6 to 26.4±1.0 meq/liter (P < 0.05). In sharp contrast to controls, colchicine treatment of phosphate-depleted rats was associated with continued bicarbonaturia (control: 0; PD: 5.8+2.4 ueq/h; P < 0.001) despite the abrupt fall in plasma bicarbonate concentration from 23 To document the presence of this extra-renal source of bicarbonate in phosphate depletion we abolished urinary bicarbonate wasting by nephrectomizing rats from both groups. Normally, this leads to the retention of fixed acids, causing the production of a progressive metabolic acidosis.…”

Section: Resultsmentioning

confidence: 90%

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

Emmett¹,

Goldfarb²,

Agus³

et al. 1977

J. Clin. Invest.

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A B S T R A C T Acid-base disturbances may develop secondary to the changes in renal tubular function and bone dynamics which attend phosphate depletion (PD). This work characterizes the acid-base status of rats fed a low phosphate diet. After 18 days, PD rats had marked calciuria (pair-fed controls: 0.3+0.2; PD 32.2+2.5 ,ueq/h; P < 0.001), severe bicarbonaturia (controls: 0; PD 17.6+0.2 ,ueq/h; P < 0.001), and negative net acid excretion (controls: 44.5+2.9; PD: -6.6+2.5 ,ueq/h; P < 0.001), but plasma pH, HCO3, and Pco2 were equal in both groups. After 45 days, plasma HCO3 fell to 21.1+0.9 meq/liter in PD (controls: 23.6+0.5 meq/liter; P < 0.05), while bicarbonaturia (controls: 0.4+0.2; PD: 3.8±1 ueq/h; P < 0.02) and calciuria were present but diminished. These data suggested the coexistence of bone HCO3 mobilization and renal HCO3 wasting in PD. To test this thesis, bicarbonaturia was eliminated by nephrectomy. 24 h later plasma HCO3 was higher in PD rats (controls: 19.3+0.02; PD: 22.6+0.8 meq/liter; P < 0.05), consistent with the presence of extrarenal HCO3 production. After inhibition of bone resorption with colchicine (1 mg/kg), plasma HCO3 decreased to 16.8±+0.6 meq/liter in PD rats (controls): 26.4±1 meq/ liter; P < 0.001) while bicarbonaturia persisted. These data indicate that the plasma HCO3 in PD is the net result of renal HCO3 wasting and bone HCO3 mobilization.

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Section: Resultsmentioning

confidence: 90%

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

Emmett¹,

Goldfarb²,

Agus³

et al. 1977

J. Clin. Invest.

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“…The fact that microtubules also show a significant increase in content when hormone release from chief cells is presumed to Received for publication 25 September 1974 and in revised form 21 February 1975. several organs (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17), including that of the parathyroid gland. Colchicine inhibits the conversion of proparathyroid hormone to parathyroid hormone in incubated slices of bovine parathyroid gland (5), and vinblastine sulfate inhibits the release of parathyroid hormone from incubated parathyroid glands (4,14).…”

mentioning

confidence: 99%

A quantitative ultrastructural study of microtubule content and secretory granule accumulation in parathyroid glands of phosphate- and colchicine-treated rats.

Reaven¹,

Reaven²

1975

J. Clin. Invest.

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“…Cortical and papillary parts of the kidney were dissected from the whole kidney and homogenized in buffered isotonic sucrose medium (0.25 M sucrose, 5 mM Tris, 3 mM MgCl2, and 1 mM EDTA, pH 7.4) as previously described (6,7). The 600 g/10-min pellet of homogenate was washed in a medium of the same composition, divided in small aliquots, frozen in dry ice, and kept frozen at -800C until assayed for adenylate cyclase activity.…”

Section: Biochemical Studiesmentioning

confidence: 99%

“…The 600 g/10-min pellet of homogenate was washed in a medium of the same composition, divided in small aliquots, frozen in dry ice, and kept frozen at -800C until assayed for adenylate cyclase activity. Adenylate cyclase activity was assayed as previously described (6,7). In experiments in which the 676 F. G. Knox, J. Preiss, J. J. Kim, and T. P. Dousa effects of added hormones or drugs were tested, the adenylate cyclase activity was measured in the absence and presence of the agent and differences were evaluated on a paired basis.…”

Section: Biochemical Studiesmentioning

confidence: 99%

Mechanism of resistance to the phosphaturic effect of the parathyroid hormone in the hamster.

Knox¹,

Preiss²,

Kim³

et al. 1977

J. Clin. Invest.

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A B S T R A C T The effect of parathyroid hormone and calcitonin on the renal excretion of phosphate, calcium, and cyclic AMP was evaluated in the thyroparathyroidectomized hamster, a mammal apparently resistant to the phosphaturic effect of parathyroid hormone. Parathyroid hormone did not increase phosphate excretion, although it decreased excretion of calcium and increased urinary excretion of cyclic AMP. This lack of a phosphaturic response to parathyroid hormone was not reversed by administration of 25-OH vitamin D or infusions of calcium or phosphate. Calcitonin, another potentially phosphaturic hormone, also failed to increase phosphate excretion but markedly elevated urinary excretion of cyclic AMP. In hamsters pretreated with infusion of ammonium chloride, which decreased plasma and urinary pH, both parathyroid hormone and calcitonin increased excretion of phosphate as well as that of cyclic AMP. Acetazolamide had no phosphaturic effect in ammonium chloride-loaded hamsters, and it decreased cyclic AMP and calcium excretion. Alkalinization of urine by acetazolamide did not prevent the phosphaturic effect of parathyroid hormone in ammonium chloride-loaded hamsters, but it blocked the increase in urinary cyclic AMP excretion. Parathyroid hormone and calcitonin both stimulated adenylate cyclase in a cell-free system (600-g pellet) from hamster renal cortex, elevated tissue cyclic AMP levels, and activated protein kinase in tissue slices from hamster renal cortex. In acid medium, the increase in cyclic AMP

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Effects of Colchicine and Vinblastine on the Cellular Action of Vasopressin in Mammalian Kidney A POSSIBLE ROLE OF MICROTUBULES

Cited by 50 publications

References 33 publications

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

A quantitative ultrastructural study of microtubule content and secretory granule accumulation in parathyroid glands of phosphate- and colchicine-treated rats.

Mechanism of resistance to the phosphaturic effect of the parathyroid hormone in the hamster.

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