UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The localisation and colocalisation of neuronal isoform (type I) nitric oxide synthase, endothelin-1, arginine-vasopressin and substance P in endothelial cells of rat coronary and femoral arteries was investigated by pre-embedding and postembedding immunocytochemistry. Nitric oxide synthase appeared in a high proportion of endothelial cells of both arteries (about 89% in the femoral artery, examined with the preembedding avidin-biotin-peroxidase method, and in almost all cells of the coronary artery, examined with the postembedding immunogold technique). Double immunogold labelling in single cells demonstrated the colocalisation of nitric oxide synthase with endothelin-1, arginine-vasopressin and substance P. The immunolabelling was mostly confined to the cytoplasmic matrix. It is suggested that nitric oxide synthase/nitric oxide and the peptides examined may be involved in local control of blood flow in coronary and femoral arteries.
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PMID:Localisation of nitric oxide synthase and its colocalisation with vasoactive peptides in coronary and femoral arteries. An electron microscope study. 752 54

The endothelins consist of a family of vasoconstrictor peptides originally isolated from endothelial tissue which are now known to be involved in neuroendocrine regulation. However, while there are data indicating the involvement of endothelins in the modulation of the hypothalamo-pituitary-adrenal (HPA) axis, the precise mechanisms involved have been unclear. We have therefore used a previously validated rat hypothalamic explant system in order to investigate the possible modulation of the neurohypophyseal hormones vasopressin and oxytocin, and corticotropin-releasing hormone (CRH), by endothelin-1 (ET-1) and endothelin-3 (ET-3). Following a period of stabilisation, the release of vasopressin, oxytocin and CRH remained approximately constant in successive 20-min incubations. Addition of ET-1 stimulated the release of vasopressin at a dose of 0.1 nmol/l (p < 0.05), and both vasopressin and oxytocin at 10 nmol/l (p < 0.01 and 0.05, respectively). The release of vasopressin and oxytocin induced by 10 nmol/l ET-1 were both totally blocked by co-incubation with either 1 or 10 mumol/l of the specific ETA receptor subtype antagonist cyclo (D-Trp-D-Asp-Pro-D-Val-Leu) (BQ-123). ET-1 had no effect on CRH release in the dose range of 0.1-1,000 nmol/l. In case any possible stimulation of CRH might be masked by simultaneous generation of nitric oxide (NO), an inhibitor of CRH secretion, addition of ET-1 was also carried out in the presence of the NO synthase inhibitor, L-NO-Arg: ET-1 was again without effect in this dose range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin-1 stimulates the in vitro release of neurohypophyseal hormones, but not corticotropin-releasing hormone, via ETA receptors. 753 87

Detection of the neurohypophysial hormones vasopressin (AVP) and oxytocin (OT) in the testis of several species has led to the proposal that these peptides may have a physiological role in the regulation of testicular function. Therefore, we investigated whether the contractile myoid cells of rat seminiferous tubules express functional receptors for AVP or OT and, thus, constitute a target for these hormones. This study used primary cultures of purified peritubular myoid cells derived from rats both before and after puberty. By several criteria, myoid cells prepared from adult rats expressed vasopressin receptors (VPRs). We detected specific and saturable [3H]AVP binding to a single population of sites with a Kd of 7.5 nM and a binding capacity of 145 fmol/mg protein. AVP stimulated the accumulation of inositol phosphates in a dose-dependent manner with an EC50 of 1.7 nM. Cloning and sequencing of the myoid cell VPR confirmed it to be the V1a subtype of VPR. VPR expression by myoid cells is under developmental control, as the receptors are present in the adult rat, but absent before puberty. In contrast, OT receptors were not expressed at any stage of development. Peritubular myoid cells are also responsive to endothelin-1 (ET-1), which potently stimulated phosphoinositidase-C. However, unlike AVP, the ET-1 responses were observed both before and after sexual maturity, suggesting different roles for AVP and ET-1 in the control of myoid cell function. Our data establish that the myoid cells of the adult rat seminiferous tubule are a target for AVP. This indicates an additional role for AVP in the regulation of testicular function and male fertility in the adult rat.
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PMID:Rat testicular myoid cells express vasopressin receptors: receptor structure, signal transduction, and developmental regulation. 753 65

