Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The vessels of the isolated rabbit ear were perfused at 23 mbar with Krebs solution with (tonic) and without (atonic) noradrenaline (5.9 x 10(-7)M) at selected temperatures of 20 degrees -38 degrees C. Peripheral resistance units (PRU) were calculated from the observed peak flow rates and alterations caused by drugs expressed as Delta% PRU.2. ACh is constrictor in the atonic vessel.3. ACh is a vasodilator of the tonic vessel perfused with NA. This effect is potentiated by anticholinesterase and by denervation, unaffected by botulinum toxin and antagonized by atropine. ACh also dilates the vessel perfused with vasopressin.4. Increasing the temperature reduces the responses to ACh but increases the effect of anticholinesterase.5. Nicotine causes a dose dependent dilatation of the tonic vessels, reduced but not abolished by C(6), by atropine, by botulinum toxin and by denervation.6. Nicotine causes a dose dependent constriction of the atonic vessels, abolished by C(6) and by phentolamine, reduced by denervation, but unaffected by botulinum toxin.
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PMID:Response to acetylcholine and nicotine of the perfused vessels of the rabbit ear. 557 56

In hydrated, conscious goats nicotine was administered into the 3rd ventricle and its effects on water and electrolyte excretion were studied. Acetylcholine (ACh.) in combination with eserine (Es.) was injected by the same route in goats pretreated with atropine. Nicotine as well as large doses of Ach + Es. induced an antidiuresis of the pituitary type. The responses to ACh. were dose-dependent. Intracerebroventricular (icv.) pretreatment with hexamethonium blocked the responses to both nicotine and ACh., whereas atropine and propranolol were ineffective. It appears likely that nicotine receptors are involved inthe ACh.-induced release of antidiuretic hormone. Phentolamine (icv.) completely blocked the effects of ACh. + Es. and partly those of nicotine, indicating that catecholamines might be involved to some extent.
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PMID:Effect of intracerebroventricular injection of nicotine and acetylcholine on renal water and salt excretion in conscious goats. 611 64

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 vasopressin antagonist and by a barbiturate and it was absent in the Brattleboro rat with congenital diabetes insipidus. These results show that the antidiuretic response to the hypotension induced by amyl nitrite is due to the release of vasopressin and that this release is mediated by a neuroendocrine reflex acting through the brain stem. Carbachol and nicotine produced an antidiuretic response on injection into a lateral cerebral ventricle (i. vent.). Carbachol was almost ineffective, but nicotine much more effective, when injected into the cisterna magna (i.cist.) from which in the rat there is no access to the ventricles. Carbachol therefore acts at a site reached from the ventricles, possibly the paraventricular nucleus. Nicotine acts at a more distal site reached from the subarachnoid space. This site may correspond with the nicotine-sensitive area on the ventral surface of the brain stem which has been described in the cat. Atropine blocked the antidiuretic response to carbachol but not that to amyl nitrite. Hexamethonium blocked the antidiuretic response to amyl nitrite as well as that to nicotine and was more effective on i.cist. than i.vent. injection. These results reveal a cholinergic link with a nicotinic but not a muscarinic receptor in the neural pathways controlling the release of vasopressin in response to hypotension. A hypothetical model is presented in which the release of vasopressin is stimulated by a pathway arising from chemoreceptors and inhibited by a second pathway arising from stretch- and baroreceptors. Hypotension acts by suppressing the normally predominant inhibitory pathway and stimulating the excitatory pathway. Hexamethonium is presumed to block transmission at a synapse in the excitatory pathway at the ventral surface or, less probably, at the paraventricular and supraoptic nuclei.
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PMID:A cholinergic link in the reflex release of vasopressin by hypotension in the rat. 614 13

Immobilization stress (1 h) induced discrete reductions in noradrenaline (NA) levels in the posterior periventricular hypothalamic region and in the paraventricular hypothalamic nucleus, and a decrease in dopamine (DA) turnover in the medial palisade zone (MPZ) of the median eminence, but failed to induce regional increases of hypothalamic NA turnover. Stress also stimulated the secretion of ACTH, corticosterone and prolactin, while vasopressin, LH and FSH serum levels were unaffected. The stress induced reduction of DA turnover in MPZ may mediate the stress induced increase of prolactin secretion. Nicotine (0.3 mg/kg, s.c., 1 h) did not by itself significantly influence catecholamine (CA) turnover in the various CA nerve terminal systems analyzed in the hypothalamus, but reduced NA levels in the subependymal layer (SEL) of the median eminence. Nicotine administration did not affect the serum levels of any of the hormones evaluated. Nicotine counteracted to a minor degree the immobilization stress-induced reduction in NA levels, and also the stress-induced secretion of ACTH, but not of prolactin suggesting the involvement of noradrenergic mechanisms possibly in the paraventricular nucleus in the nicotine modulation of stress induced increases of ACTH secretion. The nicotine-induced reduction of NA levels in SEL was blocked by stress as well as the tendency for nicotine induced increases of dopamine (DA) turnover in the medial and lateral palisade zones of the median eminence indicating opposing influences of immobilization stress and nicotine on at least some hypothalamic CA systems.
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PMID:Immobilization stress-induced changes in discrete hypothalamic catecholamine levels and turnover, their modulation by nicotine and relationship to neuroendocrine function. 630 59

