... that's what Robert Engler concluded in an editorial comment in Circulation a few years ago. Why such a bold definition by a renowned researcher?

When adenosine is outside the cell it acts as a "local hormone" by interacting with membrane proteins, the so-called adenosine receptors. It is produced on demand, just where and when it is needed. A fine example is the cardiovascular system. When we are short of oxygen, cells in the heart break down ATP (the intracellular energy store) to adenosine, which is then released from the cell. So when danger is there, local extracellular concentrations of adenosine are much higher than under normal conditions. This extracellular adenosine can interact with the membrane bound adenosine receptors that normally lead a relatively quiet life. Consequences are that our heart slows down and the force of contraction decreases, which reduces the demand for oxygen. At the same time our blood vessels in and around the heart dilate, increasing the supply of oxygen.

Now that you are visiting our web site, why not read a little bit further to find out why we here in Leiden like adenosine and its receptors so much.

Adenosine receptors come in four flavors, prosaically termed A1, A2A, A2B and A3. All four subtypes are studied in our division of Medicinal Chemistry of the Leiden/Amsterdam Center for Drug Research. Ever since 1985 when we started, this has been a fruitful area of research for us. On this web site you will find bits and pieces of the work we did and do, and relevant information of the people involved.

By the way, did you know that caffeine works via adenosine receptors? Read more...