Caffeine is really both a vasoconstrictor and a vasodilator. Which one dominates where depends upon a number of things including the dose, local sympathetic and humoral conditions and the various receptor densities (eg. alpha & beta adrenergic and adenosine) in the blood vessels in question. For example, it generally produces cerebral vasoconstriction because of adenosine receptor density. Alpha-1 ARs (mediate vasoconstriction) predominate in most smooth muscle arterioles. However, in skeletal muscle muscle beta-2 ARs (mediate vasodilation) predominate. During exercise, there are a number of things that produce vasodilation in the active muscle vascular beds, one of them being epinephine mediated beta-agonism (leading to among other things an increase in cAMP). Since caffeine and theophylline can act as physiological PDEis (there is some conflicting information out there regarding whether or not the concentration necessary to produce these effects can be achieved normally though), the cAMP signaling that produces vasodilation would be preserved, prolonged and/or amplified. Since caffeine does increase sympathetic outflow, beds where alpha-1 ARs predominate vasoconstriction would be more likely. High enough doses would also increase epinephrine and vasodilation in beta-2 AR beds.
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