Role of Various Potassium Channels in Caffeine-induced Aortic Relaxation in Rats

BACKGROUND: Studies done on caffeine-induced changes in aortic rings have demonstrated inconclusive results. Moreover, the role of various potassium channels in caffeine-induced effects has not been explored so far. The present in vitro study was designed to explore the direct effects of caffeine on rat aortic rings and the role of various potassium channels in those changes/effects. MATERIALS AND METHODS: This study was carried out in College of Medicine, University of Dammam. Aortic rings obtained from Sprague Dawley rats were mounted in the organ bath. Tension in the aortic rings was measured with an isometric force transducer and recorded with a PowerLab data-acquisition system. Aortic rings in relaxed and contractile state were exposed to caffeine and various potassium channel blockers (glyburide, 4-aminopyridine, or tetraethylammonium). RESULTS: Caffeine produced significant relaxation of isolated aortic rings (baseline tension: 1.26 ± 0.30 g, tension after adding cumulative concentrations of caffeine: 1.12 ± 0.31 g, P < 0.05) in the absence or presence of norepinephrine (NE) (tension induced by NE: 1.06 ± 0.37 g, tension after adding cumulative concentrations of caffeine: 1.01 ± 0.36 g, P < 0.05). Caffeine's vasodilatory effects were, however, blocked in aortic rings pretreated with different types of potassium channel blockers such as 4-aminopyridine (tension induced by NE: 1.52 ± 0.41 g, tension after adding cumulative concentrations of caffeine: 1.50 ± 0.37 g, P > 0.05), glyburide (tension induced by NE: 0.82 ± 0.35 g, tension after adding cumulative concentrations of caffeine: 0.79 ± 0.42 g, P > 0.05), and tetraethylammonium (tension induced by NE: 0.68 ± 0.34 g, tension after adding cumulative concentrations of caffeine: 0.67 ± 0.33 g, P > 0.05). CONCLUSION: Caffeine causes significant dilation of aortic rings, and this vasodilatory effect may involve ATP-dependent, calcium-mediated, or voltage-dependent potassium channels.