The distribution of various vasoactive agents [nitric oxide synthase (NOS)- type I, endothelin-1 (ET-1), arginine-vasopressin (AVP), serotonin (5-HT), histamine and substance P (SP)] in the thoracic aortic endothelium of aged Sprague-Dawley rats was investigated using electron microscopic immunocytochemical methods. The aged thoracic aortic intima was characterized by a large number of leukocytes that adhered to the endothelium, an accumulation of a flake-like precipitate and clusters of leukocytes and smooth muscle cells (SMC) in the subendothelium. Age-associated alterations were also seen in the medial and adventitial layers of the vascular wall. An extensive vasa-vasorum was present in the adventitia from which leukocytes penetrated into perivascular tissue. Some vasa-vasorum showed mast cells adhered to perivascular pericytes. Immunocytochemistry showed about 70% endothelial cells (EC) with positive immunostaining for the brain isoform NOS-type I, compared to 10% in adult mature rats. About 10% of cells showed a positive immunoreaction for ET-1, which is about the same as for the mature adult thoracic aorta (8-9%). Subendothelial macrophages often showed positive immunostaining for antibodies against ET-1. The percentage of EC immunopositive to AVP, 5-HT, and histamine was 16-18, 15 and 12%, respectively compared to 5-8, 7-8 and 6% in mature adult rats. A few cells showed an immunopositive reaction for SP. In summary, the ageing vessel was characterized by a large number of leukocytes adhering to the endothelium and also by the presence of many macrophages and SMC in the subendothelial layer. The percentage of EC in rat thoracic aorta showing NOS immunostaining increased substantially from 10% in mature rats to 70% in aged rats. The percentage of EC immunopositive for AVP, 5-HT and histamine also increased about twofold compared to mature adult rats, while no changes were seen for ET-1.
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PMID:An ultrastructural and immunocytochemical study of thoracic aortic endothelium in aged Sprague-Dawley rats. 758 46

A causal or supportive relationship between 1,2-diacylglycerol (DAG) content and the maintenance of tonic vasoconstriction was sought in canine basilar arteries treated in vitro with various agents reported to increase DAG levels in other tissues (platelet-derived growth factor, vasopressin, angiotensin II, and endothelin-1) and, conversely, with agents known to activate sustained constriction (high K+, phorbol ester, hemolysate, and endothelin-1). Multiple segments from individual isolated arteries were prepared. Some segments were immediately frozen as controls and others incubated in physiological saline solution at 37 degrees C for either 5 minutes or 30 minutes in the presence or absence of different concentrations of the test materials. Segments were then quickly frozen until homogenized for lipid extraction and DAG assay. The DAG content of samples incubated up to 2 hours in physiological saline solution alone did not significantly differ from that of immediately frozen control samples. Resting DAG content expressed relative to total protein measured in each sample averaged 3.82 +/- 0.26 (standard error of the mean) pmol DAG/microgram of protein (74 samples from 37 arteries). Endothelin at 2 x 10(-7) mol/L led to a statistically significant increase in DAG content of approximately 40% of basal content at 5 and 30 minutes. A smaller increase in DAG attributable to hemolysate (approximately 25%) was statistically significant at 30 minutes, whereas vasopressin provoked a notable decrease in DAG content. The other agents had no effect. No differences in these results were noted between normal canine basilar arteries and arteries constricted in vivo by subarachnoid blood clot before isolation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of vasoconstrictor agents on diacylglycerol content of normal and vasospastic canine basilar arteries in vitro. 759 11

Renomedullary interstitial cells (RMIC) are unique to the renal medulla. By virtue of their anatomic location and arrangement, RMIC may hinder axial dissipation of the concentration gradient, thereby aiding urinary concentration. A more active role in urinary concentration has been postulated on the basis of speculations about RMIC contractile potential, however, RMIC contraction has not been investigated. To determine if these cells are contractile, cultured rat RMIC were exposed to endothelin-1 (ET-1), a potent vasoconstrictor which binds to RMIC, and examined using video microscopy. ET-1 (as low as 10 pM) caused a slowly developing and dose-dependent reduction in RMIC surface area. ET-1 markedly increased the number and intensity of F-actin microfilament staining. ET-1-induced RMIC contraction was not altered by nifedipine, was partially reduced by nickel, and was completely inhibited by H7, indicating that ET-1 action is mediated by protein kinase C and is partially dependent upon receptor-operated calcium channels. The ET-1 effect does not involve nitric oxide since NG-monomethyl-L-arginine did not alter ET-1-induced RMIC contraction; in addition, ET-1 had only a minor effect on cGMP levels and no effect on nitrite production. PGE2 acts in an autocrine manner to dampen ET action since indomethacin potentiates, while PGE2 inhibits, ET-1-induced RMIC contraction. The contractile response is not unique to ET-1 since vasopressin also reduces RMIC surface area and increases F-actin microfiliment staining. These studies demonstrate that RMIC in culture are contractile. The possibility is raised that contraction of RMIC plays a role in modifying urinary concentration as well as regulation of other renal medullary functions.
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PMID:Identification of a contractile function for renal medullary interstitial cells. 761 12

