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1 eta1-adrenergic receptor) and H2R (histamine-H2-receptor).
2 s the in vitro dissociation constant for the H2-receptor.
3                                   Myocardial H2 receptor activation may promote cardiac fibrosis and
4                            Here we show that H2 receptor activation negatively modulates outward curr
5 ower doses of histamine were mimicked by the H2 receptor agonist dimaprit, and the effects of higher
6 taneously injected with TGFbeta1 or with the H2 receptor agonist dimaprit.
7 3 receptor blockers, and were mimicked by an H2 receptor agonist.
8 r prediction that cimetidine, a histamine-2 (H2) receptor agonist commonly used to treat peptic ulcer
9     Intra-CA1 injections of selective H1 and H2 receptor agonists showed that histamine exerted its e
10 tion in rabbit duodenal mucosa via histamine H2 receptors and enteric nerves.
11 s, stimulates the parietal cell directly via H2 receptors and indirectly via H3 receptors coupled to
12 an H1 receptor antagonist (pyrilamine) or an H2 receptor antagonist (cimetidine) demonstrated a prote
13 optosis in pre-clinical models and histamine H2 receptor antagonist (H2RA) use may improve symptoms i
14 5-HT1B receptor agonist and histamine H1 and H2 receptor antagonist activities.
15                                          The H2 receptor antagonist cimetidine (2 microM) blocked the
16                                  Neither the H2 receptor antagonist cimetidine (20 microM) nor the H3
17 ptor antagonist diphenhydramine, whereas the H2 receptor antagonist cimetidine had no effect.
18                               Vehicle or the H2 receptor antagonist cimetidine has no effect.
19 t was prevented by treatment with either the H2 receptor antagonist cimetidine or with the potassium
20                                       As the H2 receptor antagonist cimetidine was perfused to the ti
21 F92374, a structural analog of the histamine H2 receptor antagonist cimetidine, induces antinocicepti
22 ntage of patients who filled either a PPI or H2 receptor antagonist prescription, hospital admission
23 % to -5.36%) in patients who filled a PPI or H2 receptor antagonist prescription.
24 tor antagonist chlorpheniramine, but not the H2 receptor antagonist ranitidine, blocks the effects of
25 ever, neither a thromboxane A2/prostaglandin H2 receptor antagonist SQ29548 and a thromboxane synthas
26                                       In the H2 receptor antagonist studies, CVC in control sites was
27                     Cimetidine is a powerful H2 receptor antagonist that eliminates histamine's effec
28                          Roxatidine, a novel H2 receptor antagonist, acts through a mechanism that in
29 histamine were antagonized by cimetidine, an H2 receptor antagonist, but not by selective H1 and H3 r
30 evere thrombocytopenia after exposure to the H2 receptor antagonist, ranitidine, and identified an an
31 ore, SQ29548, a thromboxane A2/prostaglandin H2 receptor antagonist, significantly reduced CD40L-enha
32                          As cimetidine is an H2 receptor antagonist, the authors hypothesize that thi
33 , and this effect was blocked by a selective H2 receptor antagonist.
34         All patients received a histamine-2 (H2)-receptor antagonist-blocking agent during the study.
35 mys were orally administered an irreversible H2-receptor antagonist loxtidine for 0, 8, and 16 weeks,
36 ceptor antagonist YF476 and/or the histamine H2-receptor antagonist loxtidine for 3 or 6 months.
37                           Examination of the H2-receptor antagonist structures for insight into the m
38 rpose of this study was to determine whether H2-receptor antagonist use affects the overall incidence
39  to evaluate whether cimetidine, a histamine H2-receptor antagonist, interferes with the initiation a
40 licylate + metronidazole + tetracycline + an H2-receptor antagonist, was supported by two pivotal lit
41 al indications, we examined associations for H2 receptor antagonists (H2RAs) as a secondary aim.
