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11.
Emília P. Duarte Graça Baltazar Arsélio P. Carvalho 《The European journal of neuroscience》1994,6(7):1128-1135
We compared the effectiveness of Ca2+ entering by Na+/Ca2+ exchange with that of Ca2+ entering by channels produced by membrane depolarization with K+ in inducing catecholamine release from bovine adrenal chromaffin cells. The Ca2+ influx through the Na+/Ca2+ exchanger was promoted by reversing the normal inward gradient of Na+ by preincubating the cells with ouabain to increase the intracellular Na+ and then removing Na+ from the external medium. In this way we were able to increase the cytosolic free Ca2+ concentration ([Ca2+]c) by Na+/Ca2+ exchange to 325 ± 14 nM, which was similar to the rise in [Ca2+]c observed upon depolarization with 35 mM K+ of cells not treated with ouabain. After incubating the cells with ouabain, K+ depolarization raised the [Ca2+]c to 398 ± 31 nM, and the recovery of [Ca2+]c to resting levels was significantly slower. Reversal of the Na+ gradient caused an −6-fold increase in the release of noradrenaline or adrenaline, whereas K+ depolarization induced a 12-fold increase in noradrenaline release but only a 9-fold increase in adrenaline release. The ratio of noradrenaline to adrenaline release was 1.24 ± 0.23 upon reversal of the Na+/Ca2+ exchange, whereas it was 1.83 ± 0.19 for K+ depolarization. Reversal of the Na+/Ca2+ exchange appeared to be as efficient as membrane depolarization in inducing adrenaline release, in that the relation of [Ca2+]c to adrenaline release was the same in both cases. In contrast, we found that for the same average [Ca2+]c, the Ca2+ influx through voltage-gated channels was much more efficient than the Ca2+ entering through the Na+/Ca2+ exchanger in inducing noradrenaline release from chromaffin ceils. This greater effectiveness of membrane depolarization in stimulating noradrenaline release suggests that there is a pool of noradrenaline vesicles which is more accessible to Ca2+ entering through voltage-gated Ca2+ channels than to Ca2+ entering through the Na+/Ca2+ exchanger, whereas the adrenaline vesicles do not distinguish between the source of Ca2+. 相似文献
12.
13.
对广西武鸣华侨农场4158人进行基线普查,410人进行膳食调查和作8小时夜尿电解质测定,并将高血压低发区广西的资料与高发区的北京作对比.结果显示,体重指数高是高血压一个重要的危险因素,而体重过重又与膳食中摄入碳水化合物和总热量大有关.另一主要的危险因素是钠,膳食中摄入钠高,尿Na和Na/K比值高者,血压水平和高血压的患病率亦高. 相似文献
14.
Takeshi Uchida Yutaka Ohtaki Hideaki Kido Hiroshi Shinyama Kazutaka Hayashi Katsumi Yamanaga Masahiro Watanabe 《Drug development research》1992,26(2):203-212
The diuretic and the antihypertensive actions of torasemide were examined in renal and genetic hypertensive rats and compared to the effects of furosemide. Oral administration of torasemide (1 and 3 mg/kg) elicited a dose-dependent increase in the excretion of urine and electrolytes and elevated the urinary Na/K ratio in both renal and genetic hypertensive rats. Torasemide and furosemide had a similar maximum diuretic effect in the normotensive Wistar rat and the spontaneously hypertensive rat (SHR). However, the diuretic activity of furosemide was weaker in the renal hypertensive rat (RHR). Torasemide showed approximately 30 times greater diuretic potency than furosemide. Torasemide and furosemide demonstrated hypotensive action in hypertensive rat models, but not in the normotensive Wistar rat. Especially in the RHR, torasemide exhibited a more potent hypotensive action than furosemide. These results show that the diuretic and antihypertensive activities of torasemide are effective in various rat models of hypertension, while the diuretic activity of furosemide is weak in certain hypertensive rat models. © 1992 Wiley-Liss, Inc. 相似文献
15.
三七总皂甙(PNS)能抑制心肌总ATP酶活力,但对Na~( )-K~( )-ATP酶无明显影响。三七皂甙单体Rb_1及Rg_1对心肌总ATP酶活力均有抑制作用,但Rb_1的抑制效力显著大于Rg_1·Rb_1能抑制豚鼠离体心房肌的自律性和收缩性,Rg_1也能抑制豚鼠离体心房肌的自律性,但对心房肌的收缩性却无明显影响。提示PNS抑制心肌收缩力这一作用的主要有效成份是Rb_1· 相似文献
16.
体外测定青蒿琥酯钠(SA)对大鼠红细胞膜Na~( )-K~( )-交换ATP酶活性的影响.方法:在反应系统中分别加入不同浓度的SA(0,0.5,1,5和10 μmol·L~(-1)),通过测定反应系统中释放的无机磷含量,计算酶活性.结果:随着SA浓度(O,0.5,1,5和10 μmol·L~(-1))的增高,对Na~( )-K~( )-交换ATP酶活性的抑制作用也随之增强,抑制率分别为15%,29%,46%和75%.将底物ATP浓度增加为125,250,375和500 μmol·L~(-1),进行了酶的动力学测定.用直线回归分析作Eadie-Hofstee动力学曲线,结果表明,SA对该酶的抑制作用为竞争性抑制.结论:提示SA可影响宿主红细胞膜的离子转运及膜的功能. 相似文献
17.
