Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Volume 39, Issue 1, Pages 142-149Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00005344-200201000-00015
Keywords
cAMP; cardiovascular effects; purinergics
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The mechanism by which purinergic agonist adenosine triphosphate (ATP) and uridine triphosphate (UTP) decrease systemic arterial pressure in the anesthetized mouse was investigated. Intravenous injections of adenosine triphosphate (ATP) and uridine triphosphate (UTP) produced dose-dependent decreases in systemic blood pressure in the mouse. The order of potency was ATP > UTP. Vasodilator responses to ATP and UTP were altered by the cyclic adenosine monophosphate (cAMP) phosphodiesterase inhibitor rolipram. The vascular responses to ATP and UTP were not altered by a nitric oxide synthase inhibitor, a cyclooxygenase inhibitor, a cGMP phosphodiesterase inhibitor, or a particular P2 receptor antagonist. These data suggest that ATP and UTP cause a decrease in systemic arterial pressure in the mouse via a cAMP-dependent pathway via a novel P2 receptor linked to adenylate cyclase and that nitric oxide release, prostaglandin synthesis, cGMP, and P2X(1), P2Y(1), and P2Y(4) receptors play little or no role in the vascular effects of these purinergic agonists in the mouse.
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