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)

Pithed rats were used to compare the abilities of vasopressin and NG-nitro-L-arginine methyl ester (L-NAME) to prevent the early (1 h after starting an endotoxin infusion) E. coli endotoxin-induced impairment of pressor responsiveness to noradrenaline, cirazoline, BHT 933 and to sympathetic stimulation (T8). L-NAME increased arterial blood pressure and augmented pressor responses to noradrenaline and to sympathetic nerve stimulation to a similar degree in control and endotoxin-treated rats. The response to the alpha 1-adrenoceptor agonist cirazoline was augmented by L-NAME in endotoxin-treated rats only, whereas the response to the alpha 2-adrenoceptor agonist BHT 933 was unaffected. Vasopressin (0.64 I.U. kg-1 h-1) prevented the hypotension that resulted from endotoxin administration and produced a similar increase in blood pressure to that produced by L-NAME. This dose of vasopressin also augmented pressor responses to noradrenaline and sympathetic nerve stimulation similarly in both control and endotoxin-treated rats. Sodium nitroprusside, in a dose that mimicked the degree of hypotension caused by endotoxin, also impaired pressor responsiveness to cirazoline; this impairment was prevented by co-infusion of vasopressin. Thus the effects of L-NAME in preventing the early phase of endotoxin-induced impairment of vascular responsiveness may be related to its hypertensive properties, due to inhibition of the constitutive form of nitric oxide synthase, rather than inhibition of endotoxin-induced nitric oxide synthase. These data suggest that early endotoxin-induced impairment of vascular reactivity probably involves factors other than nitric oxide. The well documented effect of endotoxin in inducing nitric oxide synthase probably explains the later, more sustained loss of vascular responsiveness.
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PMID:Modification of alpha-adrenoceptor-mediated pressor responses by NG-nitro-L-arginine methyl ester and vasopressin in endotoxin-treated pithed rats. 128 May 96

1 We have determined the dermal microvascular effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 100 nmol/site), endothelin-1 (ET-1, 0.1-10 pmol/site) and ET-3 (0.1-30 pmol/site) in rats with streptozotocin (STZ)-induced diabetes mellitus. Cutaneous blood flow changes as measured by a 133xenon (133Xe) clearance technique, were determined in diabetic rats four weeks after treatment with streptozotocin (STZ) and compared with responses measured in normal rats four weeks after treatment with saline. 2 Resting skin blood flow was similar in diabetic and in normal rats, as measured by 133Xe clearance and laser Doppler flowmetry. 3 Intradermal NG-nitro-L-arginine methyl ester (L-NAME) reduced skin blood flow in normal rats by 55.2 +/- 2.6% as measured by 133Xe clearance, (n = 9). L-NAME was significantly less effective in diabetic rats, inducing a 40.9 +/- 7.7% decrease in blood flow (n = 9, P less than 0.05). The enantiomer D-NAME had no effect in either group of rats. 4 Low doses of ET-1 and ET-3 injected intradermally induced dose-dependent decreases in blood flow, measured by 133Xe clearance, which were similar in both groups of rats. However, the responses to the highest doses of ET-1 (10 pmol/site) and ET-3 (10 and 30 pmol/site) were significantly reduced in the diabetic compared with the normal rats (P less than 0.05).In addition vasoconstriction to the highest doses of vasopressin (0.3 and 3 pmol/site) and vasodilatation to the neuropeptide calcitonin gene-related peptide (CGRP, 1O pmol/site) were similarly reduced in the diabetic rats (P <0.05).5. The decrease in blood flow induced by submaximal doses of ET-1 was enhanced by co-injection with L-NAME (100 nmol/site) in both diabetic and normal rats. However, this enhanced response was significantly reduced in the diabetic rats (P<0.05). A similar pattern of responses were observed to ET-3 in the presence and absence of L-NAME.6. These results indicate that the cutaneous microvasculature of rats with STZ-induced diabetes responds differently to intradermal ET-1 and ET-3 compared with normal rats; a similarly altered vascular reactivity was observed with vasopressin and CGRP. Hence, the diabetic microcirculation has impaired responses to several vasoconstrictors and a vasodilator. The effect of the nitric oxide synthase inhibitor L-NAME is also suppressed in the diabetics, suggesting that there may be decreased local production of, or response, to nitric oxide.
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PMID:Altered microvascular reactivity to endothelin-1, endothelin-3 and NG-nitro-L-arginine methyl ester in streptozotocin-induced diabetes mellitus. 139 77

