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. Author manuscript; available in PMC: 2009 Sep 26.
Published in final edited form as: Toxicol Sci. 2007 Oct 18;102(2):207–218. doi: 10.1093/toxsci/kfm263

Fig. 3.

Fig. 3

Synopsis of proposed physiological and cellular mechanism of metal-induced hypertension. On the graph, sites 1–7 reflect endocrine or paracine vaso-active mediators/receptors, sites 8–11 reflect direct changes in vascular smooth muscle physiology and associated connective tissue caused by metal exposure. Abbreviations: αR = α adrenergic receptor; ACE = angiotensin converting enzyme; βR = β adrenergic receptor; E = epinephrine; ECM = extracellular matrix; IL = interleukin; NE = norepinephrine; NO = nitric oxide; PAI-1 = plasminogen activator inhibitor -1; PKC = protein kinase C; SMC = smooth muscle cells; TNF = tumor necrosis factor α.