The effect of NaCl and LiCl on vasopressin-sensitive adenyl cyclase

Douša, Tomáš; Hechter, Oscar

doi:10.1016/0024-3205(70)90286-9

Cited by 134 publications

(51 citation statements)

References 11 publications

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“…A correlation between reduced vasopressin-mediated activation of adenylate cyclase as measured in vitro and unresponsiveness to vasopressin in vivo has been observed in a number of other experimental circumstances: in nephrogenic diabetes insipidus induced by BAX 439 (25), by lithium (38)(39)(40), by vasopressinoic acid (16), and by demethylchlortetracycline (41). Furthermore, in all these instances, as in the present study, the maximal activity of adenylate cyclase was reduced while the affinity for vasopressin remained unimpaired.…”

Section: Resultssupporting

confidence: 82%

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Douša¹,

Valtin²

1974

J. Clin. Invest.

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A B S T R A C T Previous workand decreased to a lesser extent in DI +/+ nonsevere animals. A significant correlation was found between the activity of adenylate cyclase maximally stimulated by AVP in a given genotype, and the urine osmolality in the same animals. There were no significant differences in maximal stimulation of renal medullary adenylate cyclase in control experiments: not when stimulated nonspecifically by sodium fluoride, nor when stimulated by AVP in tissues from rats with induced water diuresis as compared to antidiuretic rats. Nor were there significant differences between VII +/+ and DI +/+ severe mice in the activity of renal cortical adenylate Preliminary reports of this work have appeared in abstract form:

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Section: Resultssupporting

confidence: 82%

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Douša¹,

Valtin²

1974

J. Clin. Invest.

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“…Although these findings with different doses in a different preparation cannot be entirely reconciled with our results, a significant rise in Uo0m, even if not above Poem, may mean a subnormal but significant increase in water transport was induced by c-AMP. Our findings are also supported by a recent study of rabbit kidney adenyl cyclase, where a direct assay of c-AMP production showed that lithium inhibited ADH interaction with adenyl cyclase (24). The methods employed in that study effectively exclude the alternative possibility that lithium increases c-AMP destruction (25).…”

Section: In Vivo Studiessupporting

confidence: 84%

“…These data suggest that the effects of lithium on ADH-induced transport are exerted at a site biochemically proximal to the action of c-AMP. Furthermore, lithium is known to inhibit the production of c-AMP by various adenyl cyclase systems in vitro, including brain, thyroid, and kidney (22)(23)(24). Recently, Forrest, Cohen, Torretti, and Epstein (5) reported that lithium produced nephrogenic diabetes insipidus in rats, and that c-AMP failed to increase Uosm above Posm under these conditions.…”

Section: In Vivo Studiesmentioning

confidence: 99%

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies

Singer¹,

Rotenberg²,

Puschett³

1972

J. Clin. Invest.

178

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A B S T R A C T The physiological basis for the polyuria and polydipsia occurring in some manic-depressive patients treated with lithium salts was studied in vivo and in vitro. Three lithium-treated polyuric patients, in whom other causes of a concentrating defect were excluded, had abnormal urinary concentrating abilities after a standard water depreviation test. Two of these patients failed to respond to exogenous vasopressin (ADH) and one had a subnormal response. The abilities of these patients to excrete solute-free water (CI20) was comparable to normal subjects during steady-state water diuresis, suggesting no gross abnormalities in sodium transport. However, each of these patients demonstrated abnormally low capacities to reabsorb solutefree water (TCHo) under hydropenic conditions after administration of hypertonic saline and vasopressin. These in vivo findings demonstrate at least a nephrogenic basis for the diabetes insipidus syndrome manifested by these three patients.The defect in water transport was further characterized in toad urinary bladders in vitro. Short-circuit current (I) and water flow (W) were studied under basal, ADH-stimulated, and cyclic adenosine 3',5'-monophosphate (c-AMP)-stimulated conditions. Increasing mucosal [Li']

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“…The results are consistent with the views of Dousa (1970) and of Thomsen (1970) that the fluid balance changes due to lithium mainly arise from inhibition of vasopressin-sensitive renal adenyl cyclase.…”

supporting

confidence: 92%

Proceedings of the Physiological Society, 8–9 November 1974, Bristol Meeting: Communications

1975

The Journal of Physiology

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The effect of NaCl and LiCl on vasopressin-sensitive adenyl cyclase

Cited by 134 publications

References 11 publications

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Cellular Action of Antidiuretic Hormone in Mice with Inherited Vasopressin-Resistant Urinary Concentrating Defects

Lithium-induced nephrogenic diabetes insipidus: in vivo and in vitro studies

Proceedings of the Physiological Society, 8–9 November 1974, Bristol Meeting: Communications

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