Excess salt consumption is a contributor to hypertension and arterial dysfunction in humans living in industrialized societies, but this phenotype is not observed in inbred, genetically identical mice that consume a high-salt (HS) diet. This study reveals that a HS diet in outbred, genetically diverse mice progressively increases systolic blood pressure and induce arterial dysfunction. These data suggest that genetically diverse mice may provide translational insight into arterial adaptations in humans that consume an HS diet.

Background and Aims. Exercise activity is an important method for managing type 2 diabetes. This investigation examined the HIIT and continuous training on apelin, APJ receptor, NO, and cardiotrophin-1 in the cardiac tissue of diabetic rats. Methods. The animals were categorized into 3 groups of HIIT, continuous (CO), and control (C) (all animals were sacrificed immediately and 2 days after exercise training period). Rats underwent the treadmill exercise program either HIIT (12 bouts at 90–95% of VO₂ max with 60 s rest at 50% of VO₂ max) or CO (60–65% VO₂ max for 40 min). Protocols performed 5 days per week for 8 weeks. Apelin, APJ receptor, NO, and cardiotrophin-1 protein expressions were measured using the Western blotting method in the left ventricle. Results. Immediately after HIIT and CO exercise protocols, apelin and CT-1 protein showed a significant difference in contrast by the C-0 group (p<0.01). However, NO values were substantially higher in HIIT-0 compared to C-0 and CO-0 groups rats (p<0.01). After two days of exercise protocols, apelin and NO protein showed a significant increase in HIIT and CO groups in contrast to the C animals (p<0.01). Moreover, APJ and CT-1 protein significantly upregulated in CO-2 and HIIT-2 compared to the other groups (p<0.01). Conclusions. This study indicates that exercise training, despite the type, is an efficient method to modify apelin, APJ receptor, NO, and cardiotrophin-1 values in animals with type 2 diabetes.