PubMed · 8841286
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J J Ply. 1996. Decrease of postoperative inflammation with diclofenac sodium.. https://doi.org/10.1016/s0161-6420(96)30503-4
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1. Exocytotic events and changes of cell volume in mucous cells from guinea-pig antrum were examined by video-enhanced optical microscopy. 2. Acetylcholine (ACh) evoked exocytotic events following cell shrinkage, the frequency and extent of which depended on the ACh concentration. ACh actions were mimicked by ionomycin and thapsigargin, and inhibited by Ca2+-free solution and Ca2+ channel blockers (Ni2+, Cd2+ and nifedipine). Application of 100 microM W-7, a calmodulin inhibitor, also inhibited the ACh-induced exocytotic events. These results indicate that ACh actions are mediated by intracellular Ca2+ concentration ([Ca2+]i) in antral mucous cells. 3. The effects of ion channel blockers on exocytotic events and cell shrinkage evoked by ACh were examined. Inhibition of KCl release (quinine, Ba2+, NPPB or KCl solution) suppressed both the exocytotic events and cell shrinkage evoked by ACh. 4. Bumetanide (inhibition of NaCl entry) or Cl--free solution (increasing Cl- release and inhibition of NaCl entry) evoked exocytotic events following cell shrinkage in unstimulated antral mucous cells and caused further cell shrinkage and increases in the frequency of exocytotic events in ACh-stimulated cells. However, Cl--free solution did not evoke exocytotic events in unstimulated cells in the absence of extracellular Ca2+, although cell shrinkage occurred. 5. To examine the effects of cell volume on ACh-evoked exocytosis, the cell volume was altered by increasing the extracellular K+ concentration. The results showed that cell shrinkage increases the frequency of ACh-evoked exocytotic events and cell swelling decreases them. 6. Osmotic shrinkage or swelling caused the frequency of ACh-evoked exocytotic events to increase. This suggests that the effects of cell volume on ACh-evoked exocytosis under anisosmotic conditions may not be the same as those under isosmotic conditions. 7. In antral mucous cells, Ca2+-regulated exocytosis is modulated by cell shrinkage under isosmotic conditions.
1. The relationship between nitric oxide (NO) concentration measured with an NO-specific microelectrode and endothelium-dependent relaxation was investigated in isolated rat superior mesenteric artery contracted with 1 microM noradrenaline. 2. Acetylcholine (10 microM) induced endothelium-dependent simultaneous increases in luminal NO concentration of 21 +/- 6 nM, and relaxations with pD2 values and maximum of 6.95 +/- 0.32 and 97.5 +/- 0.7 % (n = 7), respectively. An inhibitor of NO synthase, N G-nitro-L-arginine (L-NOARG, 100 microM) inhibited the relaxations and increases in NO concentration induced by acetylcholine. 3. Oxyhaemoglobin (10 microM) reversed the relaxations and increases in NO concentrations induced by acetylcholine, S-nitroso-N-acetylpenicillamine (SNAP) and S-morpholino-sydnonimine (SIN-1), but not the relaxations induced with forskolin. Oxyhaemoglobin also decreased the NO concentration below baseline level. 4. In the presence of L-NOARG (100 microM), a small relaxation to acetylcholine (10 microM) of noradrenaline-contracted segments was still seen; oxyhaemogobin inhibited this relaxation and decreased the NO concentration by 14 +/- 4 nM (n = 4). 5. The NO concentration-relaxation relationship for acetylcholine resembled that for SNAP and SIN-1 more than for authentic NO. Thus while 7-17 nM NO induced half-maximal relaxations in response to SNAP or SIN-1, 378 +/- 129 nM NO (n = 4) was needed for half-maximal relaxation to authentic NO. 6. The present study provides direct evidence that the relaxation of the rat superior mesenteric artery with the endothelium-dependent vasodilator acetylcholine is correlated to the endogeneous release of NO. The study also suggests that NO mediates the L-NOARG-resistant relaxations in this artery, and that there is a basal NO release.
Metabotropic and ionotropic effects evoked by the endogenous Helix heptapeptide, SEPYLRFamide, and four analogues, i.e., where the amino acid sequences at the N-terminal (EPYLRFamide, SEGYLRFamide, SRPYLRFamide and SKPYLRFamide) were modified, were compared on identified Helix lucorum LPa2, LPa3, RPa3, RPa2 neurones using two electrode voltage clamp and current clamp techniques. All peptides (bath application) reduce reversibly the inward current to local ionophoretic application of acetylcholine onto the neurone soma with an order of potency: EPYLRFamide=SEGYLRFamide=SRPYLRFamide>SEPYLRFamide+ ++>SKPYLRFamide. The reductions of the acetylcholine-induced inward current evoked by SEPYLRFamide and its analogues at concentrations of 0.01-10 microM are not accompanied by a change of amplitude of the leak inward current caused by constant negative shift of a holding potential. At concentration of 50 microM all peptides increase reversibly the resting membrane conductance to an equal degree. Local application under pressure of SEPYLRFamide and its analogues onto the soma of neurones evoke hyperpolarizations with similar values. These results indicate that the N-terminal three amino acids of the peptide molecule are not responsible for the degree of ionotropic effect on the neurones studied. In contrast the amino acid sequence at the N-terminal modifies the degree of the modulatory effects of the YLRFamide-related analogues. Changes at the SEPYLRFamide N-terminal (Ser1-Glu2-Pro3) intensify the inhibitory action of the analogues as compared with effect evoked by the endogenous peptide, that is, removal of Ser1 (Glu1-Pro2), replacement of Pro3 with Gly3 (Ser1-Glu2-Gly3), replacement of Glu2 with Arg2 (Ser1-Arg2-Pro3). Replacement of Glu2 with Lys2 (Ser1-Lys2-Pro3) reduces the modulatory potency. It is concluded that ionotropic and metabotropic effects of these YLRFamide-related peptides may occur at different membrane binding sites.