In vitro caffeine induced aortic smooth muscle reactivity in rat.

The effects of caffeine on aortic smooth muscle contractility during hypertension were studied in SHR and WKY control rats. To compare the effects of Mg++ on vascular reactivity induced by caffeine 1.2 mM MgCl2 was either included or omitted from the Krebs solution bathing the aortic tissue. The role of alpha-adrenergic receptors and verapamil-sensitive Ca++ channels in eliciting caffeine induced contraction in aortic tissues was also examined in Sprague Dawley rats. We report that the aortic smooth muscle from SHR animal was less responsive than WKY aortic smooth muscle to 10 and 20 mM concentrations of caffeine. Caffeine induced a relaxation of aortic smooth muscle contracted with 60 mM KCl or 10(-7) M NE. However, the relaxation response was slower in SHR as compared to WKY rats. To assess the involvement of alpha-adrenergic receptors in caffeine induced aortic contractility alpha 1- and alpha 2-receptors were blocked with 10(-7) M prazosin and 10(-7) M yohimbine respectively. The caffeine induced aortic contractility did not seem to involve alpha-adrenergic receptors. A blockade of verapamil sensitive Ca++ channels with 10(-7) M verapamil failed to inhibit caffeine induced aortic contractility. These results indicate that caffeine involves release of Ca++ in vascular muscle, however, Ca++ is released from a site other than the one controlled by alpha-adrenergic receptors. Also, the Ca++ channels involved are other than the Verapamil sensitive Ca++ channels. Yet it is clear that if the aortic contractility is due to Ca++ release alone, then caffeine is a potent agent for Ca++ release in the aortic smooth muscle of rat. Additionally, the caffeine-sensitive mechanism for aortic smooth muscle contraction is impaired during hypertension.