Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The endothelium-dependent relaxation is impaired in spontaneously hypertensive rats (SHR) by the release of a vasoconstrictor prostanoid. We evaluated whether such a vasoconstrictor prostanoid is masking the vasodilatation induced by nitric oxide (NO). 2. For this we observed, in SHR, whether indomethacin (INDO) modified both the pressor response to the inhibition of NO biosynthesis with L-nitro-arginine methyl ester (L-NAME) and the acute hypotensive response to acetylcholine. 3. INDO did not modify basal mean arterial pressure (MAP), either the pressor response to L-NAME, or the depressor response to acetylcholine. 4. It shows that, in awake SHR, a vasoconstrictor prostanoid, did not seem to affect the acute regulatory function of NO on MAP.
Gen Pharmacol 1994 Jan
PMID:Indomethacin does not modify the role of nitric oxide on blood pressure regulation of SHR. 802 94

The mechanism of iota-carrageenan (i-CAR)-induced protection against murine cytomegalovirus (MCMV) infection of mice was analysed. The virus titres in the target organs on the fourth day correlated with that in the plasma at 1 h after intraperitoneal inoculation of MCMV, irrespective of i-CAR treatment. Pretreatment of mice with i-CAR induced infiltration of polymorphonuclear neutrophils into the peritoneal cavity and inhibition of viral spread from the peritoneal cavity to the plasma. Although the direct relationship of these two phenomena was unclear, the inhibition by i-CAR of viral spread resulted in protection against MCMV infection of mice.
J Gen Virol 1994 Jan
PMID:Inhibition by iota-carrageenan of the spread of murine cytomegalovirus from the peritoneal cavity to the blood plasma. 811 19

The possible role of histamine (HA) locally applied into the hippocampus on memory mechanisms of the rats was studied. The acquisition of a one-way active avoidance response to an ultrasonic 40 kHz sinus-wave tone anticipating an electric shock was used as experimental model. Learning sessions consisted in placing animals into a two compartment cage were they learnt to escape to the safe compartment after an ultrasonic tone anticipating an electric feet shock. After acquiring the conditioned avoidance response, animals were implanted with microinjection cannulae and injected with 1 microliter of saline, or increasing doses of histamine (9, 22.5, 45, and 90 nmol) into the hippocampus. In the experimental sessions, 4 trials before (PRE) and 4 trials afterward treatment (POST), the percentage of conditioned avoidance responses (% CAR) and the latency time to escape (LT) were measured. Results showed that HA increased significantly the LT and this effect was grossly dose-dependent. % CAR was also affected and the score was significantly inhibited by the imidazolamine administration. Results suggest that HA may be involved in memory retrieval processes in the hippocampus.
J Neural Transm Gen Sect 1995
PMID:Effects of localized histamine microinjections into the hippocampal formation on the retrieval of a one-way active avoidance response in rats. 869 50

1. Frequency-dependent nonadrenergic, noncholinergic (NANC) relaxant responses were induced by transmural stimulation of whole tracheal tube preparations. 2. Responses at lower frequencies (< or = 10 Hz) were abolished by L-nitroarginine methyl ester (L-NAME). 3. Responses at higher frequencies (> or = 20 Hz) consisted of a rapid, short-lasting relaxation, followed by a slow, long-lasting relaxation. The former and the latter were reduced by L-NAME and alpha-chymotrypsin, respectively. 4. alpha-Chymotrypsin had little effect on the magnitude of NANC responses, but reduced the duration of responses at higher frequencies (> or = 20 Hz). 5. The results suggest that NANC relaxation of guinea pig trachea may be mediated primarily by nitric oxide, with and without concomitant release of vasoactive intestinal peptide or related peptides, and nitric oxide may act as predominant mediator providing the magnitude of relaxant response.
Gen Pharmacol 1996 Jul
PMID:Role of nitric oxide in nonadrenergic, noncholinergic relaxation of whole tracheal tube preparations isolated from guinea pigs. 884 85

1. The role of nitric oxide (NO) in the acid secretory response of the rat stomach following damage was investigated. A rat stomach was mounted in an ex-vivo chamber, perfused with saline, and the potential difference (PD), luminal pH, acid and HCO3- responses were measured before and after the mucosal exposure to 20 mM taurocholate (TC) for 30 min, with or without pretreatment with NG-nitro-L-arginine methyl ester (L-NAME). 2. Exposure of the stomach to TC caused a reduction of PD, a decrease of acid secretion and an increase in luminal HCO-. Pretreatment with L-NAME did not affect such PD and HCO3- responses, but completely attenuated the decreased acid secretory response and rather enhanced this secretion. 3. These effects of L-NAME were significantly antagonized by the co-administration of L-arginine but not D-arginine. The enhanced acid secretory response in the presence of L-NAME was significantly inhibited by prior administration of cimetidine or FPL-52694 (a mast-cell stabilizer). 4. The mucosal exposure to TC significantly decreased the number of mucosal mast cells and increased the luminal histamine output. 5. Damage in the stomach may activate the histamine-dependent acid stimulatory pathway in addition to the NO-dependent inhibitory mechanism, although the latter effect overcomes the former, resulting in a decrease of acid secretion. L-NAME unmasks the stimulation of acid secretion by suppressing the inhibitory pathway.
Gen Pharmacol 1996 Jul
PMID:Stimulation of acid secretion in rat stomach following exposure to taurocholate in the presence of the nitric oxide synthase inhibitor. 884 89