Experiments were designed to characterize the mechanism of vasopressin action in small arteries of brain stem and cerebrum and to determine the role of L-arginine pathway in reactivity of these vessels to vasopressin. Secondary branches of canine basilar arteries (425 +/- 63 microns ID, n = 6) and middle cerebral arteries (466 +/- 30 microns ID, n = 6) were dissected and mounted on glass microcannulas in organ chambers. Changes in intraluminal diameter of the pressurized arteries were measured using a video dimension analyzer. Vasopressin caused endothelium-dependent relaxation in the brain stem arteries [-log half-maximal effective concentration (EC50) = 9.2 +/- 0.4, n = 5] but not in the branches of middle cerebral arteries. In contrast, bradykinin caused identical endothelium-dependent relaxations in arteries of both regions (-log EC50 = 8.0 +/- 0.2, n = 5, and 7.7 +/- 0.1, n = 4 for brain stem and cerebrum, respectively). Relaxations to vasopressin (but not to bradykinin) were reduced in the presence of V1-vasopressinergic antagonist [1-(beta-mercapto-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5-Tyr(Me)AVP;10(-7) M], pertussin toxin (100 ng/ml), and NG-monomethyl-L-arginine (L-NMMA; 10(-4) M). The inhibitory effect of L-NMMA was prevented by L-arginine (3 x 10(-4) M) but not D-arginine (3 x 10(-4) M). These studies suggest that vasopressin causes endothelium-dependent relaxation in canine brain stem arteries. The effect of the neuropeptide appears to be mediated by activation of endothelial V1-vasopressinergic receptors coupled to nitric oxide synthase. This signal transduction pathway is not functional in endothelial cells of branches of middle cerebral arteries.
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PMID:Endothelial L-arginine pathway and regional cerebral arterial reactivity to vasopressin. 159 Apr 60

The effects of cilazaprilat were assessed on endothelium-dependent relaxations and contractions in isolated canine arteries. In coronary arteries incubated with indomethacin, cilazaprilat potentiated endothelium-dependent relaxations to bradykinin. In superfusion-perfusion bioassay studies with femoral arteries, cilazaprilat augmented the release of nonprostanoid endothelium-derived relaxing factors caused by bradykinin. To verify whether this effect was solely due to inhibition of the converting enzyme, the effects of cilazaprilat on responses to a variety of endothelium-dependent vasoactive agents were assessed. Endothelium-dependent relaxations to acetylcholine, thrombin, and vasopressin were not altered significantly by cilazaprilat. However, those induced by ADP and aggregating platelets were enhanced significantly by the compound. Endothelium-dependent relaxations to ADP-beta-S were augmented significantly but to a lesser extent. Furthermore, in the presence of the nitric oxide synthase antagonist NG-nitro-L-arginine, ADP-beta-S still caused small relaxations that were possibly mediated by endothelium-derived hyperpolarizing factor. These relaxations were augmented by cilazaprilat. Thus, the augmentation of purinergic relaxations may involve an increased production of endothelium-derived relaxing factors in addition to the protection of ADP from breakdown. Cilazaprilat did not affect endothelium-dependent contractions to acetylcholine or the calcium ionophore A23187 in canine basilar arteries, previously shown to be mediated by superoxide anions. Thus, cilazaprilat is not a scavenger of superoxide anion. Because this agent potentiates endothelium-dependent relaxations to bradykinin, ADP, and aggregating platelets, the present study suggests that, in addition to the lowering of plasmatic levels of angiotensin II, the antihypertensive and cardioprotective effects of cilazaprilat are mediated through an increased production of endothelium-derived relaxing factors.
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PMID:Effects of the converting enzyme inhibitor cilazaprilat on endothelium-dependent responses. 191 98

