-transparent.png){kind=logo}
[3H]Prostaglandin D2 binding to rabbit platelets was increased by about 150% in the presence of beta-adrenoceptor agonist, isoproterenol. The isoproterenol-induced potentiation of the [3H]prostaglandin D2 binding gave a bell-shaped dose-response relationship (maximum response at 3 X 10(-8) M) in a stereospecific manner. Similar and moderate potentiation was obtained with terbutaline. On the other hand, beta-adrenoceptor antagonists such as alprenolol, propranolol and butoxamine (beta 2-specific) had no potentiating effect on [3H]prostaglandin D2 binding; rather, they abolished the isoproterenol-induced increase of [3H]prostaglandin D2 binding. The beta 1-specific antagonist, metoprolol, did not have any effect. Rabbit platelets were found to possess one [3H]prostaglandin D2 binding site (Kd = 6 X 10(-7) M, Bmax = 787 fmol/mg protein). In the presence of isoproterenol at 3 X 10(-8) M, Bmax was increased with unaltering Kd value. Isoproterenol did not increase [3H]prostaglandin E1, [3H]prostaglandin E2 and [3H]prostaglandin F2 alpha bindings to platelets. The potential effect of isoproterenol was mimicked by forskolin, theophylline, dibutyryl cyclic AMP, prostaglandin E1 and prostaglandin I2, but it was abolished by 2', 5'-dideoxyadenosine, an inhibitor of adenylate cyclase, indicating that elevated level of cyclic AMP may be available for the induction of the increase of [3H]prostaglandin D2 binding. Prostaglandin D2-induced cyclic AMP synthesis and antiaggregation activity were also augmented in the presence of isoproterenol. These results suggest a beta 2-adrenoceptor-mediated cyclic AMP-dependent mechanism for the regulation of prostaglandin D2 receptor binding in rabbit platelets.
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
April 1992,
Biochimica et biophysica acta,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
March 1982,
The American journal of physiology,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
August 1979,
The Journal of clinical investigation,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
February 1977,
Prostaglandins,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
August 1986,
British journal of pharmacology,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
November 1983,
The American journal of physiology,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
October 1979,
Life sciences,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
June 1994,
Japanese journal of pharmacology,
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
November 2001,
Science (New York, N.Y.),
K Hanasaki, and
Y Mizuno, and
M Ikeda, and
M Shimonishi, and
S Yoshimura, and
K Tomita, and
A Ichikawa
January 2006,
The Journal of allergy and clinical immunology,