To clarify the physiological role of motilin in the pig gastrointestinal (GI) tract, effect of Leu13-porcine motilin (LMT) on the contractility of GI smooth muscle was investigated in studies using isolated muscle strips and dispersed muscle cells. LMT produced no contraction in either longitudinal muscle (LM) or circular muscle (CM) of the stomach (fundus, corpus, antrum), duodenum, ileum and colon even at 1 microM. Pretreatment with LMT (1 nM-1 microM) did not potentiate the contractile response to acetylcholine (ACh) in each muscle strip. Dispersed cells from the duodenum responded to ACh in a concentration-dependent manner (EC50 = 10 pM), but not to LMT even at a high concentration (10 microM). Electrical field stimulation (EFS) caused a frequency-dependent (0.2-10 Hz) contraction of the duodenal LM that was almost completely inhibited by atropine or tetrodotoxin. EFS caused the relaxation of duodenal CM in a frequency-dependent manner (0.1-10 Hz). This relaxation was not inhibited by atropine, propranolol, phentolamine or guanethidine, indicating the involvement of noncholinergic, nonadrenergic (NCNA) nerves. NG-nitro L-arginine methylester (L-NAME, 100 microM) attenuated the EFS-induced relaxation and the inhibition at low frequency was larger than that at high frequency. L-Arginine prevented the inhibition by L-NAME but D-arginine did not. LMT (1 nM-1 microM) had no influence on EFS-induced cholinergic contraction of LM and EFS-induced NCNA relaxation of CM layer. The present in vitro studies indicate that motilin is ineffective in producing contraction and in modulating the autonomic neuroeffector transmission of the pig GI smooth muscle, and suggest that pig GI smooth muscle lacks functional motilin receptors.
Gen Pharmacol 1996 Jun
PMID:Does motilin stimulate the gastrointestinal motility of the pig? In vitro study using smooth muscle strips and dispersed muscle cells. 885 1

1. Several previous in vivo studies demonstrated that crosslinked hemoglobin is a potent vasoconstrictor capable of significantly increasing arterial blood pressure following systemic administration. The precise mechanisms underlying the vascular effects of crosslinked hemoglobin are not clear. The present study was designed to determine the effect of crosslinked hemoglobin on the endothelial L-arginine-nitric oxide biosynthesis pathway in isolated canine arteries. 2. Isolated femoral and renal arteries were suspended in organ chambers for isometric tension recordings. Endothelium-dependent relaxations to acetylcholine and calcium ionophore A23187 were studied in the absence or in the presence of crosslinked hemoglobin or hemoglobin. A radioimmunoassay technique was used to determine levels of guanosine 3',5'-cyclic monophosphate (cyclic GMP) and adenosine 3',5'-cyclic monophosphate (cyclic AMP). 3. A nitric oxide synthase inhibitor L-NAME (10(-4)M) selectively inhibited endothelium-dependent relaxations to acetylcholine and calcium ionophore A23187. The inhibitory effect of L-NAME was reversed by L-arginine (3 x 10(-4)M). Crosslinked hemoglobin (10(-7), 10(-6) and 10(-5)M) inhibited endothelium-dependent relaxations to acetylcholine (10(-9)-10(-5)M) or A23187 (10(-9)-10(-6)M). In the same concentration range, purified bovine hemoglobin exerted a similar inhibitory effect on relaxations mediated by activation of endothelial cells. Crosslinked hemoglobin (10(-6)M) significantly reduced basal production of cyclic GMP, but did not affect production of cyclic AMP. Acetylcholine (10(-6)M) stimulated production of cyclic GMP. This effect of acetylcholine was abolished in the presence of crosslinked hemoglobin. 4. These studies demonstrate that crosslinked hemoglobin impairs endothelium-dependent relaxations in isolated large conduit arteries. This effect appears to be mediated by the chemical antagonism of crosslinked hemoglobin against nitric oxide released from the endothelium. Inhibition of the endothelial L-arginine-nitric oxide biosynthesis pathway, with subsequent decrease of cyclic GMP in smooth muscle, may help to explain vasoconstrictor and pressor effects of crosslinked hemoglobin.
Gen Pharmacol 1996 Mar
PMID:Crosslinked hemoglobin inhibits endothelium-dependent relaxations in isolated canine arteries. 891 36

