1. Rho-kinase expression and its contribution to the control of perfusion pressure in the isolated rat mesenteric vascular bed
- Author
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Mustafa Ark, İsmail Ün, Ergin Şingirik, Ata Secilmis, Onur Arıkan, Kansu Büyükafşar, and Çukurova Üniversitesi
- Subjects
Agonist ,medicine.medical_specialty ,medicine.drug_class ,Saponin ,Vasodilation ,Biology ,In Vitro Techniques ,Protein Serine-Threonine Kinases ,Gene Expression Regulation, Enzymologic ,Mesenteric Veins ,Y-27632 ,Internal medicine ,medicine ,Pressure ,Animals ,Enzyme Inhibitors ,Rats, Wistar ,Rho-kinase ,Phenylephrine ,Pharmacology ,rho-Associated Kinases ,Dose-Response Relationship, Drug ,Endothelin-1 ,Mesenteric artery ,Fasudil ,Intracellular Signaling Peptides and Proteins ,Mesenteric Arteries ,Rats ,Perfusion ,Endocrinology ,medicine.anatomical_structure ,Vascular resistance ,Female ,medicine.symptom ,Endothelin receptor ,Vasoconstriction ,medicine.drug - Abstract
PubMedID: 14757149 Rho-kinase expression was investigated in the rat mesenteric artery and the effects of its inhibitors, (+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride monohydrate (Y-27632) and fasudil (HA-1077), were examined on the increase in perfusion pressure induced by two different receptor agonists, namely the ?-adrenoceptor agonist, phenylephrine and, the endothelin ETA and ETB receptor agonist, endothelin-1. Y-27632 and fasudil produced a concentration-dependent decrease in perfusion pressure. There was no difference between the concentration-response lines of these two inhibitors. The maximum decrease in the perfusion pressure induced by 10-5 M Y-27632 was 85.8±3. 7% when the tone was increased by phenylephrine. However, it was 48.1±5.4% (P
- Published
- 2004