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Dilazep-induced vasodilation is mediated through adenosine receptors
Y Zhang1, J D Geiger, D J Légaré
1Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Life Sciences
|January 1, 1991
Summary
Dilazep, an adenosine uptake inhibitor, lowers blood pressure and increases blood flow in the superior mesenteric artery. This vasodilation effect is mediated by adenosine receptors, as shown by blocking studies with 8-phenyltheophylline.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Adenosine Signaling
Background:
- Adenosine plays a crucial role in regulating vascular tone.
- Inhibitors of adenosine uptake, like dilazep, are potential therapeutic agents.
- Understanding the precise mechanisms of adenosine-mediated vasodilation is important.
Purpose of the Study:
- To investigate the in vivo vasodilating effect of dilazep.
- To determine if adenosine mediates the vasodilating effects of dilazep.
- To elucidate the role of adenosine receptors in dilazep-induced vasodilation.
Main Methods:
- Administration of dilazep (adenosine uptake inhibitor) in vivo.
- Measurement of systemic arterial blood pressure and superior mesenteric arterial conductance.
- Administration of 8-phenyltheophylline (8-PT), an adenosine receptor antagonist, to block adenosine effects.
- Assessment of dilazep's effect after adenosine receptor blockade.
Main Results:
- Dilazep significantly reduced systemic arterial blood pressure.
- Dilazep increased superior mesenteric arterial conductance.
- 8-PT blocked the vasodilating effects of dilazep, indicating adenosine receptor involvement.
- Plasma adenosine levels remained unchanged, suggesting local or receptor-mediated effects.
Conclusions:
- Dilazep exhibits a vasodilating effect in vivo.
- This vasodilating effect is mediated by adenosine.
- Adenosine receptors are critical for dilazep's action on vascular conductance.