| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA
2 Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institutes of Health, Bethesda, MD, USA
* To whom correspondence should be addressed. E-mail: mgorman{at}u.washington.edu.
The role of P1 receptors and P2Y1 receptors in coronary vasodilator responses to adenine nucleotides was examined in the isolated guinea pig heart. Bolus arterial injections of nucleotides were made in hearts perfused at constant pressure. Peak increase in flow was measured before and after addition of purinoceptor antagonists. Both the P1 receptor antagonist 8-p-sulfophenyltheophylline (8-SPT) and adenosine deaminase inhibited adenosine vasodilation. AMP-induced vasodilation was inhibited by P1 receptor blockade but not by adenosine deaminase or by the selective P2Y1 antagonist N6-methyl-2'-deoxyadenosine 3',5'-bisphosphate (MRS 2179). ADP-induced vasodilation was moderately inhibited by P1 receptor blockade and greatly inhibited by combined P1 and P2Y1 blockade. ATP-induced vasodilation was antagonized by P1 blockade but not by adenosine deaminase. Addition of P2Y1 blockade to P1 blockade shifted the ATP dose-response curve further rightward. It is concluded that in this preparation ATP-induced vasodilation results primarily from AMP stimulation of P1 receptors, with a smaller component from ATP or ADP acting on P2Y1 receptors. ADP-induced vasodilation is largely due to P2Y1 receptors with a smaller contribution by AMP or adenosine acting via P1 receptors. AMP responses are mediated solely by P1 receptors. Adenosine contributes very little to vasodilation resulting from bolus intracoronary injections of ATP, ADP or AMP.
This article has been cited by other articles:
|
|
 |
|
  J. C. Arciero, B. E. Carlson, and T. W. Secomb Theoretical model of metabolic blood flow regulation: roles of ATP release by red blood cells and conducted responses Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1562 - H1571. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. W. Gorman, E. O. Feigl, and C. W. Buffington Human Plasma ATP Concentration Clin. Chem., February 1, 2007; 53(2): 318 - 325. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. D. Tune Withdrawal of vasoconstrictor influences in local metabolic coronary vasodilation Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2044 - H2046. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Borgdorff and G. J. Tangelder Pump-induced platelet aggregation with subsequent hypotension: Its mechanism and prevention with clopidogrel J. Thorac. Cardiovasc. Surg., April 1, 2006; 131(4): 813 - 821. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Farias III, M. W. Gorman, M. V. Savage, and E. O. Feigl Plasma ATP during exercise: possible role in regulation of coronary blood flow Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1586 - H1590. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. G. Konduri, I. Bakhutashvili, R. Frenn, I. Chandrasekhar, E. R. Jacobs, and A. K. Khanna P2Y purine receptor responses and expression in the pulmonary circulation of juvenile rabbits Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H157 - H164. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
