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Endothelial Nitric Oxide Mediates Caffeine Antagonism of Alcohol-Induced Cerebral Artery Constriction

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Endothelial Nitric Oxide Mediates Caffeine Antagonism of Alcohol-Induced Cerebral Artery Constriction 1521-0103/356/1/106–115$25.00 http://dx.doi.org/10.1124/jpet.115.229054 THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS J Pharmacol Exp Ther 356:106–115, January 2016 Copyright ª 2015 by The American Society for Pharmacology and Experimental Therapeutics Endothelial Nitric Oxide Mediates Caffeine Antagonism of Alcohol-Induced Cerebral Artery Constriction Jennifer Chang, Alexander L. Fedinec, Guruprasad Kuntamallappanavar, Charles W. Leffler, Anna N. Bukiya, and Alex M. Dopico Department of Pharmacology (J.C., G.K., A.N.B., A.M.D.) and Department of Physiology (A.L.F., C.W.L.), College of Medicine, Health Science Center, University of Tennessee, Memphis, Tennessee Received August 28, 2015; accepted November 5, 2015 ABSTRACT Downloaded from Despite preventive education, the combined consumption of independence of systemic factors and drug metabolism, but alcohol and caffeine (particularly from “energy drinks”) continues required a functional endothelium. Moreover, caffeine protection to rise. Physiologic perturbations by separate intake of ethanol against alcohol increased nitric oxide (NO•) levels over those and caffeine have been widely documented. However, the found in the presence of ethanol alone, disappeared upon biologic actions of the alcohol-caffeine combination and their blocking NO• synthase, and could not be detected in pressur- underlying subcellular mechanisms have been scarcely studied. ized cerebral arteries from endothelial nitric-oxide synthase Using intravital microscopy on a closed-cranial window and knockout (eNOS2/2) mice. Finally, incubation of de-endothelialized jpet.aspetjournals.org isolated, pressurized vessels, we investigated the in vivo and in cerebral arteries with the NO• donor sodium nitroprusside (10 mM) vitro action of ethanol-caffeine mixtures on cerebral arteries from fully restored the protective effect of caffeine. This study rats and mice, widely recognized models to address cerebro- demonstrates for the first time that caffeine antagonizes vascular pathophysiology and pharmacology. Caffeine at con- ethanol-induced cerebral artery constriction and identifies centrations found in human circulation after ingestion of one to endothelial NO• as the critical caffeine effector on smooth two cups of coffee (10 mM) antagonized the endothelium- muscle targets. Conceivably, situations that perturb endothelial • independent constriction of cerebral arteries evoked by ethanol function and/or NO availability will critically alter caffeine at ASPET Journals on October 1, 2021 concentrations found in blood during moderate-heavy alcohol antagonism of alcohol-induced cerebrovascular constriction intoxication (40–70 mM). Caffeine antagonism against alcohol without significantly disrupting endothelium-independent, alcohol- was similar whether evaluated in vivo or in vitro, suggesting induced cerebral artery constriction itself. Introduction drinking experience (CDC, 2014). Despite several years of preventive education, binge drinking prevalence across US Caffeine and alcohol (ethyl alcohol; ethanol) are the two college campuses has remained steadily high at .40% most widely used psychoactive agents in the world (Meredith (McMurtrie, 2014). Numerous epidemiologic studies have et al., 2013; Winstock 2014). In the United States, .90% of portrayed the deleterious effects of alcohol on cerebrovascular adults consume caffeine regularly, with an average intake of health (Altura and Altura, 1984; Puddey et al., 1999; Reynolds .200 mg/d; that is, more caffeine than what is contained in two 6-ounce cups of coffee or five 12-ounce cans of soft drinks et al., 2003; Patra et al., 2010). In particular, episodic drinking – (Frary et al., 2005; Juliano et al., 2012). The health risks with blood alcohol levels reaching 35 80 mM is associated imposed on the cardiovascular system by high and/or chronic with increased risk for cerebrovascular ischemia (Puddey caffeine intake as well as the health hazards resulting from et al., 1999), stroke, and death from ischemic stroke (Reynolds abrupt caffeine withdrawal are well known and reviewed et al., 2003). Cerebrovascular ischemia may result from elsewhere (Balster, 1998). impaired vasodilatation and/or enhanced constriction of cere- In turn, episodic, moderate-to-heavy ethanol intake, such as bral arteries. Using a rat model that mimics human cerebral during “binging,” constitutes the primary form of excessive artery reactivity, we showed that ethanol (10–100 mM) alcohol consumption in the United States. Indeed, ∼29% of constricted middle cerebral arteries both in vivo and in vitro females and 43% of males in the United States have binge (Liu et al., 2004; Bukiya et al., 2009, 2014). The combined use of alcohol and caffeine, the latter as the “ ” This work was supported by the National Institutes of Health National main active ingredient of power/energy supplements such as Institute on Alcohol Abuse and Alcoholism [Grant R37-AA11560 (to A.M.D.)] chewing bars, gums, gels, and beverages (i.e., “energy drinks”) and the National Heart, Lung, and Blood Institute [Grants R01-HL104631 (to A.M.D.), R01-HL42851, and R01-HL34059 (to C.W.L.)]