diabetes insipidus/nikotin

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Familial central diabetes insipidus: vasopressin and nicotine stimulated neurophysin deficiency with subnormal oxytocin and estrogen stimulated neurophysin.

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Five members of a family with dominantly inherited diabetes insipidus were diagnosed and treated with deamino-d-arginine vasopressin (DDAVP), a vasopressin analogue given intranasally. All subjects demonstrated subnormal levels of arginine vasopressin (AVP) by radioimmunoassay in response to

Antidiuretic responses of rats with hereditary hypothalamic diabetes insipidus to vasopressin, oxytocin and nicotine.

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A nicotine test for the investigation of diabetes insipidus.

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The effect of nicotine on urinary flow in diabetes insipidus.

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[Diabetes insipidus in a patient with small-cell lung cancer: a paradox?].

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We observed oat-cell lung carcinoma in a man who presented with diabetes insipidus. The chest radiograph showed a suspect nodule within a context of major nicotine addiction. Histopathological examination of the transbronchial biopsy confirmed the diagnosis of oat-cell carcinoma. Brain CT revealed

The influence of chronic subcutaneous nicotine administration on aldosterone and corticosterone plasma concentrations and the plasma renin activity.

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Since adrenocortical hormones and the renin-angiotensin system are capable of inducing defined pathophysiologic changes in the cardiovascular system, similar to those observed after nicotine, experiments were performed in rats to investigate the effect of chronic nicotine administration on the

[Radioimmunoassay for human plasma 8-arginine-vasopressin (author's transl)].

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The authors have developed a radioimmunoassay for human plasma vasopressin (AVP) which permits the estimation of antidiuretic hormon (ADH) levels as low as 0,8 pg/ml. The average plasma level of AVP after overnight water restriction was found to be 14,3 pg/ml (sd = 4,4 pg/ml) in normal subjects.

A cholinergic link in the reflex release of vasopressin by hypotension in the rat.

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Inhalation of amyl nitrite in the water-loaded rat under ethanol anaesthesia produced a brief fall of blood pressure followed by a prolonged antidiuretic response. The antidiuretic response to amyl nitrite was accompanied by increased urinary excretion of vasopressin, it was blocked by a specific

Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide.

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An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while

Increased plasma arginine vasopressin in clinical adrenocortical insufficeincy and its inhibition by glucosteroids.

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Trichloroacetic acid extracts of plasma were fractionated on a CG-50 resin column and the 50% acetic acid eluents chromatographed on silicic acid-impregnated glass paper in butanol-acetic acid-water. The specific arginine vasopressin (AVP) zone was eluted and assayed for antidiuretic activity in the

Release of an antidiuretic substance by bradykinin in the rat.

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1. Water-loaded rats under ethanol anaesthesia were used to determine whether bradykinin releases ADH and whether the release is a reflex response to hypotension or the result of direct stimulation of the central nervous system by the peptide.2. Intravenous injections of bradykinin caused

Expression, purification and NMR characterization of the cyclic recombinant form of the third intracellular loop of the vasopressin type 2 receptor.

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The vasopressin type 2 (V2R) receptor belongs to the class of G-protein coupled receptors. It is mainly expressed in the membrane of kidney tubules, where it is activated by the extracellular arginine vasopressin. In men, inactivating and activating mutations cause nephrogenic diabetes insipidus and

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