Contribution of Adenosine to the Regulation of Cerebral Blood Flow: The Role of Calcium Ions in the Adenosine-Induced Cerebrocortical Vasodilatation
It is well established that cerebral blood flow (CBF) and adenosine concentration in the brain can be elevated severalfold during arterial hypoxia and epileptic seizures (Winn et al., 1981). Since perivascularly administered adenosine dilatates pial arteries (Wahl and Kuschinsky, 1976) and the stable analog of adenosine, chloroadenosine, is an even more efficient dilatator of cerebrocortical vessels (Winn et al., 1981), it was suggested that adenosine plays a central role in the regulation of CBF (Winn et al., 1981). However, since the adenosine concentration of the normal brain is very low (Winn et al., 1981: around 10−7 mol l−1), this assumption is valid only if adenosine is present exclusively in the extracellular fluid. Besides this, it is also not yet clear whether the vasodilatator action of adenosine involves changes in calcium availability of the vascular smooth muscle (Dutta et al., 1980; Fenton et al., 1982), or adenosine dilates the vessels by some other mechanism (Kukovetz et al., 1978). In the present study the following questions were addressed: a) How efficient is topically administered adenosine when compared with arterial hypoxia and epileptic seizures in altering cerebrocortical vascular volume (CVV) ? b) Is there a possible role of adenosine-induced cortical metabolic changes in the vasodilatatory mechanism? c) What is the importance of calcium availability in the vascular action of adenosine? To answer these questions the brain cortex was superfused with various concentrations of adenosine.
KeywordsCerebral Blood Flow Epileptic Seizure Cerebral Perfusion Pressure Brain Cortex Adenosine Concentration
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