Pub Date : 1995-06-01DOI: 10.1152/AJPCELL.1996.270.6.1-A
A. G. Prat, Yong‐Fu Xiao, D. Ausiello, H. Cantiello
Protein kinase A (PKA)-activation of epithelial Na+ channels requires actin filaments. Mouse mammary adenocarcinoma cells expressing the human cystic fibrosis transmembrane conductance regulator (CFTR) or mock transfectants were used to determine whether CFTR is also modulated by the actin cytoskeleton. The actin filament disrupter cytochalasin D (CD; approximately 5 micrograms/ml) readily activated whole cell currents in CFTR but not in mock-transfected (MOCK) cells. Addition of actin to the cytosolic side of quiescent excised inside-out patches of CFTR but not MOCK cells also activated CFTR. The actin-activated Cl- channels (symmetrical Cl-) had a linear conductance of 9.3 pS and were inhibited by diphenylamine-2-carboxylate and monoclonal antibodies raised against CFTR. Channel activity was also blocked by addition of the actin-binding proteins deoxyribonuclease I and filamin. Incubation of CFTR cells with CD (approximately 15 micrograms/ml) for > 6 h prevented CFTR activation by the addition of either 8-bromoadenosine 3',5'-cyclic monophosphate plus forskolin under whole cell conditions or PKA under excised inside-out conditions. However, CFTR activation was restored by subsequent addition of actin. The data indicate that CFTR is regulated by actin filaments whose effect may, in turn, be associated with the PKA-dependent pathway.
{"title":"cAMP-independent regulation of CFTR by the actin cytoskeleton.","authors":"A. G. Prat, Yong‐Fu Xiao, D. Ausiello, H. Cantiello","doi":"10.1152/AJPCELL.1996.270.6.1-A","DOIUrl":"https://doi.org/10.1152/AJPCELL.1996.270.6.1-A","url":null,"abstract":"Protein kinase A (PKA)-activation of epithelial Na+ channels requires actin filaments. Mouse mammary adenocarcinoma cells expressing the human cystic fibrosis transmembrane conductance regulator (CFTR) or mock transfectants were used to determine whether CFTR is also modulated by the actin cytoskeleton. The actin filament disrupter cytochalasin D (CD; approximately 5 micrograms/ml) readily activated whole cell currents in CFTR but not in mock-transfected (MOCK) cells. Addition of actin to the cytosolic side of quiescent excised inside-out patches of CFTR but not MOCK cells also activated CFTR. The actin-activated Cl- channels (symmetrical Cl-) had a linear conductance of 9.3 pS and were inhibited by diphenylamine-2-carboxylate and monoclonal antibodies raised against CFTR. Channel activity was also blocked by addition of the actin-binding proteins deoxyribonuclease I and filamin. Incubation of CFTR cells with CD (approximately 15 micrograms/ml) for > 6 h prevented CFTR activation by the addition of either 8-bromoadenosine 3',5'-cyclic monophosphate plus forskolin under whole cell conditions or PKA under excised inside-out conditions. However, CFTR activation was restored by subsequent addition of actin. The data indicate that CFTR is regulated by actin filaments whose effect may, in turn, be associated with the PKA-dependent pathway.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"100 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120813354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-04-01DOI: 10.1016/0016-5085(95)28828-7
M. Nathanson, K. Mariwalla
{"title":"Characterization and function of ATP receptors on hepatocytes from the little skate Raja erinacea.","authors":"M. Nathanson, K. Mariwalla","doi":"10.1016/0016-5085(95)28828-7","DOIUrl":"https://doi.org/10.1016/0016-5085(95)28828-7","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116070791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-04-01DOI: 10.1016/0016-5085(95)29112-1
T. Yamada, M. Hoshino, T. Hayakawa, Y. Kamiya, H. Ohhara, K. Mizuno, H. Yamada, T. Nakazawa, T. Inagaki, A. Uchida, M. Miyaji, T. Takeuchi
{"title":"Bile secretion in rats with indomethacin-induced intestinal inflammation.","authors":"T. Yamada, M. Hoshino, T. Hayakawa, Y. Kamiya, H. Ohhara, K. Mizuno, H. Yamada, T. Nakazawa, T. Inagaki, A. Uchida, M. Miyaji, T. Takeuchi","doi":"10.1016/0016-5085(95)29112-1","DOIUrl":"https://doi.org/10.1016/0016-5085(95)29112-1","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"270 5 Pt 1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130844045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-03-01DOI: 10.1016/0006-355X(95)92146-2
K. Gooch, J. Frangos
