![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
RM Johnson and TM Lincoln
The effects of nitroprusside (NP), glyceryl trinitrate (GTN), and the 8- bromo analog of cyclic GMP (8-Br-cGMP) on norepinephrine (NE)- stimulated phosphorylase a formation and myosin light chain (MLC) phosphorylation were examined in the rat aorta. NE produced a time- dependent increase in tension, phosphorylase a formation, and MLC phosphorylation. The formation of phosphorylase a and phosphorylation of MLC were transient, since both processes declined to basal levels within 30 min after the addition of NE even though tension remained elevated. NP and GTN inhibited tension, phosphorylase a formation, and MLC phosphorylation although inhibition of phosphorylase was greater when strips were treated with submaximal (i.e., 0.01 microM) NE concentrations. GTN was a more effective inhibitor of phosphorylase a formation than NP in NE-treated strips, although both agents and 8-Br- cGMP inhibited MLC phosphorylation. The guanylate cyclase inhibitor methylene blue (10 microM) effectively prevented the effects of NP and GTN. The results suggest that NP, GTN, and 8-Br-cGMP inhibit phosphorylase kinase and MLC kinase activation by lowering Ca2+ in the cell. This hypothesis is supported by the observations that 8-Br-cGMP inhibited the Ca2+-dependent, KCl-induced phosphorylase a formation most markedly at reduced concentrations of extra-cellular Ca2+. In addition, neither NP, GTN, nor 8-Br-cGMP inhibited phosphorylase a formation in forskolin-treated tissues, which occurred in response to cAMP-dependent phosphorylation of phosphorylase b kinase.
This article has been cited by other articles:
|
|
 |
|
  T. Hashimoto, M. Kihara, J. Ishida, N. Imai, S.-i. Yoshida, Y. Toya, A. Fukamizu, H. Kitamura, and S. Umemura Apelin Stimulates Myosin Light Chain Phosphorylation in Vascular Smooth Muscle Cells Arterioscler. Thromb. Vasc. Biol., June 1, 2006; 26(6): 1267 - 1272. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M. Lincoln, N. Dey, and H. Sellak Signal Transduction in Smooth Muscle: Invited Review: cGMP-dependent protein kinase signaling mechanisms in smooth muscle: from the regulation of tone to gene expression J Appl Physiol, September 1, 2001; 91(3): 1421 - 1430. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. K. Hennan and J. Diamond Effect of NO donors on protein phosphorylation in intact vascular and nonvascular smooth muscles Am J Physiol Heart Circ Physiol, April 1, 2001; 280(4): H1565 - H1580. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. K. Davda, K. T. Stepniakowski, G. Lu, M. E. Ullian, T. L. Goodfriend, and B. M. Egan Oleic Acid Inhibits Endothelial Nitric Oxide Synthase by a Protein Kinase C-Independent Mechanism Hypertension, November 1, 1995; 26(5): 764 - 770. [Abstract] [Full Text]
|
|
 |
 |
 |
|
 |
 |
 |
