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)

Receptors for neurotransmitters can be visualized and characterized using in vitro tissue slice binding techniques and quantitative autoradiography. In this article, the general methods used in studies of this type are outlined and specific application to the study of catecholamine and neuropeptide receptors in rat and human brain tissue are described. Receptor autoradiography is used to examine regulation of dopamine receptor density in response to denervation and replacement of dopamine using brain transplants. Morphological and pharmacological aspects of vasopressin receptor ontogeny in the rat brain are examined. Finally, autoradiographic data on catecholamine receptor localization and characterization in the human hypothalamus, locus coeruleus, and frontal cortex are presented and discussed with reference to their applications in the study of neuropsychiatric disorders such as schizophrenia and senile dementia of the Alzheimer's type.
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PMID:Localization and measurement of neurotransmitter receptors in rat and human brain by quantitative autoradiography. 253 20

The quality of the postjunctional alpha adrenoceptors involved in the increase in diastolic pressure caused by 2-N,N-dimethylamino-5, 6-dihydroxy-1,2,3,4-tetrahydronaphthalene (M-7) were re-evaluated in pithed normotensive rats. The antagonism by yohimbine (1 mg/kg) was most pronounced, whereas prazosin (0.1 mg/kg) had no effect on the hypertensive responses to low doses of M-7, but clearly attenuated those to the higher amounts (greater than 10 micrograms/kg i.v.). A pretreatment with the combination of both alpha adrenoceptor antagonists markedly depressed slope and maximum of the log dose-pressor response curve to M-7. The selective beta-2 adrenoceptor antagonist ICI 118, 551 caused an enhancement of the pressor effects of the higher doses of M-7 which was most profound after the combined treatment with prazosin and yohimbine. M-7 showed a dose-dependent depressor effect in phentolamine (30 mg/kg)-treated pithed rats of which diastolic pressure was raised by infusion of vasopressin. It is concluded that M-7, in addition to its reported alpha-2 adrenoceptor agonistic properties, stimulates postsynaptic alpha-1 adrenoceptors in higher doses. In pithed normotensive rats, however, M-7 also interacts with vascular beta-2 adrenoceptors giving rise to vasodilatation. This action can strongly interfere with the vasoconstrictor effect of M-7.
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PMID:Re-evaluation of the selectivity of 2-N,N-dimethylamino-5,6-dihydroxy-1,2,3, 4-tetrahydronaphthalene (M-7) as an agonist of postjunctional alpha-2 adrenoceptors in the pithed normotensive rat. 613 92

The central actions of angiotensin II (ANG II) include the release of vasopressin (AVP) from the supraoptic nucleus (SON) via the pituitary gland into the blood. In conscious rats, we investigated whether catecholamines in the SON are involved in this release process. It was found that i.c.v. injections of ANG II (100 ng) selectively increased the release of norepinephrine (NA) from the SON. Like the ANG II i.c.v.-induced AVP release, this effect was prevented by i.c.v. pretreatment with the ANG II AT1 receptor antagonist, losartan (5 micrograms). The alpha-1 adrenoceptor antagonist, prazosin (0.7 nmol), injected bilaterally into the SON, significantly reduced the ANG II 100-ng i.c.v.-induced AVP release. Pretreatment with the alpha-2, beta-1 and beta-2 adrenoceptor antagonists, idazoxan, atenolol and ICI 118551, respectively, had no effect. Injections of NA into the SON increased plasma AVP at doses up to 10 nmol but not at higher doses (30-100 nmol). The effects of NA were mimicked by the alpha-1 adrenoceptor agonist, methoxamine (1-5 nmol). Bilateral pretreatment of the SON with losartan (5 micrograms) markedly inhibited the i.c.v. ANG II 100 ng-induced AVP release. The increase in AVP release after ANG II injections into the SON was also inhibited by losartan pretreatment into the SON, whereas prazosin had no effect. These results demonstrate that the ANG II-induced release of AVP is initiated through periventricular ANG II AT1 receptors and involves postsynaptic alpha-1 adrenoceptor stimulation in the SON. In addition, ANG II AT1 receptors in the SON can contribute to AVP release after periventricular ANG II receptor stimulation.
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PMID:Angiotensin II-induced vasopressin release is mediated through alpha-1 adrenoceptors and angiotensin II AT1 receptors in the supraoptic nucleus. 824 29

Vasopressin is a potent vasopressor for improving organ perfusion during septic shock. The rationale for the use of vasopressin is its relative deficiency of plasma levels and hypersensitivity to its vasopressor effects during septic shock. Growing evidence suggests that low-dose (<0.04 U/min) vasopressin is safe and effective for the treatment of vasodilatory shock. Although it is being used more frequently, there are no randomized clinical trials comparing vasopressin as a first-line agent to commonly used vasopressors. However, vasopressin causes arterial smooth muscle cell contraction through a non-catecholamine receptor pathway, thus it represents an attractive adjunct to the management of septic shock, especially when catecholamines are ineffective.
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PMID:Role of vasopressin in the management of septic shock. 1527 69

The activity of many signaling receptors is regulated by their endocytosis via clathrin-coated pits (CCPs). For G protein-coupled receptors (GPCRs), recruitment of the adaptor protein arrestin to activated receptors is thought to be sufficient to drive GPCR clustering in CCPs and subsequent endocytosis. We have identified an unprecedented role for the ubiquitin-like protein PLIC-2 as a negative regulator of GPCR endocytosis. Protein Linking IAP to Cytoskeleton (PLIC)-2 overexpression delayed ligand-induced endocytosis of two GPCRs: the V2 vasopressin receptor and beta-2 adrenergic receptor, without affecting endocytosis of the transferrin or epidermal growth factor receptor. The closely related isoform PLIC-1 did not affect receptor endocytosis. PLIC-2 specifically inhibited GPCR concentration in CCPs, without affecting membrane recruitment of arrestin-3 to activated receptors or its cellular levels. Depletion of cellular PLIC-2 accelerated GPCR endocytosis, confirming its regulatory function at endogenous levels. The ubiquitin-like domain of PLIC-2, a ligand for ubiquitin-interacting motifs (UIMs), was required for endocytic inhibition. Interestingly, the UIM-containing endocytic adaptors epidermal growth factor receptor protein substrate 15 and Epsin exhibited preferential binding to PLIC-2 over PLIC-1. This differential interaction may underlie PLIC-2 specific effect on GPCR endocytosis. Identification of a negative regulator of GPCR clustering reveals a new function of ubiquitin-like proteins and highlights a cellular requirement for exquisite regulation of receptor dynamics.
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PMID:The ubiquitin-like protein PLIC-2 is a negative regulator of G protein-coupled receptor endocytosis. 1819 83

Vasopressin is a potent vasopressor used for improving organ perfusion during cardiac arrest, septic and catecholamine-resistant shock; with reference to this, it is useful for the treatment of vasoplegic shock because, restoring organ perfusion pressure by contraction of vascular smooth muscle through a non-catecholamine receptor pathway, it can be employed when catecholamines are ineffective. A 49-yr-old woman was admitted to the Emergency Department after having intentionally taken 95.2g of metformin, 1.6g of pioglitazone and 40 UI of insulin glargine in a suicide attempt. Despite fluid resuscitation, CVVHDF (continuous veno-venous hemodiafiltration) treatment, norepinephrine and epinephrine infusion, she developed a severe lactic acidosis and a catecholamines-refractive vasodilatory shock. Only the vasopressin infusion, in association with catecholamines, gradually stabilized the patient's hemodynamic status.
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PMID:Metformin intoxication: Vasopressin's key role in the management of severe lactic acidosis. 2908 89