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Potassium and calcium channel gene expression in small arteries in porcine and rat models of diet‐induced obesity (676.4)

Obesity is an increasing problem worldwide leading to cardiovascular morbidity. Only limited information exists on the transcriptional regulation of arterial K+ and Ca2+ channels in obesity. We quantified, by real‐time PCR, mRNA expression of K+ channels and L‐type Ca2+ channels (LTCC) in small mesenteric (MA), middle cerebral (MCA), and left coronary arteries (LCA) of lean vs. obese rats and minipigs. Male Sprague Dawley rats were fed a high‐fat (FAT; N=5), high‐fructose (FRUC; N=7), high‐fat/high‐fructose (FAT/FRUC; N=7) or standard diet (STD; N=7‐11) for 28 Weeks. FAT and FAT/FRUC became obese, whereas FRUC and STD were lean. Systolic blood pressure (SBP) averaged over 14 weeks was increased (P<0.001) in FRUC and FAT/FRUC but not in FAT. Kir, Kv1.2, Kv1.5, and Kv7.4 channels were up‐regulated in FAT, whereas SKca and IKca channels were down‐regulated in FAT/FRUC (P<0.05). There were no transcriptional changes in FRUC. Castrated male Göttingen minipigs with or without diabetes were fed a diet rich in fat, cholesterol and fructose (OB+DIAB; N=3 vs. OB; N=2, respectively) or a standard diet (STD; N=3) for 22‐45 weeks. Body weight, total body fat content and plasma triglyceride levels were increased in OB and OB+DIAB. BKca, IKca, SKca and/or LTCC mRNA was up‐regulated in LCA from OB and OB+DIAB (n.s.). Expression of BKca mRNA was increased, whereas IKca mRNA decreased in MCA from OB (n.s.). SKca mRNA was decreased in MA from OB (n.s.). Diet‐induced obesity in rats and minipigs lead to complex changes in K+ and Ca2+ channel gene expression, which, in rats, did not seem to be linked with changes in SBP. These transcriptional changes may lead to disturbances in microvascular flow patterns in obesity.