Effects of sitagliptin on ß-adrenoceptor mediated relaxation in streptozotocin-diabetic rat aorta.

Background/aim: Dipeptidyl peptidase-4 (DPP4) inhibitors, a class of oral antidiabetic drugs, have been shown to be protective on the vascular system because of their antiinflammatory, antiatherosclerotic, and vasodilatory effects. ß2-adrenoceptors (ß2-ARs) mediate the vasorelaxation in the aorta. However, ß3-adrenoceptor-mediated relaxation has not been studied in diabetic aorta yet.

Beta-3 adrenoceptors: A potential therapeutic target for heart disease.

As heart failure (HF) is a growing public health problem worldwide, rapid therapeutic development is required to improve HF management. Decreased myocardial contractility in HF is associated with the persistent sympathetic activation of β/β-adrenoceptors (β/β-ARs). Although it is initially activated to compensate for a decline in myocardial contractility, it plays a pivotal role in organ damage and functional deterioration over time, resulting in the desensitization of receptors involved.

Contributions of Rho-kinase and AMP-related kinase signaling pathways to responses mediated by endothelium-derived contracting factors in diabetic rat aorta.

Diabetes-induced endothelial damage leads to vascular dysfunction. The current study investigated the effects of short-term (4-week) streptozotocin (STZ)-induced diabetes on responses mediated by endothelium-derived contracting factors (EDCFs) as well as possible contributions of Rho-kinase and AMP-activated kinase (AMPK) signaling pathways. The effects of STZ-diabetes on vascular function were examined in isolated thoracic aorta preparations of 30-week-old rats ( = 27).

Role of the β-adrenergic receptor subtype in catecholamine-induced myocardial remodeling.

β-Adrenoceptors (AR) stimulate cardiac Na/K pump in healthy hearts. β-ARs are upregulated by persistent sympathetic hyperactivity; however, their effect on Na/K ATPase activity and ventricular function in this condition is still unknown. Here, we investigate preventive effects of additional β-AR activation (BRL) on Na/K ATPase activity and in vivo hemodynamics in a model of noradrenaline-induced hypertrophy.

Onset of decreased heart work is correlated with increased heart rate and shortened QT interval in high-carbohydrate fed overweight rats.

Mechanical activity of the heart is adversely affected in metabolic syndrome (MetS) characterized by increased body mass and marked insulin resistance. Herein, we examined the effects of high carbohydrate intake on cardiac function abnormalities by evaluating in situ heart work, heart rate, and electrocardiograms (ECGs) in rats. MetS was induced in male Wistar rats by adding 32% sucrose to drinking water for 22-24 weeks and was confirmed by insulin resistance, increased body weight, increased blood glucose and serum insulin, and increased systolic and diastolic blood pressures in addition to significant loss of left ventricular integrity and increased connective tissue around myofibrils.