Effect of thyroxine on ion movement in isolated toad bladder

Matty, A. J.; Green, K.

doi:10.1016/0016-6480(64)90030-9

Cited by 12 publications

(8 citation statements)

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“…Thyroid hormone has been shown to decrease the resistance of toad bladders (40). In addition, the bath to lumen flux of 36 C and 32 P increased with thyroid hormone administration, consistent with a decrease in the paracellular permeability to these anions (39,40). However, passive phosphate and calcium transport across the small intestine was less in rats that received thyroid hormone for 7 d than in control rats, consistent with a decrease in paracellular movement of these ions with thyroid hormone treatment (38).…”

Section: Discussionmentioning

confidence: 81%

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Developmental Changes in Proximal Tubule Tight Junction Proteins

et al. 2005

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We demonstrated previously that neonatal proximal tubules have a lower passive paracellular permeability to chloride ions and higher resistance than that of adult proximal tubules. In addition, administration of thyroid hormone to neonates, before the normal maturational increase in serum thyroid hormone levels, prematurely accelerates the developmental increase in chloride permeability to adult levels. To test the hypothesis that there is a maturational change in tight junction proteins and that thyroid hormone mediates these changes, we examined the two known tight junction proteins present in proximal tubules, occludin and claudin 2. Using immunoblot and immunohistochemistry, we demonstrated that claudin 2 has a 4-fold greater abundance in neonatal proximal tubules than in adult tubules. Occludin, however, has a 4-fold greater expression in adult tubules than in neonatal tubules. Administration of thyroid hormone to neonates did not affect claudin 2 expression, occludin expression, or the transepithelial resistance in rat proximal tubule cells in vitro. In conclusion, there are postnatal maturational changes in tight junction proteins. The factors that cause these maturational changes are unknown but unlikely to be due solely to the maturational increase in thyroid hormone.The proximal tubule receives an ultrafiltrate from the glomerulus and reabsorbs two thirds of the ultrafiltrate in a nearly iso-osmotic manner. In addition to active transcellular fluid transport, the proximal tubule reabsorbs solutes via passive diffusion across the paracellular pathway. The early proximal tubule reabsorbs glucose and amino acids and preferentially reabsorbs bicarbonate over chloride ions (1,2), which leaves the luminal fluid delivered to the late proximal tubule with a higher chloride concentration and lower bicarbonate concentration than that in the peritubular plasma (1,2). Passive solute transport is dependent on the gradients that develop between lumen and peritubular capillary and permeability properties of the paracellular pathway.Approximately two thirds of the filtered chloride is reabsorbed by the adult proximal tubule (1,3 active and transcellular and half is passive and paracellular (3-5). Active NaCl transport is mediated by the parallel operation of the Na+/H+ exchanger and a Cl−/base exchanger (3,4). Passive Cl absorption is mediated by diffusion of chloride ions down its concentration gradient generated in the early proximal tubule (6,7). Thus, the permeability properties of the paracellular pathway can affect a significant amount of proximal tubule NaCl transport.Furthermore, the permeability properties of the paracellular pathway serve as a barrier to prevent the back diffusion of glucose, amino acids, phosphate, bicarbonate, and other solutes that are in higher concentration in the peritubular fluid than in the lumen of the late proximal tubule. In previous in vitro rabbit microperfusion studies, our laboratory demonstrated that unlike the adult segment, the neonatal proximal tubule was impermeab...

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Section: Discussionmentioning

confidence: 81%

“…Other studies suggested that thyroid hormone may be involved in the regulation of the permeability of the paracellular pathway (38)(39)(40). Thyroid hormone has been shown to decrease the resistance of toad bladders (40).…”

Section: Discussionmentioning

confidence: 99%

Developmental Changes in Proximal Tubule Tight Junction Proteins

et al. 2005

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“…Thyroid hormone was shown 35 years ago to affect passive paracellular anion permeability in isolated toad bladders (20,21). After thyroxine treatment, there was an increase in shortcircuit current but no change in electrical potential, consistent with a concomitant increase in paracellular permeability.…”