We have used the patch-clamp technique to study the effect of angiotensin II (AII) on the activity of the apical 70 pS K+ channel and used Na(+)-sensitive fluorescent dye (SBFI) to investigate the effect of AII on intracellular Na+ concentration (Na+i) in the thick ascending limb (TAL) of the rat kidney. Addition of 50 pM AII reversibly reduced NPo, a product of channel open probability (Po) and channel number (N), to 40% of the control value and reduced the Na+i by 26%. The AII (50 pM)-induced decrease in channel activity defined by NPo was partially reversed by addition of 5 microM 17-octadecynoic acid (17-ODYA), an agent which blocks the cytochrome P450 monooxygenase. The notion that P450 metabolites of arachidonic acid (AA) may mediate the inhibitory effect of AII was further suggested by experiments in which addition of 10 nM of 20-hydroxyeicosatetraenoic acid (20-HETE) blocked the channel activity in cell-attached patches in the presence of 17-ODYA. We have used gas chromatography mass spectrometry (GC/MS) to measure the production of 20-HETE, a major AA metabolite of the P450-dependent pathway in the TAL of the rat. Addition of 50 pM AII increased the production of 20-HETE to 260% of the control value, indicating that 20-HETE may be involved in mediating the effect of AII (50 pM). In contrast to the inhibitory effect of 50 pM AII, addition of 50-100 nM AII increased the channel activity to 270% of the control value and elevated the Na+i by 45%. The effect of AII on the activity of the 70 pS K+ channel was also observed in the presence of 5 microM 17-ODYA and 5 microM calphostin C, an inhibitor of protein kinase C. However, addition of 100 microM NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, abolished completely the AII (50-100 nM)-induced increase in channel activity and addition of an exogenous nitric oxide (NO) donor, S-nitroso-N-acetyl-penicillamine (SNAP), increased channel activity in the presence of L-NAME. These data suggest that the stimulatory effect of AII is mediated by NO. We conclude that AII has dual effects on the activity of the apical 70 pS K+ channel. The inhibitory effect of AII is mediated by P450-dependent metabolites whereas the stimulatory effect may be mediated via NO.
J Gen Physiol 1996 Dec
PMID:Effect of angiotensin II on the apical K+ channel in the thick ascending limb of the rat kidney. 897 91

1. The biphasic reflex tracheal response (constriction followed by dilatation) occurred during bronchoconstriction induced by inhalation of ovalbumin antigen (OA) in sensitized guinea pigs. 2. The reflex tracheal constriction was largely reduced by atropine, and the dilatation was inhibited by propranolol and N omega-nitro-L-arginine methyl ester (L-NAME). The noradrenaline, adrenaline, cyclic AMP, and cyclic GMP contents in the tracheal segment were significantly higher during reflex tracheal dilatation. 3. These findings suggest that cholinergic nerves may mediate reflex tracheal constriction and that adrenergic and NOergic nerves may mediate the ensuing reflex tracheal dilatation.
Gen Pharmacol 1997 Mar
PMID:Neural reflex-mediated tracheal response during bronchoconstriction induced by ovalbumin antigen in guinea pigs. 906 80

1. This article examines the effects of hypoxia on the contractile response of isolated human umbilical artery strips to 5-hydroxytryptamine (5-HT). 2. Hypoxic conditions produce a large increase in the contractile response to 5-HT without a significant alteration of the sensitivity evaluated at the level of the pD2 value. Indomethacin (10 microM) reduced hypoxia-induced potentiation of the response to 5-HT and decreased the response to the monoamine under oxygenated conditions. 1-NAME (100 microM) did not further increase the effect of hypoxia on the vessel response to 5-HT and increased the response to 5-HT under oxygenated conditions. 3. Taken together, these results suggest that, at least partially, the response of human umbilical artery strips to 5-HT depends on 5-HT release of a contracting prostanoid which is a product of the cyclooxygenase pathway. Furthermore, during hypoxia in human umbilical artery strips, there appears to be impairment of the basal production and/or release of EDRF/NO. 4. A subthreshold concentration of prostaglandin F2 alpha (1 nM) potentiates the response to 5-HT in indomethacin-pretreated umbilical artery strips. The data raise the possibility that prostaglandin F2 alpha might be the prostanoid released during hypoxia, which in turn potentiates the response of the human umbilical artery to 5-HT.
Gen Pharmacol 1997 Jan
PMID:Hypoxia and response of human umbilical artery strips to 5-hydroxytryptamine: role of prostaglandin F2 alpha. 911 81


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