Drugs online research references
Invest Ophthalmol Vis Sci. 1994 Jul;35(8):3268-77.
Nonadrenergic noncholinergic vasodilation in bovine ciliary artery involves CGRP and neurogenic nitric oxide.
Wiencke AK, Nilsson H, Nielsen PJ, Nyborg NC.
Department of Pharmacology, University of Aarhus, Denmark.
PURPOSE. Characterization of the nonadrenergic noncholinergic (NANC) vasodilator innervation in the anterior segment in the bovine eye. METHODS. The neurogenic tetrodotoxin-sensitive response to electrical field stimulation (EFS) of the intraocular segment of the bovine long posterior ciliary artery supplying the ciliary body was recorded using isolated ring segments of this artery mounted on an isometric myograph. After adrenergic and cholinergic receptor blockade (with phentolamine, propranolol, and atropine), the preconstricted vessels were subjected to EFS by passing constant current pulses (0.3 msec, 35 mA, 0.5 to 32 Hz) between two electrodes on either side of the vessel segments. RESULTS. EFS resulted in 60% relaxation of the active tone in 40 vessels. Treatment with capsaicin reduced the NANC response by 16 +/- 2% (P < 0.001) and inhibition of the NO synthase with 1 x 10(-4) M L-NOARG reduced the NANC response by 83 +/- 10% (P < 0.001). Desensitization of the vessels to substance P had no effect. The CGRP(8-37) fragment (1 x 10(-6) M) in the presence of 1 x 10(-4) M L-NOARG reversibly and competitively inhibited the NANC response. L-arginine partly antagonized the inhibition induced by L-NOARG. About 60% of the L-NOARG-sensitive component of the NANC response was inhibited by methylene blue. Combined incubation with capsaicin and L-NOARG nearly abolished the NANC response. The L-NOARG-sensitive/capsaicin-resistant relaxation was present in endothelium denuded vessels. The responses to EFS were blocked by TTX. CONCLUSIONS. The neurogenic NANC vasodilator response in the intraocular part of the bovine long posterior ciliary artery supplying the ciliary body is endothelium independent and consists of two components: a capsaicin-sensitive component mediated by CGRP released from sensory nerve endings and a larger L-NOARG sensitive component mediated by a direct "nitroxidergic" neurotransmission. The size of the nitroxidergic NANC response indicates that it has a physiological relevance in vivo.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7519182&dopt=Abstract
Neuroscience. 1994 Apr;59(4):1043-50.
Serotonin protects C6 glioma cells from glutamate toxicity.
Shinagawa S.
Department of Neurobiology, University of Kanazawa School of Medicine, Ishikawa, Japan.
It was recently shown that addition of L-glutamate in millimolar amounts to a culture of C6 glioma cells induced cell death within 24 h. The mechanism for glutamate toxicity in the C6 glioma cells is linked to the inhibition of cystine uptake, leading to glutathione depletion through the cystine/glutamate antiporter (Xc) system. In the present study, neurotransmitters, whose receptors were localized on the glioma (glial) cells, were evaluated for their ability to protect C6 cells from glutamate toxicity through this amino acid antiporter. Among them, only 100 microM serotonin suppressed cell death by glutamate in a constant co-existence culture. The suppressive dose of serotonin was relatively low and the half-effective dose was about 35 microM. 8-Hydroxy-2-(DL-n-propylamino)tetralin, a specific serotonin1A agonist, showed a comparable suppression to glutamate damage, while 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane, a specific serotonin2 agonist, and quipazine, a non-selective serotonin1B agonist, did not suppress it. Furthermore, propranolol and pindolol significantly blocked the serotonin effect, but spiperone, mianserin and ketanserin did not block it. These results strongly indicate that this protective action of serotonin to glutamate toxicity was receptor (serotonin1A) mediated. Serotonin did not protect the C6 cells from glutathione depletion by glutamate. The cellular level of glutathione was depleted even under the co-existence of serotonin and glutamate. Serotonin induced a significant inhibition of lipid peroxide accumulation in the C6 glioma cells to glutamate exposure and the low rate of lipid peroxide accumulation was controlled.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7520131&dopt=Abstract
Jpn J Physiol. 1978;28(6):833-45.
Developmental changes of the contractile activity and the drug sensitivity of smooth muscle of the alimentary tract of guinea pig.
Ohkawa H.
The mechanical activity of the smooth muscle of guinea pig alimentary tract changed during fetal and postnatal development. At the F20 (fetus, body weight 20 g) stage of the fetus, the antrum, small intestinal and colonic preparations showed no spontaneous activity. After this stage, spontaneous activity occurred but the patterns of contractile activity of various regions of the alimentary tract differed from those of the adult. However, at later fetal stages (F50 or later), the mechanical patterns of various regions, except the lower region of colon, were similar to adult patterns. An excitatory response to acetylcholine was observed in all regions at the F20 stage but catecholamines were not effective at this stage. Responses to catecholamines appeared later than those to acetylcholine but they were not constant. During development of the colon, the excitatory effect of adrenaline was significant and the effect was blocked by phenoxybenzamine, and isoprenaline inhibited the spontaneous activity. However, sympathetic nerve stimulation at F70 inhibited the mechanical activity and propranolol blocked the inhibitory action of sympathetic nerves. These results indicate the co-existence of alpha-excitatory and beta-inhibitory receptors on the developing colonic smooth muscle cell membrane.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=752095&dopt=Abstract
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