{"title":"Flow- and bradykinin-induced nitric oxide production by endothelial cells is independent of membrane potential.","authors":"K. Gooch, J. Frangos","doi":"10.1016/0006-355X(95)92146-2","DOIUrl":"https://doi.org/10.1016/0006-355X(95)92146-2","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"122 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129501668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-02-01DOI: 10.1016/0300-9572(96)83749-X
W. Karzai, J. M. Reilly, W. Hoffman, R. Cunnion, R. Danner, S. Banks, J. Parrillo, C. Natanson
{"title":"Hemodynamic effects of dopamine, norepinephrine, and fluids in a dog model of sepsis.","authors":"W. Karzai, J. M. Reilly, W. Hoffman, R. Cunnion, R. Danner, S. Banks, J. Parrillo, C. Natanson","doi":"10.1016/0300-9572(96)83749-X","DOIUrl":"https://doi.org/10.1016/0300-9572(96)83749-X","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"110 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127984908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1995-02-01DOI: 10.1016/0735-1097(95)92233-U
T. Morioka, M. Kitakaze, T. Minamino, S. Takashima, K. Node, Y. Okazaki, H. Sato, Y. Shinozaki, M. Chujo, H. Mori
{"title":"Downward shift of coronary pressure-flow relationship following a brief period of ischemia in dogs.","authors":"T. Morioka, M. Kitakaze, T. Minamino, S. Takashima, K. Node, Y. Okazaki, H. Sato, Y. Shinozaki, M. Chujo, H. Mori","doi":"10.1016/0735-1097(95)92233-U","DOIUrl":"https://doi.org/10.1016/0735-1097(95)92233-U","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"41 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1995-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115173936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-12-01DOI: 10.1097/00024382-199512001-00093
S. Tsuchida, M. Hiraoka, M. Sudo, S. Kigoshi, I. Muramatsu
We investigated the effects of prolonged treatment with Escherichia coli lipopolysaccharide (LPS) on the responses to sodium nitroprusside (SNP) in endothelium-denuded rat aortic strips. Incubation of the aortic strips with LPS for 24 h dramatically attenuated relaxation and guanosine 3',5'-cyclic monophosphate (cGMP) formation by SNP, which were significantly restored by the inhibition of nitric oxide (NO) production with N omega-nitro-L-arginine. In the aorta coincubated with LPS and protein synthesis inhibitor (dexamethasone or cycloheximide, which prevents induction of endotoxin-inducible NO synthase), no attenuation of the relaxation was observed and the cGMP formation was significantly restored. Relaxation response to 8-bromo-cGMP or papaverine was not attenuated, even after 24 h of incubation. These results suggest that the attenuation of SNP responses is mainly associated with a decrease in the activation of guanylate cyclase (GC) as a consequence of the prolonged exposure to muscle-derived NO. Moreover SNP in the presence of methylene blue evoked a small but apparent relaxation of 24-h-incubated aorta without significant elevation of cGMP, suggesting the involvement of cGMP-independent pathways in the remaining relaxation produced by SNP.
我们研究了大肠杆菌脂多糖(LPS)长期治疗对去内皮大鼠主动脉条带对硝普钠(SNP)反应的影响。用LPS孵育主动脉条带24小时后，SNP可显著减弱松弛和鸟苷3′，5′-环单磷酸(cGMP)的形成，而N - omega-硝基- l -精氨酸抑制一氧化氮(NO)的产生可显著恢复cGMP。在与LPS和蛋白质合成抑制剂(地塞米松或环己亚胺，阻止内毒素诱导的NO合成酶的诱导)共孵生的主动脉中，未观察到松弛的衰减，cGMP的形成明显恢复。8-溴- cgmp或罂粟碱的松弛反应即使在24小时后也没有减弱。这些结果表明，SNP反应的衰减主要与鸟苷酸环化酶(GC)激活的减少有关，这是长期暴露于肌肉来源的NO的结果。此外，在亚甲基蓝存在的情况下，SNP引起了24小时培养主动脉的小而明显的松弛，但没有显著的cGMP升高，这表明cGMP无关的途径参与了SNP产生的剩余松弛。
{"title":"Attenuation of sodium nitroprusside responses after prolonged incubation of rat aorta with endotoxin.","authors":"S. Tsuchida, M. Hiraoka, M. Sudo, S. Kigoshi, I. Muramatsu","doi":"10.1097/00024382-199512001-00093","DOIUrl":"https://doi.org/10.1097/00024382-199512001-00093","url":null,"abstract":"We investigated the effects of prolonged treatment with Escherichia coli lipopolysaccharide (LPS) on the responses to sodium nitroprusside (SNP) in endothelium-denuded rat aortic strips. Incubation of the aortic strips with LPS for 24 h dramatically attenuated relaxation and guanosine 3',5'-cyclic monophosphate (cGMP) formation by SNP, which were significantly restored by the inhibition of nitric oxide (NO) production with N omega-nitro-L-arginine. In the aorta coincubated with LPS and protein synthesis inhibitor (dexamethasone or cycloheximide, which prevents induction of endotoxin-inducible NO synthase), no attenuation of the relaxation was observed and the cGMP formation was significantly restored. Relaxation response to 8-bromo-cGMP or papaverine was not attenuated, even after 24 h of incubation. These results suggest that the attenuation of SNP responses is mainly associated with a decrease in the activation of guanylate cyclase (GC) as a consequence of the prolonged exposure to muscle-derived NO. Moreover SNP in the presence of methylene blue evoked a small but apparent relaxation of 24-h-incubated aorta without significant elevation of cGMP, suggesting the involvement of cGMP-independent pathways in the remaining relaxation produced by SNP.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1994-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124656321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-11-01DOI: 10.1016/0928-4680(94)90843-5
