Tyrosine kinase participates in vasoconstriction through a Ca(2+)- and myosin light chain phosphorylation-independent pathway.
This study was undertaken to determine the role of tyrosine kinase on intracellular Ca(2+) ([Ca(2+)](i)), myosin light chain (MLC) phosphorylation, and contraction caused by norepinephrine (NE) in rat aorta. NE induced a sustained contraction with an increase of [Ca(2+)](i). On the other hand, NE increased the phosphorylation of the 20 kDa MLC transiently. Pretreatment with genistein and tyrophostin 25, tyrosine kinase inhibitors, significantly inhibited NE-induced contraction, but did not affect the increase of [Ca(2+)](i) and MLC phosphorylation. These results suggest that tyrosine kinase may regulate the NE-mediated contraction without altering [Ca(2+)](i) and MLC phosphorylation in rat aorta.
Fang
Lian Hua
LH
Department of Pharmacology, College of Medicine, Chungbuk National University, 361-763, Cheongju, South Korea.
Kwon
Seong Chun
SC
Zhang
Yong He
YH
Ahn
Hee Yul
HY
D058646:Adrenergic alpha-1 Receptor Agonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D019833:Genistein / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D018994:Myosin Light Chains / Q000378:metabolism*; D009638:Norepinephrine / Q000494:pharmacology; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D051381:Rats; D020032:Tyrphostins / Q000494:pharmacology; D014661:Vasoconstriction / Q000502:physiology*
D058646:Adrenergic alpha-1 Receptor Agonists; D000316:Adrenergic alpha-Agonists; D018994:Myosin Light Chains; D020032:Tyrphostins; C079836:tyrphostin 25; D019833:Genistein; D011505:Protein-Tyrosine Kinases; D002118:Calcium; D009638:Norepinephrine