scholarly journals Identification of protein kinase C isoforms in porcine coronary artery and their involvement in contractile potentiation induced by endothelin-1

1998 ◽  
Vol 76 ◽  
pp. 217
Author(s):  
Mayumi Uchino ◽  
Kazuo Obara ◽  
Masayo Koide ◽  
Yoshiyuki Tanabe ◽  
Koichi Nakayama
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Porcine Coronary Artery ◽  
Endothelin 1 ◽  
Kinase C ◽  
Protein Kinase C Isoforms

scholarly journals Contractile Potentiation by Endothelin-1 Involves Protein Kinase C-.DELTA. Activity in the Porcine Coronary Artery.

1999 ◽  
Vol 49 (2) ◽  
pp. 175-183 ◽  
Author(s):  
Kazuo OBARA ◽  
Shinzo HATA ◽  
Katsura SATO ◽  
Masayo KOIDE ◽  
Kunio ISHII ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Protein Kinase C Delta ◽  
Porcine Coronary Artery ◽  
Endothelin 1 ◽  
Kinase C ◽  
Delta Activity

scholarly journals Selective Protein Kinase C Isoforms Are Involved in Endothelin-1-Induced Human Uterine Contraction at the End of Pregnancy

2000 ◽  
Vol 63 (5) ◽  
pp. 1567-1573 ◽  
Author(s):  
Isabelle Eude ◽  
Brigitte Paris ◽  
Dominique Cabrol ◽  
Françoise Ferré ◽  
Michelle Breuiller-Fouché
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Uterine Contraction ◽  
Endothelin 1 ◽  
Kinase C ◽  
Protein Kinase C Isoforms

2-Chloroadenosine prevents phorbol ester-induced depletion of protein kinase C in porcine coronary artery

1993 ◽  
Vol 264 (5) ◽  
pp. H1465-H1471 ◽  
Author(s):  
R. B. Marala ◽  
K. Ways ◽  
S. J. Mustafa
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Chronic Exposure ◽  
Porcine Coronary Artery ◽  
Kinase C ◽  
Adenosine Analogue ◽  
Presence And Absence

In this study we investigated the role of the adenosine analogue 2-chloroadenosine (CAD) in the regulation of protein kinase C (PKC) in porcine coronary artery. Arterial rings were contracted with endothelin-1 (ET-1; 10(-10) to 10(-7) M) and phorbol 12,13-dibutyrate (PDBu; 10(-7) M) after incubating them for 1 and 2 days with PDBu (200 nM) in the presence and absence of CAD (10(-4) M). Chronic exposure to PDBu alone attenuated ET-1-induced contractions, while inclusion of CAD during incubation protected against the PDBu-induced blunting of ET-1-induced contraction. Similarly, PDBu (10(-7) M)-induced contraction of the arterial rings was attenuated upon chronic incubation with PDBu, and once again, inclusion of CAD showed an improved response to PDBu-induced contraction when compared with PDBu alone. Incubation with PDBu (200 nM) for 20 min caused the PKC translocation from cytosol to membrane, whereas CAD totally blocked this translocation. Chronic (1 and 2 days) incubation with PDBu caused a substantial depletion of PKC activities in cytosol and membrane. The presence of CAD protected the PDBu-induced depletion of PKC in both cytosol and membrane. To replete PKC, after incubation with the drugs, the arteries were incubated in the absence of drugs for another 2 days. Arteries incubated with PDBu in the presence and absence of CAD recovered significantly in their response to ET-1 as well as PDBu. These results indicate that CAD protects against the PDBu-induced activation and depletion of PKC in porcine coronary artery.

scholarly journals High glucose alters the response of mesangial cell protein kinase C isoforms to endothelin-1

1999 ◽  
Vol 55 (2) ◽  
pp. 486-499 ◽  
Author(s):  
Emily ANNE Glogowski ◽  
Evangelia Tsiani ◽  
Xiaopeng Zhou ◽  
Ivan GEORGE Fantus ◽  
Catharine Whiteside
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
High Glucose ◽  
Mesangial Cell ◽  
Cell Protein ◽  
Endothelin 1 ◽  
Kinase C ◽  
Protein Kinase C Isoforms

Inhibitory Effects of Lidocaine and Mexiletine on Vasorelaxation Mediated by Adenosine Triphosphate–sensitive K+Channels and the Role of Kinases in the Porcine Coronary Artery

2005 ◽  
Vol 102 (3) ◽  
pp. 581-587 ◽  
Author(s):  
Yoshiki Kimoto ◽  
Hiroyuki Kinoshita ◽  
Katsutoshi Nakahata ◽  
Mayuko Dojo ◽  
Yoshio Hatano
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Adenosine Triphosphate ◽  
Antiarrhythmic Drugs ◽  
K Channels ◽  
Porcine Coronary Artery ◽  
Calphostin C ◽  
Kinase C

Background Effects of antiarrhythmic drugs on coronary vasodilation mediated by K channels have not been studied. Modulator roles of protein kinase C and tyrosine kinase in the activity of K channels have also been unclear in the coronary artery. The current study examined whether lidocaine and mexiletine in the porcine coronary artery modify the vasorelaxation mediated by adenosine triphosphate-sensitive K channels via activation of protein kinase C and tyrosine kinase. Methods Porcine coronary arteries without endothelium were suspended for isometric force recording, and vasorelaxation to levcromakalim (10 to 10 m) was obtained. Changes in membrane potentials produced by levcromakalim (10 m) were also recorded. Results Glibenclamide completely abolished vasorelaxation as well as hyperpolarization in response to levcromakalim. Lidocaine and mexiletine significantly reduced these responses. Calphostin C, Go 6976, genistein, and erbstatin A partly restored vasorelaxation or hyperpolarization in response to levcromakalim in arteries treated with mexiletine but not in those with lidocaine, whereas these inhibitors did not alter the vasorelaxation to levcromakalim. Phorbol 12-myristate 13-acetate produced reduction of vasorelaxation in response to levcromakalim, which is recovered by calphostin C or Go 6976. Conclusions Therefore, lidocaine and mexiletine inhibit vasorelaxation mediated by the activation of adenosine triphosphate-sensitive K channels in the coronary artery. Protein kinase C and tyrosine kinase seem to have roles in the inhibitory effect of mexiletine but not in that of lidocaine. Class Ib antiarrhythmic drugs may reduce coronary vasodilation mediated by adenosine triphosphate-sensitive K channels via the differential modulator effects on these kinases.

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