Perivascular adipose tissue (PVAT) function in a model of metabolic syndrome

Obesity and the metabolic syndrome are risk factors for cardiovascular disease. In normal conditions, perivascular adipose tissue (PVAT) exerts vascular anticontractile effects. We hypothesized that in obesity/metabolic syndrome, despite increases in visceral fat mass, PVAT function would be impaired, contributing to the associated vascular dysfunction. We treated 5 week‐old male Sprague‐Dawley rats with a lard‐sucrose choice diet and after 3 weeks we measured metabolic parameters and contractile function in second order mesenteric arteries. There were no changes in total body weight, waist circumference or tail length between diet and control groups. There was a significant increase in fat pad weight (retroperitoneal, epididymal, inguinal and brown adipose) in diet vs control rats. Fasted glycemia was increased and glucose tolerance was decreased in diet vs control rats. There were no significant changes in the responses to PE, 5‐HT, ET‐1, ACh and SNP between groups. The presence of PVAT had a similar anticontractile effect on all contractile agonists in both groups. Contraction to the TxA2 agonist U46619 was significantly decreased in the absence of PVAT in diet compared to control rats. We conclude that PVAT function is not altered in mesenteric arteries in this model of metabolic syndrome. However, our data do not exclude alterations in PVAT function in the face of hypertensive or inflammation challenges.