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51.
A. A. Galkin D. A. Sarkisyan E. N. Timin B. I. Khodorov 《Bulletin of experimental biology and medicine》1978,85(2):172-175
Experiments were carried out on isolated strips of guinea pig taenia coli. The smooth muscle was depolarized in a solution with high potassium concentration (120 mM KCl). The effect of papaverine (in concentrations of 10–5 to 3.10–5 g/ml) on the tone and off-response to a prolonged and strong hyperpolarizing current was investigated on the denervated muscle. Papaverine was found: 1) to abolish contractile responses to application of histamine, bradykinin, and acetylcholine; 2) to reduce the tone of the depolarized muscle and abolish the effect of an increase in the Ca++ concentration in the external medium on muscle tone; 3) to have no effect on the amplitude and velocity of the ascending phase of the off-response; 4) to accelerate the descending phase of the off-response. The following hypotheses are put forward to explain the result: 1) in the cell membrane there are chemically excitable calcium channels which are blocked by papaverine; 2) in the membrane there are calcium leakage channels responsible for the maintenance of tone and blocked by papaverine; 3) papaverine has negligible effect on electrically excitable calcium channels.A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. Bio-Inorganic Chemicals BIKhS Research Institute, Kupavna, Moscow Region. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 85, No. 2, pp. 177–180, February, 1978. 相似文献
52.
Nabil Nakhostine Daniel Lamontagne 《Pflügers Archiv : European journal of physiology》1994,428(5-6):526-532
The mechanism of hypoxia-induced coronary vasodilatation was studied in isolated, saline-perfused rabbit hearts under constant flow conditions. Reduction in the perfusion solution PO2 (from 520±6 to 103±9 mm Hg) under control conditions halved the coronary resistance and was accompanied by a significant release of the prostaglandin (PG) 6-keto-PGF1 (from 1.8±0.3 to a maximum of 4.4±0.9 pmol min–1 g–1). The cyclooxygenase inhibitor, diclofenac (1 M), blocked the release of PGI2 and reduced hypoxia-induced vasodilatation (from 47±8% to 25±5%, P<0.05). The relative contribution of adenosine, prostaglandins, and adenosine triphosphate (ATP)-sensitive K+ channel (KATP channel) activation in hypoxia-induced vasodilatation was assessed by comparing the differential change (control response minus response after treatment) in coronary perfusion pressure (CPP) during infusion of 8-phenyltheophylline (8-PT), diclofenac, and glibenclamide, respectively. The differential change in CPP with 8-PT and diclofenac given together (–48 ±7%) was found to be equivalent to the sum of their respective effects (–24±7 and –19±4%, respectively). Glibenclamide (0.3 M) reduced significantly hypoxia-induced vasodilatation (differential change in CPP of –27±6%) as well as the dilator response to 10 M adenosine and to the stable PGI2-analogue, iloprost. Forskolin-induced coronary vasodilatation in arrested hearts was slightly, but significantly, reduced by glibenclamide. Our results suggest that both cyclooxygenase products and adenosine, acting independently and concomitantly, contribute to the dilator response of coronary resistance vessels to hypoxia, in part through the activation of KATP channels. KATP channel activation by prostacyclin and adenosine may involve both cyclic adenosine monophosphate-dependent and independent pathways. 相似文献
53.
目的: 通过通道蛋白特定位点(P266T)突变,观察对ATP敏感性钾通道电生理特性的影响。 方法: 将Kir6.2及其突变子P266T的cDNA导入人胚肾细胞,表达ATP敏感性钾通道,用膜片钳方法研究KATP电生理特性。 结果: KATP(P266T)开放能力是野生型的2倍; KATP(P266T)密度仅是野生型20%; KATP(P266T)对ATP敏感性降低;对pH敏感性增高。 结论: KATP特定位点(P266T)突变可改变KATP电生理特性。 相似文献
54.
Shear stress induced membrane currents and calcium transients in human vascular endothelial cells 总被引:3,自引:0,他引:3
Gero Schwarz Guy Droogmans Bernd Nilius 《Pflügers Archiv : European journal of physiology》1992,421(4):394-396
We have measured membrane currents induced by shear stress together with intracellular calcium signals in endothelial cells from human umbilical cord veins. In the presence of extracellular calcium (Ca2+]o), shear stress induced an inward current at a holding potential of 0 mV which is accompanied by a rise in intracellular Ca2+ ([Ca2+]i). In the absence of extracellular calcium shear stress was unable to evoke a calcium signal but still induced a membrane current. The voltage dependence of the shear stress induced current was obtained from difference currents evoked by linear voltage ramps before and during application of shear stress. Its reversal potential Erev shifted from –2.3±0.8 mV (n=4) in a nominally Ca2+ free solution to +1.5±1.6 mV at 1.5 mM [Ca2+]o (n=4) and to +21.9±4.4 mV (n=7) at 10 mM [Ca2+]o. From our data we conclude that shear stress opens an ion channel that is 12.5±2.9 (n=7) times more permeable for calcium than for sodium or cesium. 相似文献
55.
