PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7905278-3 1994 IFN-gamma caused a rapid concentration-dependent rise in [Ca2+]i, which was partly inhibited by diltiazem, a calcium channel blocker, TMB-8, an inhibitor of intracellular calcium redistribution, and in calcium-free medium. Diltiazem 96-105 carbonic anhydrase 2 Homo sapiens 58-61 27751805-0 2017 Effect of Ca+2 ion on the release of diltiazem hydrochloride from matrix tablets of carboxymethyl xanthan gum graft polyacrylamide. Diltiazem 37-60 carbonic anhydrase 2 Homo sapiens 10-14 16581067-3 2006 The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem. Diltiazem 135-144 carbonic anhydrase 2 Homo sapiens 23-26 16581067-3 2006 The maitotoxin-induced Ca2+ influx was suppressed by various voltage-dependent Ca2+ channel blockers such as Co2+, Mn2+, verapamil and diltiazem. Diltiazem 135-144 carbonic anhydrase 2 Homo sapiens 79-82 14600078-5 2003 Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%. Diltiazem 36-45 carbonic anhydrase 2 Homo sapiens 0-3 14600078-5 2003 Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%. Diltiazem 36-45 carbonic anhydrase 2 Homo sapiens 95-98 7516710-6 1994 Ca2+ efflux was induced by Na+, Li+ and K+ through a diltiazem-insensitive reaction. Diltiazem 53-62 carbonic anhydrase 2 Homo sapiens 0-3 9049653-9 1997 The increase in cytosolic Ca2+ concentration occurred via the influx of extracellular Ca2+ independent of L-type Ca2+ channels blocked by verapamil or diltiazem. Diltiazem 151-160 carbonic anhydrase 2 Homo sapiens 26-29 2257435-2 1990 Using front-surface fluorometry with fura-2-loaded porcine coronary arterial strips, we simultaneously measured effects of a Ca2+ antagonist, diltiazem, on cytosolic Ca2+ concentrations [( Ca2+]i) and on tension development. Diltiazem 142-151 carbonic anhydrase 2 Homo sapiens 125-128 1507210-0 1992 Synthesis, characterization, and Ca2+ antagonistic activity of diltiazem metabolites. Diltiazem 63-72 carbonic anhydrase 2 Homo sapiens 33-36 2148481-2 1990 Verapamil and diltiazem (0.01 to 5 mM) inhibited both (Ca2+ + Mg2+)-ATPase activity and initial rates of 45Ca2+ net uptake analogously. Diltiazem 14-23 carbonic anhydrase 2 Homo sapiens 55-58 2148481-5 1990 Verapamil and diltiazem inhibited the calmodulin-Ca2+ transport concentration-effect relationship by changing its apparent affinity as well as the maximal velocity of the process. Diltiazem 14-23 carbonic anhydrase 2 Homo sapiens 49-52 2148481-8 1990 Our results suggest that verapamil, diltiazem and bepridil (0.01 to 0.3 mM), but not nifedipine (1 nM to 0.01 mM), in relatively high concentrations can antagonize the calmodulin-stimulated Ca2(+)-pump, i.e. the ATPase as well as the transport process. Diltiazem 36-45 carbonic anhydrase 2 Homo sapiens 190-193 2257435-8 1990 Diltiazem, 10(-8)M to 10(-5)M, concentration-dependently inhibited the second component of [Ca2+]i elevation and tension development induced by histamine (10(-5) M). Diltiazem 0-9 carbonic anhydrase 2 Homo sapiens 92-95 2257435-9 1990 Only at higher concentrations (over 10(-5) M) did diltiazem inhibit the first component of increases in [Ca2+]i and tension development induced by histamine, both in the presence and absence of extracellular Ca2+. Diltiazem 50-59 carbonic anhydrase 2 Homo sapiens 105-108 2257435-11 1990 Diltiazem (10(-6) M) inhibited increases in [Ca2+]i and tension development induced by cumulative applications of extracellular Ca2+ during K(+)-depolarization. Diltiazem 0-9 carbonic anhydrase 2 Homo sapiens 45-48 2257435-11 1990 Diltiazem (10(-6) M) inhibited increases in [Ca2+]i and tension development induced by cumulative applications of extracellular Ca2+ during K(+)-depolarization. Diltiazem 0-9 carbonic anhydrase 2 Homo sapiens 128-131 2257435-12 1990 The curve of [Ca2+]i against tension of these Ca2(+)-induced contractions obtained in diltiazem-treated strips overlapped with that obtained in untreated strips. Diltiazem 86-95 carbonic anhydrase 2 Homo sapiens 14-17 2257435-12 1990 The curve of [Ca2+]i against tension of these Ca2(+)-induced contractions obtained in diltiazem-treated strips overlapped with that obtained in untreated strips. Diltiazem 86-95 carbonic anhydrase 2 Homo sapiens 46-49 2257435-15 1990 In contrast, the histamine-induced Ca2(+)-tension curve (second component) was shifted in parallel to the left by diltiazem. Diltiazem 114-123 carbonic anhydrase 2 Homo sapiens 35-38 2257435-17 1990 We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i. Diltiazem 17-26 carbonic anhydrase 2 Homo sapiens 95-98 2257435-17 1990 We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i. Diltiazem 17-26 carbonic anhydrase 2 Homo sapiens 125-128 2257435-17 1990 We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i. Diltiazem 17-26 carbonic anhydrase 2 Homo sapiens 125-128 2257435-17 1990 We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i. Diltiazem 17-26 carbonic anhydrase 2 Homo sapiens 125-128 2257435-17 1990 We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i. Diltiazem 17-26 carbonic anhydrase 2 Homo sapiens 125-128 2145465-7 1990 It is concluded that 1,4-dihydropyridines and verapamil and diltiazem did differently influence Ca2(+)-mediated increase in force of contraction. Diltiazem 60-69 carbonic anhydrase 2 Homo sapiens 96-99 3993799-2 1985 The Ca2+ channel antagonists, diltiazem and verapamil, competitively inhibited adenosine influx (Ki = 158 +/- 17.4 and 13.5 +/- 1.3 microM at 10 microM adenosine, respectively), despite no apparent effect on transport by Ca2+, Mg2+, Na+, or K+. Diltiazem 30-39 carbonic anhydrase 2 Homo sapiens 4-7 3993799-2 1985 The Ca2+ channel antagonists, diltiazem and verapamil, competitively inhibited adenosine influx (Ki = 158 +/- 17.4 and 13.5 +/- 1.3 microM at 10 microM adenosine, respectively), despite no apparent effect on transport by Ca2+, Mg2+, Na+, or K+. Diltiazem 30-39 carbonic anhydrase 2 Homo sapiens 221-224 7241862-4 1980 Diltiazem also depressed the Ca2+ uptake was not due to an increased permeability for Ca2+, since release of Ca2+ from the microsomes was not significantly affected by either drug. Diltiazem 0-9 carbonic anhydrase 2 Homo sapiens 29-32 7241862-5 1980 It is proposed that verapamil and diltiazem inhibit Ca2+ transport by interfering with an active process of Ca2+ accumulation in microsomes of the renal cortex. Diltiazem 34-43 carbonic anhydrase 2 Homo sapiens 52-55 7241862-5 1980 It is proposed that verapamil and diltiazem inhibit Ca2+ transport by interfering with an active process of Ca2+ accumulation in microsomes of the renal cortex. Diltiazem 34-43 carbonic anhydrase 2 Homo sapiens 108-111