Abstract

Intracellular cyclic adenosine monophosate (AMP) levels regulate the generation of thromboxane by platelets by inhibiting the hydrolysis of arachidonic acid from membrane phospholipids. However, there is conflicting evidence regarding the role of cyclic AMP in the control of the subsequent oxygenation of arachidonic acid by cyclooxygenase. We studoed the regulation of cyclooxygenase activity by agents that elevate platelet cyclic AMP (dibutyryl cyclic AMP and prostaglandins), measuring arachidonate-induced aggregation, O2 consumption, and malonaldehyde formation. In platelet-rich cyclic AMP. This inhibitory effect of cyclic AMP was absent in gel-filtered platelets suspended in buffer containing 0.5% albumin, and was progressively restored as plasma was added in increasing concentrations. Increasing the albumin concentration in platelet buffer suspensions likewise increased the ability of cyclic AMP to block the arachidonate-induced O2 burst and MDA production. We conclude that (1) the presence of plasma proteins is important in investigating platelet plasma milieu or at least in the presence of physiologic albumin concentrations.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.