Biochemical, cytochemical and immunological methods were used to compare the metabolic and neuroendocrine properties of the subfornical organ (SFO) with the hypothalamo-neurohypophysial system (HNS) in the rat. The SFO resembles the HNS in that both have (a) increased label incorporation into RNA during dehydration; (b) an intense reaction for glucose-6-phosphate dehydrogenase; (c) NADPH-diaphorase and the Type I pathway for hydrogen utilization from NADPH, presumably as part of the mixed-function oxidase system for the metabolism of endogenous substrates and xenobiotics; (d) immunoreactive vasopressin and oxytocin. Gel filtration of extracts of the SFO area using Sephadex G-25 chromatography resulted in immunoreactive peaks for both AVP and OT which were similar to synthetic hormones. One other fraction in the SFO extract, containing a substance(s) of higher molecular weight than AVP, was detected using the antiserum for AVP. The concentration of immunoreactive AVP in the SFO area was increased after colchicine, decreased by hypophysectomy, and unaltered by: (a) infusion (4.6 pg/min for 3 hr) or injection (1 or 6 ng) of AVP into the lateral cerebroventricle; (b) dehydration; (c) renin administered intracerebroventricularly; (d) pinealectomy; or (e) hypertension in the spontaneously hypertensive rat. In conclusion, cells in the SFO have specialized metabolic and neuroendocrine properties similar to the HNS. It can be inferred from these biochemical specializations that the SFO has metabolic and secretory activities.
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PMID:The subfornical organ: biochemical and neuroendocrine comparisons with the hypothalamo-neurohypophysial system. 402 8

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. 751 50

There is increasing evidence that nitric oxide (NO) plays a role within the central nervous system as a novel messenger. Neuronal culture work suggests NO to be involved specifically in mediating actions of angiotensin II (ANG). The present study examined the potential role of NO within the paraventricular nucleus (PVN), a structure involved in mediating the cardiovascular changes initiated by activation of the subfornical organ (SFO). The pressor response to stimulation of SFO, which can be divided into a short (SD) and long duration (LD) component was enhanced following administration of an NO synthase inhibitor (L-NAME) (SD control: 101 +/- 4 vs. post L-NAME: 145 +/- 10 mmHg.s (P < 0.05); LD control: 387 +/- 167 vs. post L-NAME: 1737 +/- 617 mmHg.s (P < 0.05)). This effect was specific to activation of SFO efferents as the blood pressure responses to either, stimulation of PVN, or systemic administration of vasopressin were not potentiated by administration of L-NAME. These findings suggest that NO may be acting within PVN to inhibit further release of ANG, thereby attenuating the cardiovascular response to stimulation of SFO.
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PMID:Angiotensin II neurotransmitter actions in paraventricular nucleus are potentiated by a nitric oxide synthase inhibitor. 751 40

The present study aims at investigating the effect of pharmacological manipulation of nitric oxides (NOs) formation in the rat neurohypophysis on the secretion of vasopressin (AVP). We found that the NO synthase antagonist L-NAME and free-ferrous hemoglobin (an NO inactivator) produced a transient and significant enhancement of basal secretion of AVP from incubated glands. Conversely, the NO precursor L-arginine (but not its inactive counterpart D-arginine) antagonized the stimulatory influence of L-NAME on both AVP and oxytocin (OT) output. Elevation of NOs formation triggered by means of the NO donor SIN-1 likewise dampened spontaneous, as well as stimulated, AVP release. It is concluded that NOs molecules show up as potent regulators of neuropeptide secretion at the level of nerve terminals in the neurohypophysis.
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PMID:Evidence for an inhibitory effect of nitric oxides on neuropeptide secretion from isolated neural lobe of the rat pituitary gland. 751 25

Rat aortic smooth muscle cells produced large quantities of nitric oxide (NO) after exposure to interleukin-1 beta, and this was depressed in the presence of the protein kinase C inhibitor bisindolylmaleimide. Intracellular cAMP levels were elevated mildly in cytokine-treated smooth muscle cells, and the presence of forskolin enhanced both the cAMP levels and NO production. Inhibition of GTP:cyclohydrolase I by 2,4-diamino-6-hydroxypyrimidine attenuated NO production by interleukin-1 beta-treated cells. GTP:cyclohydrolase is the regulatory enzyme for de novo tetrahydrobiopterin synthesis, and the latter is a required cofactor for NO synthase activity. Treatment of smooth muscle cells with forskolin induced GTP:cyclohydrolase mRNA expression, and simultaneous treatment of cells with forskolin and phorbol esters elicited NO production. Angiotensin II and arginine-vasopressin, acknowledged agonists for protein kinase C, elicited production of NO by forskolin-treated smooth muscle cells. These observations confirm the importance of GTP:cyclohydrolase activity for NO production by cultured smooth muscle cells and implicate both adenylyl cyclase and protein kinase C in this process.
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PMID:Simultaneous activation of adenylyl cyclase and protein kinase C induces production of nitric oxide by vascular smooth muscle cells. 752 13

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


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