Drugs online research references
Eur J Neurosci. 1992;4(5):433-437.
The Role of Ca2+ in the Elimination of Polyneuronal Innervation of Rat Soleus Muscle Fibres.
Zhu PH, Vrbova G.
Department of Anatomy and Developmental Biology, Centre for Neuroscience, University College London, Gower Street, London WC1E 6BT, UK.
The mechanism by which nerve - muscle contacts are reduced during postnatal development of the rat soleus muscle was investigated using electrophysiological methods. Between days 7 and 9 after birth, soleus muscle fibres lose 0.19 - 0.24 terminals per muscle fibre within 24 h. A much more rapid loss of contacts is seen when muscles are exposed in vitro to acetylcholine (10-3 g/ml). In this case 0.67 - 0.87 terminals per muscle fibre lose contact within 2 h. The loss of neuromuscular contacts induced by acetylcholine can be reduced by preincubating the muscles in solutions containing acetoxymethyl ester of 1,2-bis(2-aminophenoxylethane-N,N1,N;N1-tetraacetic acid (BAPTA-AM), a Ca2+ chelating agent that enters cells and reduces the Ca2+ transients inside the cell. Treatment of muscles with nifedipine, which blocks dihydropyridine-sensitive (L-type) Ca2+ channels, also reduced the acetylcholinesterase-induced loss of neuromuscular contacts. The results indicate that transient increases in Ca2+ inside nerve terminals contribute to loss of neuromuscular contacts, and that these increases occur by Ca2+ entry through L-type channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12106352&dopt=Abstract [PubMed - as supplied by publisher]
rs.noda.sut.ac.jp
We examined the mechanisms of the elevation of glutathione level induced in macrophage-like RAW 264.7 cells by low doses of gamma-rays. The level increased soon after exposure of the cells to 50 cGy of gamma-rays, peaked between 3 hours and 6 hours and returned almost to the time 0 value by 24 hours post-irradiation. Doses between 25 and 100 cGy significantly increased the glutathione level at 4 hours post-irradiation. However, there was no significant elevation at doses of more than 100 cGy or less than 25 cGy. When the effect of dose rate was examined at a constant absorbed dose of 50 cGy, dose rates of more than 50 cGy/minute significantly increased the GSH level at 4 hours post-irradiation. It was also shown that the elevation of glutathione level in cells irradiated with low doses of gamma-rays followed the induction of mRNA coding for gamma-glutamylcysteine synthetase (gamma-GCS), a rate-limiting enzyme of the de novo glutathione synthesis pathway. When the cells were exposed to the radiation in the presence of genistein, calphostin C or nifedipine, the elevations of glutathione and gamma-GCS mRNA expression were both mostly blocked. EGTA also strongly inhibited these elevations. These results suggest that the tyrosine kinase, calcium channel and protein kinase C activities play an essential role in the low-dose-radiation-induced elevation of cellular glutathione.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10928075&dopt=Abstract
Gen Pharmacol. 1992 Mar;23(2):263-7.
Vasoconstrictive responses elicited by endothelin in bovine cerebral arteries.
Encabo A, Ferrer M, Marin J, Villamor J, Balfagon G.
Departamento de Fisiologia, Facultad de Medicina, Universidad Autonoma, Madrid, Spain.
1. Endothelin (ET-1) induced concentration-dependent contractions, which were slowly developed in segments of bovine cerebral arteries. Furthermore, this agent produced tachyphylaxis. 2. The contractions evoked by ET-1 were markedly reduced in Ca-free medium containing 1 mM EGTA and by the Ca channel antagonist, nifedipine (1 microM), but increased by the Ca channel agonist, BAY K 8644 (10 nM). 3. The contractions caused by ET-1 were significantly reduced by the protein kinase C (PKC) inhibitor, staurosporine (1 and 10 nM). 4. These results indicate that ET-1 induced potent vasoconstrictive responses, probably mediated by PKC activation, which were mainly dependent on extracellular Ca; this Ca enters the smooth muscle cells via dihydropyridine sensitive Ca channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1379205&dopt=Abstract
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