| There are different opinions about the effect of Lig on cardiac muscle. But the common one is that Lig brings the change of [Ca2+ ]j after using it. It is known that intracellular Ca2+ mostly comes from two ways: influx of extracellular Ca2+ and Ca2+ release from ER (Endoplasmic reticulum)/SR (Sarcoplasmic reticulum) calcium pool. Study showed that Lig reducing [Ca2+]j was related to the cell membrane Ca2+ channels. lig inhibited L-type calcium channels current in a concentration-dependent manner in the ventricular cells of guineu pigs using whole cell patch clamp technique. So Lig was named "a new calcium inhibitor".But other people think that Lig was not special calcium inhibitor but related to Ca2+ release induced by receptor.However,this mechanism is still not clear. In this experiment, we try to investigate Lig's target on cardiac muscle and its mechanism using the receptor inhibitor or activor.Physiological recoder was used to measure the contractile force (FC) and contractile ratio (V) of papillary muscles.And laser confocal microscope was used to scan the change of fluorescent intensity. Intracellular free Ca2+ concentration ([Ca2+]j) was showed by even fluorescent intensity. In this experiment,five kinds receptor inhibitor or activor were applied.They were calcium channel activor A23187,and L-type calcium channel inhibitorVer; a1-receptor inhibitor Phentolamine and a1-receptor activor Phe; B1-receptor inhibitor Ate and B1-receptor activor Dob;AT1R inhibitor Val;IP3R inhibitor Hep. The result showed:1. Lig (200μg/ml) had the negative function on FC and V.2. Lig(200 μ g/ml) decreased the effect of Phe on FC and V in cardiac muscle.3. IP3R inhibitor Hep (100 μ g/ml) prevented Lig(200 μ g/ml) from reducing FC and V,which showed that the role of Lig(200 μ g/ml) in cardiac muscle was related with IP3R.4. AT1R inhibitor Val (1 X 10-5mol/L) had no effect on Lig(200 μ g/ml) decreasing FC and V,which showed that AT1R was not a target of Lig(200 μ g/ml) in cardiac muscle.However,Val (1 X 10-5mol/L ) inhibited Lig(30 μ mol/L) debaseing [Ca2+]i , which showed that the function of Lig(30 μ mol/L) on [Ca2+]i was connectedwith AT1R.The two results were not consistent with each other.5. β1 receptor inhibitor Ate (1 X 10-6mol/L) inhibited the effect of Lig(200 μ g/ml) on FC and V.and Ate (900 μmol/L) prevented Lig(30 μ mol/L) from decreasing [Ca2+]i .That showed β1-receptor was a target of Lig(200 μ g/ml) in cardiac muscle.6. Lig (30μmol/L) decreased cell [Ca2+]i obviously in cardiac muscle of mouse.7. Lig (30 μmol/L) reduced the role of A23187 in increasing [Ca2+]; in cardiac muscle.And Val (40 μmol/L) inhibited Lig (30μmol/L) decreasing [Ca2+]i.All these showed that Lig ( 30μmol/L) decreasing (Ca2+]i was achieved by calcium channel,mainly by L-type calcium channel in cardiac muscle.8. α1-receptor inhibitor Phentolamine (1 X 105mol/L) inhibited Lig(200 μ g/ml) decreasing [Ca2+]i ,and Lig(30 μ mol/L) prevented α1 i-receptor activor Phe from increasing [Ca2+], .That showed α1-receptor was a target of Lig(200 μ g/ml) in cardiac muscle.This experiment showed that Lig decreased [Ca2+]i by inhibiting L-type calcium channel, a1-receptor and B1-receptor etc,which leaded to the decrease of FC and V.And the excitement of L-type calcium channel, a1-receptor and B1-receptor may arouse the influx of extracellular Ca2+ and Ca2+ release from SR (Sarcoplasmic reticulum) calcium pool.In cardiac muscle,a little influx of extracellular Ca2+ is the impetus of Ca2+ release from SR calcium pool.So Lig may prevent the influx of extracellular Ca2+ by debasing the excitement of L-type calcium channel, a i-receptor and Bi-receptor,which holded back the Ca2+ release from SR calcium pool As a result,reduced [Ca2+],,FC and V.At the same time.Lig could decrease [Ca2+]i by inhibiting the function of Hep on EP3R in SR.It shows that Lig also could affect calcium pool directly,decreasing [Ca2+]tBut whether ATiR is the target of Lig on cardiac mu...
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