The effect of nicotine on the ultrastructural changes and hormone contents of the neural lobe of the pituitary were studied in the rat. Nicotine caused a significant release of both vasopressin and oxytocin from the neural lobe. The examination of the neural lobe with electron microscope reveals the nerve terminals depleted of neurosecretory granules. These results suggest that a definite correlation exists between hormone contents and ultrastructural morphology.
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PMID:Ultrastructural changes in the neural lobe of the rat pituitary following nicotine pretreatment. 668 53

Intravenous nicotine was administered to a group of six subjects during the concurrent intravenous infusion of either the opiate antagonist naloxone, or of saline. Nicotine stimulated vasopressin secretion in all subjects. Naloxone infusion increased both the plasma vasopressin response to nicotine and the resulting rise in urine osmolality.
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PMID:Naloxone increases the nicotine-stimulated rise of vasopressin secretion in man. 709 61

The plasma vasopressin response to intravenous nicotine (2 mg) and smoking cigarettes of high (1.2 mg) and low (0.6 mg) nicotine content was studied in healthy young subjects with a history of cigarette smoking. Nicotine administered intravenously had no effect on plasma vasopressin. There was a statistically significant increase in plasma vasopressin after both the low and high content cigarettes, with the high content cigarettes resulting in a significantly greater increase. All three interventions resulted in transient increases in blood pressure and pulse of similar magnitude. These studies indicate that cigarette smoking-induced vasopressin release is not mediated via an action of circulating nicotine, and suggest the presence of an airway-specific mechanism for vasopressin release.
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PMID:Evidence in man that cigarette smoking induces vasopressin release via an airway-specific mechanism. 738 Sep 90

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 on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.
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PMID:Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide. 746

Epidemiological and experimental evidence have shown that nicotine has harmful effects on the gastric mucosa. The mechanisms by which cigarette smoking or nicotine adversely affect the gastric mucosa have not been fully elucidated. In this report, clinical and experimental data are reviewed. The effects of nicotine from smoking on gastric aggressive or defensive factors are discussed. Nicotine potentiates gastric aggressive factors and attenuates defensive factors; it also increases acid and pepsin secretions, gastric motility, duodenogastric reflux of bile salts, the risk of Helicobacter pylori infection, levels of free radicals, and platelet-activating factor, endothelin generation, and vasopressin secretion. Additionally, nicotine impairs the therapeutic effect of H2-receptor antagonists and decreases prostaglandin synthesis, gastric mucosal blood flow, mucus secretion, and epidermal growth factor secretion. Although many of the studies provide conflicting results, the bulk of the evidence supports the hypothesis that nicotine is harmful to the gastric mucosa.
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PMID:Effects of smoking and nicotine on the gastric mucosa: a review of clinical and experimental evidence. 769 7

The rapid secretion of ACTH in response to nicotine is mediated by a central mechanism involving brainstem catecholaminergic regions. To identify specific brainstem regions involved in activating the hypothalamo-pituitary-adrenal axis and other areas of the brain by iv nicotine, immunocytochemical detection of cFos protein was used as a marker for neuronal activation. Nicotine (0.05 mg/kg) stimulated cFos expression in the parvocellular paraventricular nucleus (pcPVN; containing CRH-positive neurons mediating ACTH secretion); this correlated with the expression of cFos in the A2 (norepinephrinergic) and C2 (epinephrinergic) regions of the brainstem nucleus tractus solitarius, which project directly to the pcPVN. The selectivity of this brainstem activation was shown by the absence of responses in the locus coeruleus (LC), A1, and C1 catecholaminergic regions to this low dose of nicotine. In contrast, a high dose of nicotine (0.1 mg/kg), which produced a brief episode of tremor, was required for expression of cFos in the LC. This was associated with a further increase in the number of cFos-positive cells in the PVN, primarily through recruitment in the magnocellular region, a known projection field of LC. The higher dose of nicotine also induced cFos in the vasopressinergic region of the supraoptic nucleus (SON), whereas the lower dose of nicotine exclusively induced cFos in the oxytocinergic region of the SON. Limbic regions that receive catecholaminergic inputs, such as the the central nucleus of the amygdala (involved in PVN regulation) and the cingulate gyrus of the cortex, showed a dose-dependent increase in the number of cFos-positive cells after nicotine, whereas the dentate gyrus of the hippocampus only responded to the high dose. Thus, nicotine is a potent and selective stimulus for neuronal activation in brainstem catecholaminergic regions and their projection fields in the pcPVN and SON, which regulate the hypothalamo-pituitary-adrenal axis and vasopressin/oxytocin secretion, respectively.
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PMID:Nicotine stimulates the expression of cFos protein in the parvocellular paraventricular nucleus and brainstem catecholaminergic regions. 838 11


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