42 stopped at least 7 days before the study and H2 receptor antagonists were stopped for at least 24 hou
43                Antithrombotics, antibiotics, H2 receptor antagonists, and corticosteroids were often
44 illed, facilitated electronic prescribing of H2 receptor antagonists, and education for patients and
45 s from those patients who were not receiving H2 receptor antagonists, but did not change significantl
46 samples from the patients who were receiving H2 receptor antagonists.
47 nges, which were blocked by histamine H1 and H2 receptor antagonists.
48                              Although use of H2-receptor antagonists (adjusted OR, 1.84; 95% CI, 1.71
49 f PPI (n=173,321) and new users of histamine H2-receptor antagonists (H2 blockers; n=20,270) and foll
50 as lower charges than initial endoscopy when H2-receptor antagonists are used to prevent recurrence o
51 e combination of CCK2/gastrin- and histamine H2-receptor antagonists has synergistic inhibitory effec
52                                The histamine H2-receptor antagonists have been identified as inhibito
53 he quad does not have drug interactions with H2-receptor antagonists or proton pump inhibitors, does
54 sociated with cimetidine and other histamine H2-receptor antagonists, splenectomy, gonorrhea, and bod
55 ations suggest an immune-enhancing effect of H2-receptor antagonists.
56  sequencing to explore the effects of H1 and H2 receptor blockade on the exercise transcriptome in hu
57 ocomial pneumonia associated with the use of H2-receptor blockade in critically ill patients, but oth
58  but was completely blocked by the histamine H2 receptor blocker cimetidine.
59 n ratio, antimicrobial therapy, histamine-2 (H2) receptor blocker use, immune status, parenteral nutr
60 lation, even after the standard treatment of H2 receptor blockers or proton pump inhibitors.
61  symptoms and involves treatment with H1 and H2 receptor blockers, leukotriene receptor antagonist an
62  combination use of proton pump inhibitor or H2 receptor blockers, plus clarithromycin or metronidazo
63  to cystic fibrosis and the use of histamine H2-receptor blockers, corticosteroids, or recombinant hu
64  anti-inflammatory drugs, statins, histamine H2-receptor blockers, or calcium-channel blockers seems
65 KF92374 lacked significant activity on H1 or H2 receptors, but had weak activity on H3 receptors.
66    In particular, histamine, acting upon the H2 receptor for a short period of time, increased IL-10
67 topenia associated with the use of histamine H2 receptor (H2R) antagonists has been described, a drug
68 ies of long-chained guanidine-type histamine H2-receptor (H2R) agonists are lower at the H2R of human
69 7BL/6J (B6) mice deficient for the histamine H2 receptor (H2RKO) are less susceptible to EAE and exhi
70 s study, we show that mice lacking histamine H2 receptor (H2RKO) are similar to H1RKO mice in that th
71 s, new signaling phenomena related to H1 and H2 receptors have been described that make them suitable
72 infection, also respond to histamine through H2 receptors, leading to a marked down-regulation of IFN
73 post-exercise activation of histamine H1 and H2 receptors localized to the previously exercised muscl
74 ceptor function in the neostriatum through a H2 receptor-mediated regulation of potassium channels.
75 s and produce histamine, which activates the H2 receptor on MB-HSCs to promote their quiescence and s
76 he hippocampal formation to innervate H1 and H2 receptors on both principal and inhibitory interneuro
77 c enterochromaffinlike cells, interacts with H2 receptors on parietal cells that are coupled via sepa
78          Thus, histamine, via stimulation of H2 receptors on peripheral monocytes and subsequent elev
79                  Histamine seems to act, via H2 receptor, on inflammatory processes by stimulating in
80          In addition, blocking the histamine H2 receptor restored neutrophil migration, enhanced CXCR
81 inin 2 (CCK2)/gastrin receptor and histamine H2-receptor signaling in the development of gastric atro
82 hacin or celecoxib) or of TXA2/prostaglandin H2 receptors (SQ-29548).
83 tion plays a role in bone metabolism via the H2 receptor, stimulating bone resorption.
84 S nitration and thromboxane A2/prostaglandin H2 receptor stimulation.
85 electrical activity of oxytocin neurones via H2 receptors, then they may have a dual effect, increasi