165 blocker  (Vector Laboratories)

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on cytosolic Ca 2+ in H9C2 in nonperoxidative conditions. (a) Dose-response and time-course study. The results are the mean ± standard deviation of 5 experiments. (b) An example taken from one experiment

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques: Standard Deviation

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on cytosolic Ca 2+ in H9C2 in the presence or absence of various agents in nonperoxidative conditions. (a-d) A = 2 min asenapine (10 μM). (a and c) C = Basal. (a and b) EGTA = Ethylene glycol tetraacetic acid 50 mM; A23 = A23187 (1 μM); H89 = H89 (1 μM); KN93 = KN93 (1 μM); U73 = U73122 (1 μM); L-NAME = Nω-nitro-L-arginine methyl ester (10 mM). The results are the mean ± standard deviation of five experiments for each experimental protocol. (b and d) The effects of asenapine on Ca 2+ in comparison to basal values are reported as %. (a) b, c, e, P < 0.05 versus a; d, f, h, l, n, P P < 0.05 versus b. (b) c, b, d, e, f, g P < 0.05 versus a. (c and d) Amlodip = Amlodipine (1 μM); ML218 = ML218 (1 μM); propionyl = Propionyl promazine (1 μM); Nefaz = Nefazodone (1 μM); NAD = NAD-299 (1 μM). (c) b P < 0.05 versus a; d, f, h, l, n P < 0.05 versus b. (d) b, c, d, e, f P < 0.05 versus a. One-way ANOVA followed by Newman–Keuls post hoc test

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques: Standard Deviation

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on cytosolic Ca 2+ in H9C2 in presence or absence of Ca 2+ chelator and Ca 2+ ionophor, intracellular signaling pathways, and nitric oxide synthase inhibitors in nonperoxidative conditions. An example of each experimental protocol is shown. (a) 2 min asenapine (A) with Ca 2+ chelator, ethylene glycol tetraacetic acid; (b) with Ca 2+ ionophor A23187; (c) with PKA inhibitor, H89; (d) with PLC inhibitor, U73122 (U73); (e) with CaMKII inhibitor, KN93; (f), with nitric oxide synthase inhibitor, Nω-nitro-L-arginine methyl ester. The layout is the same as in

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques:

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on cytosolic Ca 2+ in H9C2 in the presence or absence of serotoninergic and dopaminergic receptor blockers and L- and T-type Ca 2+ channels inhibitors. An example of each experimental protocol is shown. (a) 2 min asenapine (A) with 5-HT 1A inhibitor, NAD-299 (NAD); (b) with L type Ca 2+ channel blocker, amlodipine (Amlod); (c) with T type Ca 2+ channel blocker, ML218; (d) with D2 receptor inhibitor, propionyl promazine (Propionyl); (e) with 5-HT 2A inhibitor, nefazodone (Nefaz). The layout is the same as in

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques:

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on ATP and thapsigargin-dependent Ca 2+ pools in H9C2. The results are the mean ± standard deviation of five experiments for each experimental protocol. C = Basal. (a) asenapine (A) was administrated either before or after ATP. c, b P < 0.05 versus a; e, f P < 0.05 versus d. (b) Asenapine was administrated alone or after 1 min thapsigargin (Tapsi) administration. The effects of thapsigargin alone and after 1 min and 3 min (alone or with asenapine) are shown. b, c, d, e, f P < 0.05 versus a; c, e P < 0.05 versus b; f P < 0.05 versus d. One-way ANOVA followed by Newman–Keuls post hoc test

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques: Standard Deviation

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on ATP and thapsigargin-dependent Ca 2+ pools in H9C2. An example of each experimental protocol is shown. (a and b) Asenapine was given before and after ATP. (c) Asenapine was given alone or in co-administration with thapsigargin. The layout is the same as in

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques:

Journal: Journal of Pharmacology & Pharmacotherapeutics

Article Title: Asenapine modulates nitric oxide release and calcium movements in cardiomyoblasts

doi: 10.4103/0976-500X.179358

Figure Lengend Snippet: Effects of asenapine on cytosolic Ca 2+ in H9C2 in peroxidative conditions. (a) Dose-response and time-course study. The results are the mean ± standard deviation of five experiments. (b) An example taken from one experiment. (c) Effects of asenapine on Ca 2+ in the presence or absence of various blockers. C = Basal; A = Asenapine; Nefaz = Nefazodone (1 μM); propionyl = Propionyl promazine (1 μM); NAD = NAD-299 (1 μM); amlodip = Amlodipine (1 μM); ML218 = ML218 (1 μM); L-NAME = Nω-nitro-L-arginine methyl ester (10 mM). The results are the mean ± standard deviation of five experiments for each experimental protocol. (c) b, d, e P < 0.05 versus a; c, d, e, f, g, h P < 0.05 versus b. One-way ANOVA followed by Newman–Keuls post hoc test

Article Snippet: In addition, in other samples, asenapine was given alone or in presence of the adenylyl cyclase blocker 2'5'-dideoxyadenosine (1 μM; Sigma; 15 min), the selective cAMP-dependent PKA inhibitor, H89 (1 μM; Sigma; 15 min), the PLC γ inhibitor, U73122 (1 µM, sigma; 15 min), the Ca 2+ -calmodulin protein kinase (CaMKII) inhibitor, KN93 (1 µM; sigma; 15 min), the L-type Ca 2+ channel blocker, amlodipine (1 μM, Santa Cruz Biotechnology; Dallas, USA; 15 min), the T-type Ca 2+ channel blocker, ML218 (1 μM, Alomone Labs, Jerusalem, Israel; 15 min), the selective 5-HT 1A antagonist, NAD-299 hydrochloride (1 μM, Tocris Bioscience, Bristol, United Kingdom; 15 min), the selective 5-HT 2A antagonist, nefazodone hydrochloride (1 μM, Tocris Bioscience; 15 min), the selective D 2 receptor antagonist, propionylpromazine hydrochloride (1 μM, Tocris Bioscience; 15 min), or the NOS blocker, Nω-nitro-L-arginine methyl ester (L-NAME; 10 mM; sigma; 15 min).

Techniques: Standard Deviation