product name Nifedipine
Description: Nifedipine is a dihydropyridine calcium channel blocker, used to lower hypertension and to treat angina. It targets L-type voltage-sensitive calcium channels. Nifedipine is a vasodilator that is selective for inotropic over chronotropic cardiac effects. Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family.
References: J Pharmacol Exp Ther. 2000 Feb;292(2):606-9; Br J Pharmacol. 2000 Dec;131(8):1521-30.
346.33
Formula
C17H18N2O6
CAS No.
21829-25-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 69 mg/mL (199.2 mM)
Water: <1 mg/mL
Ethanol: 15 mg/mL (43.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403898
| In Vitro |
In vitro activity: Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family. Nifedipine dose-dependently decreases the values of [(3)H]-thymidine incorporation and total cellular protein content as well as the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) 1/2, mitogen-activated protein kinase kinase (MEK) 1/2, and even the phosphorylation of Pyk2, in vascular smooth muscle cells (VSMC). Nifedipine suppresses the levels of proliferative cell nuclear antigen (PCNA) dose-dependently in both VSMC and balloon-injured thoracic aortae in VSMC. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Nifedipine (3 mg/kg) slightly lowers the level of systolic and/or diastolic blood pressure or increased the heart rate in rats. Nifedipine (1 μm) produces a maximal inhibition of the store-operated pathway in choroidal arteriolar smooth muscle. Nifedipine (20 and 40 mg/kg) markedly prevents the HCl plus ethanol-induced gastric mucosal injury and the increase in the content of thiobarbituric acid-reactive substances in the injured mucosa in rats. Nifedipine (20 and 40 mg/kg) dose-dependently promotes the ulcer healing and inhibites the increase in the content of thiobarbituric acid-reactive substances in the ulcerated mucosa in rats. |
| Animal model | |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 2000 Feb;292(2):606-9; Br J Pharmacol. 2000 Dec;131(8):1521-30. |
Related Posts
product name Nifedipine
Description: Nifedipine is a dihydropyridine calcium channel blocker, used to lower hypertension and to treat angina. It targets L-type voltage-sensitive calcium channels. Nifedipine is a vasodilator that is selective for inotropic over chronotropic cardiac effects. Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family.
References: J Pharmacol Exp Ther. 2000 Feb;292(2):606-9; Br J Pharmacol. 2000 Dec;131(8):1521-30.
346.33
Formula
C17H18N2O6
CAS No.
21829-25-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 69 mg/mL (199.2 mM)
Water: <1 mg/mL
Ethanol: 15 mg/mL (43.3 mM)
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403898
| In Vitro |
In vitro activity: Nifedipine causes a significant concentration-dependent increase in eNOS protein expression by cultured human coronary artery endothelial cells. Nifedipine antagonizes L-type Ca+ channels found throughout the cardiovascular system, but also blocks Kv channels, which are members of the same supergene family. Nifedipine dose-dependently decreases the values of [(3)H]-thymidine incorporation and total cellular protein content as well as the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) 1/2, mitogen-activated protein kinase kinase (MEK) 1/2, and even the phosphorylation of Pyk2, in vascular smooth muscle cells (VSMC). Nifedipine suppresses the levels of proliferative cell nuclear antigen (PCNA) dose-dependently in both VSMC and balloon-injured thoracic aortae in VSMC. Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Nifedipine (3 mg/kg) slightly lowers the level of systolic and/or diastolic blood pressure or increased the heart rate in rats. Nifedipine (1 μm) produces a maximal inhibition of the store-operated pathway in choroidal arteriolar smooth muscle. Nifedipine (20 and 40 mg/kg) markedly prevents the HCl plus ethanol-induced gastric mucosal injury and the increase in the content of thiobarbituric acid-reactive substances in the injured mucosa in rats. Nifedipine (20 and 40 mg/kg) dose-dependently promotes the ulcer healing and inhibites the increase in the content of thiobarbituric acid-reactive substances in the ulcerated mucosa in rats. |
| Animal model | |
| Formulation & Dosage | |
| References | J Pharmacol Exp Ther. 2000 Feb;292(2):606-9; Br J Pharmacol. 2000 Dec;131(8):1521-30. |