| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J. Biol. Chem., Vol. 263, Issue 6, 2658-2663, 02, 1988
LR Grillone, MA Clark, RW Godfrey, F Stassen and ST Crooke
The rat thoracic aortic smooth muscle cell line, A-10, expresses
vasopressin receptors of the V1 subtype. Vasopressin treatment of these
cells stimulated the release of arachidonic acid and the formation of
diacylglycerol and phosphocholine. These responses to vasopressin were
inhibited by the V1-specific antagonist SK&F 100273, indicating that
these were receptor-mediated phenomena. The mechanisms by which V1
receptors mediate arachidonic acid release appeared to be unaffected by
cycloheximide or actinomycin D, suggesting that the release is independent
of protein and RNA synthesis. The V1 receptors also appeared to be coupled
to a phospholipase C which can hydrolyze phosphatidylcholine, a possible
source of the released arachidonic acid. Phosphocholine and diacylglycerol
were also generated. The release of arachidonic acid, phosphocholine, or
diacylglycerol was not affected by prior treatment of the cells with
pertussis toxin (islet- activating protein). Thus, the release of these
second messengers is not mediated by the guanine nucleotide-binding protein
Gi or other pertussis toxin-sensitive substrates. We conclude that V1
receptors induce the release of arachidonic acid and the formation of
diacylglycerol and phosphocholine via the activation of both a
phosphatidylinositol- and phosphatidylcholine-specific phospholipase C.
Vasopressin induces V1 receptors to activate phosphatidylinositol- and phosphatidylcholine-specific phospholipase C and stimulates the release of arachidonic acid by at least two pathways in the smooth muscle cell line, A-10
Smith Kline & French Laboratories, Philadelphia, Pennsylvania 19101.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  J. S. Smeda Stroke Development in Stroke-Prone Spontaneously Hypertensive Rats Alters the Ability of Cerebrovascular Muscle to Utilize Internal Ca2+ to Elicit Constriction Stroke, June 1, 2003; 34(6): 1491 - 1496. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. R. Goldsmith Vasopressin antagonists in CHF: ready for clinical trials? Cardiovasc Res, April 1, 2002; 54(1): 13 - 15. [Full Text] [PDF]
|
|
|
|
 |
|
 T. Ito, O. Kozawa, K. Tanabe, M. Niwa, H. Matsuno, N. Sakai, H. Ito, K. Kato, and T. Uematsu p38 MAP Kinase Is Required for Vasopressin-Stimulated HSP27 Induction in Aortic Smooth Muscle Cells Hypertension, February 1, 2000; 35(2): 673 - 678. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Wolf, J. Wang, J. Turk, and R. W. Gross Depletion of Intracellular Calcium Stores Activates Smooth Muscle Cell Calcium-independent Phospholipase A2. A NOVEL MECHANISM UNDERLYING ARACHIDONIC ACID MOBILIZATION J. Biol. Chem., January 17, 1997; 272(3): 1522 - 1526. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y Nishizuka Intracellular signaling by hydrolysis of phospholipids and activation of protein kinase C Science, October 23, 1992; 258(5082): 607 - 614. [Abstract] [PDF]
|
|
|
|
|
|
M. Tsai, C. Yu, and D. Stacey A cytoplasmic protein inhibits the GTPase activity of H-Ras in a phospholipid-dependent manner Science, November 16, 1990; 250(4983): 982 - 985. [Abstract] [PDF]
|
|
|
|
|
|
M. Tsai, C. Yu, F. Wei, and D. Stacey The effect of GTPase activating protein upon ras is inhibited by mitogenically responsive lipids Science, January 27, 1989; 243(4890): 522 - 526. [Abstract] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
