Distribution of aldosterone receptors in rat kidney cortical tubules enriched in proximal and distal segments

Scholer, D; Mishina, Takao; Edelman, Isidore S.

doi:10.1152/ajprenal.1979.237.5.f360

Cited by 3 publications

(2 citation statements)

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“…The independence of the efferent ducts from mineralocorticoid control is consistent with the common embryonic origin of the efferent ducts and the proximal kidney tubules (the efferent ducts are derived from embryonic mesonephric kidney tubules: Torrey, 1943;Du Bois, 1969). The proximal tubules do not have specific receptors for aldosterone (Scholer, Mishina & Edelman, 1979;Doucet & Katz, 1981), and Na+-K+-ATPase activity in the proximal tubule of the rabbit is unaffected by adrenalectomy or aldosterone supplementation (Garg, Knepper & Burg, 1981;b, 1984, and only slightly depressed by adrenalectomy in the rat (presumably by indirect effects from factors such as a reduced glomerular filtration rate: El Mernissi & Doucet, 1983a). After some initial controversy, it is also now generally accepted that mineralocorticoids do not directly affect water and electrolyte reabsorption in the proximal tubule.…”

Section: Discussionsupporting

confidence: 70%

Adrenal independence of fluid and electrolyte reabsorption in the ductuli efferentes testis of the rat

Clulow²,

La³

et al. 1997

Experimental Physiology

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SUMMARYThe ductuli efferentes testis (efferent ducts) of the rat were studied to determine whether fluid and electrolyte reabsorption by the ducts is under the control of adrenal mineralocorticoids. Testicular fluid output and the rate of fluid reabsorption by the ducts were determined in sham-operated controls and in rats which had been adrenalectomized 10 days previously, adrenalectomized 10 days previously and given aldosterone therapy (75 jug kg-' day-' s.c.) from day 3 to day 10 post adrenalectomy, and in rats given injections of the aldosterone antagonist, spironolactone, for 10 days (10 mg kg-' day-' s.c.). The values for testicular fluid output and fluid flow from the efferent ducts (means + S.E.M.) in the sham-operated rats were 36 0 + 7-8 and 1-23 + 0-12 Jul h-', respectively, resulting in an estimate of fluid reabsorption by the efferent ducts of 94.8 + 1 6 % of the testicular fluid output. None of the treatments resulted in a significant change in testicular fluid output or in fluid reabsorption from the efferent ducts. Similarly, the treatments did not significantly alter the osmolality or electrolyte concentrations in fluid samples from the rete testis or the distal end of the efferent ducts (sham-operated values for rete testis and efferent duct fluid, respectively, were: osmolality, 311.2 + 1 7 and 302-7 + 5-7 mosmol kg-'; [Na+], 151-2 + 5-6 and 150 8 + 8-1 mmol 1'; [ClF], 147-9 + 6-6 and 126-7 + 2-2 mmol 1-'; [K+], 15 2 + 0 7 and 13-5 + 2 4 mmol 1-'). It is concluded that, like the homologous proximal tubule of the metanephric kidney, fluid reabsorption from the efferent ducts is independent of adrenal mineralocorticoid control.

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Section: Discussionsupporting

confidence: 70%

Adrenal independence of fluid and electrolyte reabsorption in the ductuli efferentes testis of the rat

Clulow²,

La³

et al. 1997

Experimental Physiology

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“…Glucocorticoids increase acid excretion in the form of ammonia excretion in response to an acid load with little effect on urine acidification, whereas mineralocorticoids increase acid secretion and acidify the urine with a limited effect on ammoniagenesis (20,48). Glucocorticoid receptors are enriched in the proximal tubule, whereas mineralocorticoid receptors are enriched in more distal regions (12,29,34). The differential distribution of these receptors is consistent with the restriction of ammoniagenesis induction to the proximal tubules.…”

Section: Discussionmentioning

confidence: 67%

Glucocorticoids have a role in renal cortical expression of the SNAT3 glutamine transporter during chronic metabolic acidosis

Karinch¹,

Lin²,

Meng³

et al. 2007

American Journal of Physiology-Renal Physiology

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Glucocorticoids are involved in many aspects of regulation of acid-base homeostasis, including the stimulation of renal ammoniagenesis during chronic metabolic acidosis. Plasma glutamine is the principal substrate for ammoniagenesis under these conditions. Expression of the System N glutamine transporter SNAT3 is increased in the renal proximal tubules during acidosis. In vivo studies in rats using 1) sham and adrenalectomized rats, 2) the glucocorticoid receptor antagonist RU486, and 3) dexamethasone treatment demonstrated involvement of glucocorticoids in regulation of SNAT3 expression. Adrenalectomy attenuated the acidosis-induced increase in renal cortical SNAT3 mRNA approximately 40%, and treatment with dexamethasone (1 mg x kg(-1) x day(-1) sc) partially reversed this effect. RU486 also blunted the acidosis-induced increase in SNAT3 expression approximately 50%. Chronic dexamethasone treatment (0.1 mg x kg(-1) x day(-1) sc, 6 days) of normal rats slightly increased SNAT3 expression. In all cases, renal glutamine arteriovenous difference mirrored SNAT3 expression and activity in the proximal tubules, suggesting that SNAT3 regulates glutamine uptake during acidosis. These studies indicate that glucocorticoids regulate acid-base homeostasis during metabolic acidosis in part by regulating expression of the System N transporter SNAT3.

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Glucagon receptors along the nephron: [125I]glucagon binding in rat tubules

Butlen

Morel

1985

Pflugers Arch.

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Binding of [125I]glucagon was measured in microdissected pieces of tubules from the rat nephron. Specific glucagon binding sites were found only in nephron segments containing a glucagon-sensitive adenylate cyclase activity. At 7.5 nM labelled hormone, higher levels of specific binding (16-27 X 10(-18) mol mm-1) were found in the thick ascending limb of the Henle's loop and in the distal convoluted tubule and lower binding levels (2-5 X 10(-18) mol mm-1) in the collecting tubule whereas specific binding could not be detected in the proximal tubule and in the thin segments of the Henle's loop. In the medullary thick ascending limb, Scatchard analysis of specific [125I]glucagon binding indicated an apparent equilibrium dissociation constant of 2.4 nM. The stereospecificity of binding sites in medullary thick ascending limbs and medullary collecting tubules, was assessed by competition experiments using unlabelled glucagon, enteroglucagon and unrelated hormones (vasopressin, calcitonin, parathyroid hormone and insulin); in both segments, glucagon was more active than enteroglucagon in displacing labelled glucagon from its tubular binding sites, whereas all other hormones tested were inactive. These results indicate that tubule binding sites might be the physiological receptors for glucagon involved in adenylate cyclase activation.

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Distribution of aldosterone receptors in rat kidney cortical tubules enriched in proximal and distal segments

Cited by 3 publications

References 0 publications

Adrenal independence of fluid and electrolyte reabsorption in the ductuli efferentes testis of the rat

Adrenal independence of fluid and electrolyte reabsorption in the ductuli efferentes testis of the rat

Glucocorticoids have a role in renal cortical expression of the SNAT3 glutamine transporter during chronic metabolic acidosis

Glucagon receptors along the nephron: [125I]glucagon binding in rat tubules

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