目的: 研究肾上腺髓质素( adrenomedullin, ADM)抑制豚鼠心室肌细胞L-型钙通道的信号转导机制。方法: 应用全细胞膜片钳技术,记录应用ADM(1-100 nmol·L-1)前后L-型钙电流(ICa,L),以及分别记录应用ADM特异性受体拮抗剂ADM22-52(100 nmol·L-1)+ADM(100 nmol·L-1)、蛋白激酶A (PKA) 特异性拮抗剂H-89(10 μmol·L-1) + ADM(100 nmol·L-1)、蛋白激酶C (PKC) 特异性拮抗剂PKC19-36(10 μmol·L-1)+ADM(100 nmol·L-1)、PKC特异性激动剂PMA(1 μmol·L-1)前后ICa,L。结果: ADM(1-100 nmol·L-1)浓度依赖性地抑制豚鼠心室肌细胞ICa,L,并可被ADM22-52(100 nmol·L-1)完全阻断;H-89(10 μmol·L-1)对ADM抑制ICa,L的作用无影响。PKC19-36(10 μmol·L-1)可完全阻断ADM 对ICa,L的抑制效应,且PMA(1 μmol·L-1)可模拟ADM 对ICa,L的抑制效应。结论: ADM作用于特异性ADM受体可浓度依赖性地抑制豚鼠心室肌细胞ICa,L,此作用有可能与PKC激活相关。 相似文献
56.
Ken Nakazawa 《Pflügers Archiv : European journal of physiology》1994,427(1-2):129-135
Modulation by protein phosphorylation of the relation between acetylcholine (ACh)-activated current (I
ACh) and adenosine triphosphate-(ATP)-activated current (I
ATP) was investigated with the whole-cell voltage-clamp technique in rat sympathetic neurons. During simultaneous activation by 100 M ATP of an inward current, the current evoked by 100 M ACh was reduced to 60–70% of that in the absence of ATP. Effects of compounds that are known to modulate protein phosphorylation were tested by including them in the intracellular solution. The reduction ofI
ACh by ATP was not observed when K252a (1 M), a non-selective protein kinase inhibitor, adenosine 5-O-(3-thiotriphosphate) (ATP[S], 1 mM) or,-methylene ATP (1 mM) were included in the intracellular solution. Activators of protein kinases, adenosine 3,5-cyclic monophosphate (cAMP, 100 M), guanosine 3,5-cyclic monophosphate (cGMP, 100 M), phorbol 12-myristate 13-acetate (PMA, 1 M), also abolished the reduction by ATP ofI
ACh. The effects of okadaic acid, a protein phosphatase inhibitor, were paradoxical: okadaic acid (2 M) itself abolished the reduction by ATP ofI
ACh but it antagonized the abolishment by cAMP or cGMP of the reduction ofI
ACh. Okadaic acid did not affect the disappearance of the reduction ofI
ACh by ATP in the presence of intracellular PMA. The results suggest that the interaction betweenI
ACh andI
ATP is regulated by protein phosphorylation/dephosphorylation. Possible mechanisms underlying the effects of these modulators of protein phosphorylation are discussed. 相似文献
57.
58.
Y. Maruyama A. Nishiyama T. Izumi N. Hoshimiya O. H. Petersen 《Pflügers Archiv : European journal of physiology》1986,406(1):69-72
The K+ channel in rat parotid gland acinar cells were investigated by ensemble current noise analysis in single isolated cells employing the giga-seal whole cell current recording mode. Sets of 20–40 identical de- and hyperpolarization voltage steps were applied and the resultant current records were processed by computer to obtain the mean and the variance of the current. The time-course of the mean current could be fitted by the sum of two exponentials, suggesting a 3-state model. The simplest plausible hypothesis is a model with one open and two closed states. Assuming this model, the relationship between the variance (2) and the mean current (I) could be fitted by the function 2/I=i–I/N. The estimated single channeli/V-relations were similar to those taken from single channel current recordings, and the size of the population of channels per cell (N) was 76±26 (n=12). The validity of the model was tested by a successful simulation of the time-course of the variance. 相似文献
59.
Planar bilayer membranes were made from commercially available lipids. With various lipids, originating from biological sources, such as egg yolk phosphatidylcholine, soybean phosphatidylcholine or bovine brain phosphatidylserine, spontaneously fluctuating channels could be observed. Spontaneous channel activity could not be observed in planar bilayers made from synthetic lipids, such as 1,2 diphytanoyl 3-sn-phosphatidylcholine. It is concluded that the observed channels are due to proteolipids, being present as impurities in the lipid material. 相似文献
60.
Max Deist Holger Repp Florian Dreyer 《Pflügers Archiv : European journal of physiology》1992,421(2-3):292-294
We studied the effect of the KATP channel blockers tolbutamide and glibenclamide on presynaptic membrane currents in the mouse M. triangularis sterni preparation using the perineural recording technique. Both sulfonylureas blocked part of the fast K+ component within 2 min after application. The block was much more pronounced under glucose-free conditions and was completelyreversible by washing. Addition of glucose to glucose-free bath solution also reduced the K+ component. A further effect of the sulfonylureas was observed under glucose-free conditions. With a delay of 5 to 10 min, the nodal Na+ component began to diminish and disappeared within 30 min. This was associated with a dramatic increase in spontaneous quantal transmitter release suggesting that the block of sulfonylurea-sensitive K+ channels causes depolarization of motor nerve terminals and fibres thus inactivating Na+ channels. Tetraethylammonium (TEA) which blocks ATP-dependent K+ channels in high concentrations caused, under glucose-free conditions, the same delayed effect as the sulfonylureas. This delayed effect was fully reversible by washing with glucose-containing, but not with glucose-free solution. Our findings strongly suggest that KATP channels exist in mammalian motor nerve endings and that under hypoglycemic conditions these channels open and become essential for the maintenance of the membrane potential. 相似文献