. is increasing sharply, particularly among adolescent and dx.doi.org/10.1124/jpet.115.229054. college students. More than 50% of US college students have ABBREVIATIONS: Emax, concentration of a ligand needed to reach its maximal effect; eNOS, endothelial nitric-oxide synthase; KO, knockout; L-NNA, N-omega-nitro-L-arginine; NO•, nitric oxide; NOS, nitric oxide synthase; PSS, physiologic saline solution; RyR, ryanodine receptors; SNP, sodium nitroprusside. 106 Caffeine Protection against Alcohol-Induced Vasoconstriction 107 reported mixing energy drinks with alcohol in the past month Laboratories (Indianapolis, IN). Adult 8- to 12-week-old male homo- 2 2 (Malinauskas et al., 2007). Remarkably, energy drinks in- zygous eNOS (Nos3tm1Unc/J) KO (eNOS / ) and C57BL/6 control mice crease the risk of alcohol dependence (Arria et al., 2011). In were purchased from the Jackson Laboratory (Bar Harbor, ME). Rats addition, people who co-consume caffeine and alcohol are 3 and mice were decapitated using a guillotine and sharp scissors, , m , m times more likely to binge drink than drinkers who do not mix respectively. Middle cerebral arteries ( 260 mand 150 m external diameter in rat and mouse species, respectively) were these agents (Mintel International Group, 2007), and their isolated and cannulated as described in our earlier work (Bukiya desire to drink alcohol is more pronounced than in subjects et al., 2013). When required, endothelium was removed by passing an exposed to the same dose of alcohol alone (Marczinski, 2015). air bubble into the vessel lumen for 90 seconds before vessel Some studies suggest that the combined use of caffeine and cannulation. The presence/absence of functional endothelium was ethanol may increase the rate of alcohol-related injury experimentally verified by the arterial response to 10 mM acetylcho- (Reissig et al., 2009). On the other hand, the combination of line, an endothelium-dependent vasodilator, versus the response to these two drugs has been proposed as neuroprotection against 10 mM sodium nitroprusside (SNP), an endothelium-independent ischemic stroke in rat models (Aronowski et al., 2003) and vasodilator (Liu et al., 2004; Bukiya et al., 2007). The chamber humans (Sacco, 2007). However, whether ethanol and caffeine containing the cannulated artery was continuously perfused at a rate actually modulate each other’s action on cerebral vessels of 3.75 ml/min with physiologic saline solution (PSS) (mM): 119 NaCl, 4.7 KCl, 1.2 KH PO , 1.6 CaCl , 1.2 MgSO , 0.023 EDTA, 11 glucose, remains unknown. More generally, in spite of increased co- 2 4 2 4 and 24 NaHCO . PSS was equilibrated at pH 7.4 with a 21%/5%/74% consumption of alcohol and caffeine in the US population, the 3 mix of O2/CO2/N2 and maintained at 35–37°C. Arteries were observed subcellular targets and mechanisms that are perturbed by the with a charge coupled device camera (Sanyo VCB-3512T; Sanyo Downloaded from presence of this drug combination are mostly unknown. Electric Co., Moriguchi, Japan) attached to an inverted Nikon Eclipse Using a combination of in vivo and in vitro arterial tone TS100 microscope (Nikon, Tokyo, Japan). The external diameter of the determinations in a rat model and selective pharmacology, and arterial wall was measured using the automatic edge-detection func- the endothelial nitric-oxide synthase knockout (eNOS2/2 KO) tion of IonWizard software (IonOptics, Milton, MA) and was digitized mouse model, our study documents that caffeine at concentra- at 1 Hz with a personal computer. tions commonly found in human circulation antagonizes con- Experiments were performed on arteries subjected to 60 mm Hg jpet.aspetjournals.org striction of cerebral arteries evoked by ethanol concentrations intravascular pressure to ensure both development and maintenance of myogenic tone (Bukiya et al., 2007). Once myogenic tone developed equivalent to blood alcohol levels found during alcohol in- and artery diameter remained stable for at least 10 minutes, the toxication. This action of caffeine does not require neuronal artery was exposed to a high K1 solution (mM): 63.7 NaCl, 60 KCl, integrity, circulating factors, or systemic drug metabolism but 1.2 KH2PO4, 1.6 CaCl2, 1.2 MgSO4, 0.023 EDTA, 11 glucose, occurs at the cerebral artery level itself. In contrast to ethanol 24 NaHCO3, pH 7.4. Drugs were applied to the artery by chamber or caffeine individual
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