T. Shibamoto, T. Hayashi, F. Sawano, Y. Saeki, Y. Matsuda, M. Kawamoto, S. Koyama
{"title":"Pulmonary vascular response to anaphylaxis in isolated canine lungs.","authors":"T. Shibamoto, T. Hayashi, F. Sawano, Y. Saeki, Y. Matsuda, M. Kawamoto, S. Koyama","doi":"10.1016/0928-4680(94)90843-5","DOIUrl":"https://doi.org/10.1016/0928-4680(94)90843-5","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"29 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128714017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-11-01DOI: 10.1016/0928-4680(94)90572-X
A. Yamauchi, A. Miyai, K. Yokoyama, T. Itoh, T. Kamada, N. Ueda, Y. Fujiwara
{"title":"Response to osmotic stimuli in mesangial cells: role of system A transporter.","authors":"A. Yamauchi, A. Miyai, K. Yokoyama, T. Itoh, T. Kamada, N. Ueda, Y. Fujiwara","doi":"10.1016/0928-4680(94)90572-X","DOIUrl":"https://doi.org/10.1016/0928-4680(94)90572-X","url":null,"abstract":"","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131574384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-05-01DOI: 10.1249/00005768-199405001-00403
L. Lamont, A. McCullough, S. Kalhan
The purpose of this study was to assess the interaction between beta-blockade and exercise on amino acid kinetics. This was a three-way crossover experiment using beta 1-blockade, beta 1,beta 2-blockade, and a placebo control. Three 6-h L-[1-13C]leucine and L-[alpha-15N]lysine infusions were performed. The first 3 h established an isotopic steady state, and 1 h of exercise (approximately 50% of maximal O2 consumption) and 2 h of recovery followed. Plasma glucose decreased with exercise during all trials (P < 0.0001). During beta 1- and beta 1,beta 2-blockade, plasma free fatty acids were reduced during rest and exercise (P < 0.001). Leucine and lysine rates of appearance were unaffected by beta-blockade during rest but were decreased with placebo exercise. Leucine oxidation increased with beta-blockade (P < 0.01) and exercise (P < 0.001). There was a statistical interaction between both treatments (P < 0.004). In conclusion, leucine oxidation increased with exercise, further increased with beta 1-blockade, and was additionally heightened with beta 1,beta 2-blockade. This cumulative response indicates that leucine oxidation was regulated through beta 1- and beta 2-receptors.
{"title":"Beta-adrenergic blockade heightens the exercise-induced increase in leucine oxidation.","authors":"L. Lamont, A. McCullough, S. Kalhan","doi":"10.1249/00005768-199405001-00403","DOIUrl":"https://doi.org/10.1249/00005768-199405001-00403","url":null,"abstract":"The purpose of this study was to assess the interaction between beta-blockade and exercise on amino acid kinetics. This was a three-way crossover experiment using beta 1-blockade, beta 1,beta 2-blockade, and a placebo control. Three 6-h L-[1-13C]leucine and L-[alpha-15N]lysine infusions were performed. The first 3 h established an isotopic steady state, and 1 h of exercise (approximately 50% of maximal O2 consumption) and 2 h of recovery followed. Plasma glucose decreased with exercise during all trials (P < 0.0001). During beta 1- and beta 1,beta 2-blockade, plasma free fatty acids were reduced during rest and exercise (P < 0.001). Leucine and lysine rates of appearance were unaffected by beta-blockade during rest but were decreased with placebo exercise. Leucine oxidation increased with beta-blockade (P < 0.01) and exercise (P < 0.001). There was a statistical interaction between both treatments (P < 0.004). In conclusion, leucine oxidation increased with exercise, further increased with beta 1-blockade, and was additionally heightened with beta 1,beta 2-blockade. This cumulative response indicates that leucine oxidation was regulated through beta 1- and beta 2-receptors.","PeriodicalId":125752,"journal":{"name":"The American journal of physiology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"1994-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129988080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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