Section: Discussionmentioning

confidence: 83%

Maturation of proximal straight tubule NaCl transport: role of thyroid hormone

Shah¹,

Quigley²,

Baum

2000

American Journal of Physiology-Renal Physiology

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We have recently demonstrated that the rates of both active and passive proximal straight tubule (PST) NaCl transport in neonatal rabbits were less than in adults. In this segment NaCl entry across the apical membrane is via parallel Na + /H + and Cl − /OH − exchangers, which increases in activity with maturation. The present in vitro microperfusion study examined whether thyroid hormone plays a role in the maturational increase in PST NaCl transport. Neonatal and adult PST were perfused with a high-chloride-low bicarbonate solution without organic solutes, simulating late proximal tubule fluid. Thyroid hormone-treated neonates had a higher rate of PST total and passive NaCl transport. In 8-wk-old animals that were hypothyroid since birth, the maturational increase in total and passive NaCl transport was prevented. Thyroid treatment for 4 days in hypothyroid 8-wk-old rabbits increased the rate of both total and passive NaCl transport. The maturational increases in both Na + /H + and Cl − /OH − exchange activities were blunted in 8-wk-old hypothyroid animals and increased to control levels with thyroid treatment. This study demonstrates that thyroid hormone is a factor responsible for the maturational increase in both active and passive PST NaCl transport.Keywords sodium/hydrogen antiporter; chloride/base exchanger; kidney development; passive transportThe Proximal Tubule Reabsorbs ~60% of the filtered NaCl. The preferential reabsorption of organic solutes and bicarbonate by the early proximal tubule leaves the luminal fluid with a higher chloride and lower bicarbonate concentration than the peritubular plasma (19,24). In the proximal tubule approximately one-half of NaCl transport is passive and paracellular (4,25). The parallel operation of the apical membrane Na + /H + antiporter and Cl − /base exchangers mediate NaCl entry into the proximal tubule cell (1,18,25 We have recently examined the postnatal developmental changes in proximal straight tubule (PST) NaCl transport (25). In rabbit PST perfused with a high chloride-low bicarbonate solution simulating late proximal tubular fluid and bathed in a serum-like albumin solution, the rate of volume absorption, a reflection of both active and passive NaCl transport, was over twofold higher in the adult than neonatal segment (25). NaCl transport was inhibited by 50% by bath ouabain in adult tubules and totally inhibited in the neonatal segment. Thus the rates of active and passive NaCl transport were higher in the adult tubule than were those in the neonate (25).In the rabbit PST there was a fivefold increase in the Na + /H + antiporter activity during postnatal development (25). Cl − /base exchange in neonatal and adult PST was not affected by cyanide and acetazolamide, CO 2 and bicarbonate, or the addition of formate, consistent with Cl − /OH − exchange (18, 25). There was a sixfold maturational increase in apical membrane PST Cl − /OH − exchange activity (25).The factors that produce the profound postnatal changes in active and passive proximal tubular t...

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“…However, it is known that thyroxine has a direct metabolic effect on the myocardium which leads, for example, to a stimulation of protein anabolism (19) and a change in the primary energy source used by heart muscle from one of carbohydrates to one of fatty acids (20). In addition, thyroxine may also have a direct effect on the cell membrane to alter transport of electrolytes and result in changes in myocardial contractility (21). Finally, the increased myocardial contractility of hyperthyroid animals is demonstrable in vitro, without nervous and humoral influences (10).…”

Section: Circuutwit Rtit a Rcb Vol XXII M*j 1968mentioning

confidence: 99%

Left Ventricular Myocardial Contractile Response to Aortic Constriction in the Hyperthyroid Guinea Pig

Goodkind

1968

Circulation Research

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Maximum left ventricular systolic pressure response to aortic constriction served as a measure of myocardial contractility in anesthetized euthyroid and hyperthyroid guinea pigs. This response in hyperthyroid guinea pigs (155.4 ± 1.40 mm Hg) was significantly greater than in euthyroid animals (147.3 ± 1.33 mm Hg) (P<.001) and developed at a lower end-diastolic pressure in hyperthyroid (11.27 ±0.418 mm Hg) than in euthyroid guinea pigs (14.15 ±0.521 mm Hg) (P<.001). Beta-adrenergic receptor blockade with propranolol decreased the heart rate in both groups of animals but did not alter the contractile response. After propranolol, the heart rate of the hyperthyroid animals, though decreased, was still greater than that of euthyroid controls. Cardiac stimulation at a rate similar to that of the hyperthyroid animals (430 beats/min) did not change the left ventricular contractile response of normal guinea pigs. It is concluded that myocardial contractility in hyperthyroid guinea pigs is greater than normal. Increased activity of the sympathetic nervous system is probably present in hyperthyroidism, is reflected in the tachycardia, but does not appear to increase myocardial contractility. The increased myocardial contractility therefore is probably due in large part to a direct effect of thyroid hormone on cardiac muscle. ADDITIONAL KEY WORDSpropranolol hemodvnamic function beta-receptor blockade pressure work tachycardia cardiac stimulation • Many attempts have been made to define the relationship of the sympathetic nervous system to the cardiovascular changes produced by excess thyroid hormone. For years the hyperkinetic circulation of thyrotoxicosis was thought to be related to a hypersensitivity to catecholamines (1). However, recent reports have shown that thyroxine does not

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Effect of thyroxine on ion movement in isolated toad bladder

Cited by 12 publications

References 11 publications

Developmental Changes in Proximal Tubule Tight Junction Proteins

Developmental Changes in Proximal Tubule Tight Junction Proteins

Maturation of proximal straight tubule NaCl transport: role of thyroid hormone

Left Ventricular Myocardial Contractile Response to Aortic Constriction in the Hyperthyroid Guinea Pig

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