本文对夹竹桃甙抑制Na~+、K~+-ATP酶的动力学作了探讨,并与乌本甙的作用进行了比较。结果表明:夹竹桃甙抑制Na~+、K~+-ATP酶,在Na~+、K~+浓度改变对均为非竞争性抑制,Na~+/K~+比例6:1时,为混合性抑制,而ATP对夹竹桃甙的作用几无影响。 相似文献
18.
《Journal of molecular neuroscience : MN》1996,29(1):67-78
We studied the activity and kinetic parameters of synaptosomal Na, K-ATPase during 15 min of forebrain ischemia and following
60 min of reperfusion produced by reversible common carotid occlusion in Mongolian gerbils. A synaptosomal fraction was obtained
by both differential centrifugation of brain tissue homogenate and centrifugation of crude mitochondrial fraction at a discontinual
sucrose density gradient. We found two components of ATP concentration dependence of ATP hydrolysis that represent two types
of ATP-binding sites: high affinity and low affinity. Neither ischemia nor reperfusion affected kinetic parameters of a high-affinity
site. However, lowaffinity site parameters were affected by both ischemia and ischemia followed by reperfusion. Maximal velocity
(V
max) decreased by 43 and 42% after ischemia and after ischemia/reperfusion, respectively. The apparentK
m for ATP decreased by 52% after ischemia and by 47% after ischemia/reperfusion. The apparent affinities for K+ and Na+ were determined from the ATP hydrolysis rate as a function of Na+ and K+ concentrations. We found the half-maximal activation constant for K+ (K
a
K+) increased by 60% after ischemia and by 146% after ischemia/reperfusion. On the other hand, we found thatK
aNa+ decreased significantly after ischemia/reperfusion (16%). We concluded that it is the dephosphorylation step of the ATPase
reation cycle that is primarily affected by both ischemia and ischemia/reperfusion. This might be caused by alteration of
the protein molecule and/or its surroundings subsequent to ischemia. 相似文献
19.
P Darwin Bell Jean-Yves Lapointe 《Clinical and experimental pharmacology & physiology》1997,24(7):541-547
1. Macula densa (MD) cells are located within the thick ascending limb (TAL) and have their apical surface in contact with tubular fluid and their basilar region in contact with the glomerulus. These cells sense changes in luminal fluid sodium chloride concentration ([NaCl]) and transmit signals resulting in changes in vascular resistance (tubuloglomerular feedback) and renin release. 2. Current efforts have focused on understanding the cellular transport mechanisms of MD cells. Progress in this area has benefited from the use of the isolated perfused TAL-glomerular preparation, which permits direct access to MD cells. 3. Using microelectrodes to measure basolateral membrane potential (VBL) of MD cells, it was found that VBL was very sensitive to changes in luminal fluid [NaCl]. As [NaCl] was elevated from 20 to 150mmol/L, VBL was found to depolarize by over 30 mV. 4. Basolateral membrane potential measurements were also used to identify an apical Na+: 2CI?: K+ cotransport pathway in MD cells that is the major pathway for NaCl entry into these cells. 5. Other work identified a basolateral chloride channel that is presumed to be responsible for changes in VBL during alterations in luminal [NaCl]. This channel, which is the predominant conductance across the basolateral membrane, may be regulated by intracellular Ca2+ and cAMP. 6. An apical Na+: H+ exchanger in MD cells was detected by measuring changes in intracellular pH using the fluorescent probe 2′,7′-bis-(2-carboxyethyl)-5(and-6) carboxyfluorescein. 7. Using patch-clamp techniques, a high density of pH- and Ca2+-sensitive K+ channels was observed at the apical membrane of MD cells. 8. Other studies found that, at the normal physiological conditions prevailing at the end of the TAL (luminal [NaCl] of 20–60 mmol/L), reabsorption mediated by MD cells is very sensitive to changes in luminal [NaCl]. 相似文献
20.
We have previously established a cell damage model, with damage induced by either acid or pepsin treatment for 30 min, involving a rat gastric epithelial cell line (RGM1). In the present study, pretreatment of cells with epidermal growth factor (EGF; 0.1–10ng/mL) or sucralfate (0.1–3 mg/mL) for 4 h prevented such cell damage in a concentration-dependent manner. Protection of cells by these drugs was not affected by pretreatment with indomethacin (10−5 mol/L) for 4 h. Removal of Na− , but not Ca2+ , from the acidified medium totally abolished the inhibitory effect of EGF, but not that of sucralfate. Genistein (a tyrosine kinase inhibitor) apparently reduced the inhibitory effect of EGF. DNA synthesis by RGM1 cells did not increase when cells were incubated with EGF for 4 h. We conclude that both EGF and sucralfate protect RGM1 cells from acid- and pepsin-induced damage and that the mechanism of protection by EGF against acid-induced damage seems to be via activation of Na+ /H+ exchangers. 相似文献