To determine whether inhibition of generation of endothelium-derived relaxing factor or nitric oxide (NO) resulted in elevated blood pressure and its effect on resistance arteries, rats were offered NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase, in their drinking water. Blood pressure (BP) rose slightly from 100 +/- 2 mmHg in controls to 130 +/- 5 mmHg with 25 mg/Kg L-NAME per day and to 173 +/- 9 mmHg with 100 mg/Kg per day for 2 1/2 to 4 weeks. Rats were studied after 1-2 weeks of hypertension (BP > 150 mmHg). The concentration of cyclic guanosine monophosphate, the intracellular second messenger of NO, was significantly depressed in aorta and in the mesenteric vascular bed in L-NAME-treated rats. Mesenteric resistance arteries studied on a wire-myograph exhibited similar external and lumen diameters, whereas media width and media/lumen ratio were greater (p < 0.01). Cross-sectional area of the media was similar. Active wall tension in response to norepinephrine tended to be greater in blood vessels from L-NAME-treated rats, while responses to vasopressin and endothelin-1 were unaltered. Sensitivity to norepinephrine was significantly enhanced in L-NAME-treated rats (p < 0.001), while that to endothelin-1 and arginine8 vasopressin was similar. In conclusion, administration of an NO synthase inhibitor produces hypertension, with exaggerated media/lumen ratio in resistance arteries and enhancement of response to norepinephrine, which together with decreased NO generation may contribute to elevation of blood pressure.
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PMID:Effect of hypertension induced by nitric oxide synthase inhibition on structure and function of resistance arteries in the rat. 768 50

This study describes the localization of endothelin-1-, vasopressin- and substance P-like immunoreactivity in a subpopulation of endothelial cells of the basilar and posterior communicating arteries of the (i) normal rabbit brains and (ii) rabbit brains perfused with a perfluorocarbon emulsion (PFC). Following perfusion with the PFC at increased flow the endothelial cell ultrastructure appeared normal, although there was a decrease of immunoreactivity to these peptides. This suggests that these peptides may be involved in endothelial control of blood flow in cerebral vessels.
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PMID:Electron-immunocytochemistry of peptides in endothelial cells of rabbit cerebral vessels following perfusion with a perfluorocarbon emulsion. 768 5

Previously we found intragranular colocalization of immunoreactive endothelin-1 and neurohypophysial hormones in the axon terminals of the rat neural lobe. To investigate the function of endothelin-1 in the rat neural lobe, immunoreactive endothelin-1 in plasma and the neural lobe was measured by enzyme immunoassay in rats subjected to hemorrhage and in other rats who were deprived of water for 2 days to induce dehydration. Changes in plasma arginine vasopressin were determined by radioimmunoassay. In addition, morphometric analysis was performed in the neural lobe of rats exposed to these stresses. Plasma concentrations of immunoreactive endothelin-1 were unchanged following hemorrhage or dehydration, whereas those of immunoreactive vasopressin were remarkably increased. In the neural lobe, immunoreactive endothelin-1 content and the number of neurosecretory granules decreased significantly after dehydration. However, immunoreactive endothelin-1 in tissue increased nearly three-fold in hemorrhaged rats, whereas the endothelin-1-immunolabeling in the axon terminals was unchanged. These results suggest that endothelin-1 in the hypothalamo-hypophysial system may be involved in the local modulation of vasopressin secretion when an animal is exposed to hypovolemic and/or osmotic stress.
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PMID:Immunoreactive endothelin-1 in the neural lobe of the rat pituitary following hemorrhage and dehydration. 770 93

Neurally mediated syncope is the most frequent cause of syncope in patients who do not have structural heart disease. Neurally mediated syncope is believed to be a reflex triggered by excessive afferent discharge from mechanoreceptors located in the arterial tree or viscera, particularly the left ventricle of the heart. In response to these signals, a CNS-mediated sudden rise in parasympathetic efferent activity occurs, causing relative or absolute bradycardia and sympathoinhibition with arterial vasodilation and hypotension. Although our understanding of the pathophysiology of this syndrome is still incomplete, it is well established that sympathetic nerve activity and norepinephrine release fall inappropriately during neurally mediated syncope, whereas appropriate increases in plasma concentrations of epinephrine, angiotensin II, vasopressin, and endothelin-1 occur. Recent studies from our laboratory suggest that synthesis of the vasodilator nitric oxide increases during neurally mediated syncope. This suggests that nitric oxide-mediated arterial vasodilation could contribute to the profound hypotension characteristic of this syndrome. The diagnosis of neurally mediated syncope can be made with acceptable levels of specificity and sensitivity by the upright tilt test. Explaining the mechanisms responsible for arterial vasodilation in neurally mediated syncope may lead to effective treatment.
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PMID:Neurally mediated syncope: pathogenesis, diagnosis, and treatment. 774 68

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