Disease relevance of Lopac-D-8190

• Dichlorobenzamil inhibits stimulated bone resorption in vitro [1].
• The addition of 3',4'-dichlorobenzamil hydrochloride, an inhibitor of the Na+/Ca2+ exchanger (NCX), prevented the increase of eNOS activity with alkalosis [2].
• Contracture developed with 3',4'-dichlorobenzamil [3].
• Dichlorobenzamil (DCB), the most specific inhibitor of Na(+)-Ca2+ exchanger, infused for 10 min before induction of ischemia in a dose of 10(-5) M, which produced a definite suppression of CMF (over 80%), inhibited the accumulation of Ca2+ and Na+ and the loss of K+ and ATP after 40 min-ischemia and reperfusion [4].
• With external Ca2+ absent, LNNA pretreatment further reduced [Ca2+]i in unheated cells, and heating failed to enhance [Ca2+]i. We determined (with external Ca2+ present) that the heat-stress induced increase in [Ca2+]i in T84 cells was blocked by dichlorobenzamil, a Na+/Ca2+ exchanger inhibitor, suggesting that the exchanger mediates Ca2+ entry [5].

High impact information on Lopac-D-8190

• 3',4'- Dichlorobenzamil ( DCB ) is one of the most active inhibitors (IC50 = 17 microM) [6].
• Interpretation of mechanical responses elicited by paired pulses suggests that 40 microM but not 100 microM DCB decreases release of Ca2+ from the sarcoplasmic reticulum [6].
• In electrically stimulated papillary muscles isolated from guinea pig heart, 10-40 microM DCB decreases contractile force [6].
• In the present study, employing two unrelated Na+/Ca2+ exchange inhibitors, 3',4'-dichlorobenzamil (DCB) and bepridil, we investigated the role of NCX in platelet activation induced by various agonists in detail [7].
• This effect was abolished by inhibitors of the plasmalemmal Na(+)/Ca(2+) exchanger (dichlorobenzamil) and the SGLT-1 (phlorizin), which was found to be expressed in aortic and coronary endothelium [8].

Chemical compound and disease context of Lopac-D-8190

• Myocardial Na+ during ischemia and accumulation of Ca2+ after reperfusion: a study with monensin and dichlorobenzamil [4].
• Nifedipine (5 x 10(-7) M) or dichlorobenzamil (3 x 10(-5) M), however, did not affect the magnesium-deficiency related relaxations [9].

Biological context of Lopac-D-8190

• 5. The amiloride derivative 3',4'-dichlorobenzamil potently suppressed the photocurrent (K1/2 approximately 5 microM), without affecting its kinetics or operating range [10].
• Similar inhibition, as well as reversal, of magnesium deficiency-induced vasorelaxation was also observed with dichlorobenzamil, a known inhibitor of the Na+/Ca++ exchange mechanism, but not with nifedipine, a known inhibitor of the voltage-operated calcium channel [11].
• 3',4'-Dichlorobenzamil inhibited with the same potency Na-K-ATPase, sarcotubular Ca-ATPase, Na-Ca-exchange carrier, cAMP-dependent phosphodiesterase isolated from bovine heart and oxidative phosphorylation of mitochondria isolated from rat liver [3].

Anatomical context of Lopac-D-8190

• Here, we report that a derivative of amiloride, 3',4'-dichlorobenzamil (DCPA), completely suppresses the dark current and light response recorded from rod photoreceptors [12].
• Dialysis of the cytosol with 3',4'-dichlorobenzamil, an organic inhibitor of the Na-Ca exchange, increased the magnitude of Icont and changed the voltage dependence, consistent with a parallel shift of the charge/voltage curve [13].
• Inhibition of Na/Ca exchange in pancreatic islet cells by 3',4'-dichlorobenzamil [14].
• 3,4 dichlorobenzamil-sensitive, monovalent cation channel induced by palytoxin in cultured aortic myocytes [15].
• It is concluded that 3',4'-dichlorobenzamil is a potent inhibitor of the process of Na/Ca exchange in the pancreatic B cell [14].

Associations of Lopac-D-8190 with other chemical compounds

• 1. In electrically driven guinea pig left atria, micromolar concentrations (2 mumol/l to 80 mumol/l) of N-chlorobenzyl derivatives of amiloride (o-chlorobenzamil and 3',4'-dichlorobenzamil) produced quantitatively similar positive inotropic effects [3].
• The role of the Na+/Ca2+ exchanger was studied using dichlorobenzamil (DCB, 50 microM) and quinacrine (1 mM), inhibitors of this exchanger [16].
• 1. We studied the effect of verapamil, nitrendipine, 3',4'-dichlorobenzamil (DCB) and Cd2+ on the increase in cytosolic free Ca2+ ([Ca2+]c) and the rate of O2-uptake induced by depolarization of isolated rat cardiac myocytes with veratridine [17].

Gene context of Lopac-D-8190

• There was a dramatic reduction of bone resorption following NCX-1 inhibition by dichlorobenzamil and XIP (but not with S-XIP) [18].
• Inhibition of Na(+)-Ca2+ exchange by dichlorobenzamil prevented the effects of EGF [19].
• Dichlorobenzamil, an inhibitor of the Na(+)-Ca2+ exchanger, tended to block the neurite stabilizing effect of gangliosides, suggesting that the mechanism might involve potentiation of this antiporter [20].
• Blockade of endothelin-induced contractions by dichlorobenzamil: mechanism of action [21].
• Dichlorobenzamil significantly ameliorated reoxygenation-induced Ca overload, as did catalase and superoxide dismutase [22].

Analytical, diagnostic and therapeutic context of Lopac-D-8190

• The DHPG current was potentiated in a Ca2+-free external solution and was diminished by intracellular dialysis with BAPTA and by perfusion with Na+-Ca2+ exchanger blockers, KB-R7943 or 3',4'-dichlorobenzamil [23].

References