Alteration of perivascular adipose tissue function in angiotensin II-induced hypertension.

We studied the role of perivascular adipose tissue (PVAT) in the control of vascular function in an in vivo experimental model of hypertension produced by angiotensin II infusion by osmotic minipump in adult male Wistar rats. Two weeks after infusion with angiotensin II, blood pressure in treated rats was significantly elevated but heart rate was reduced compared with control rats infused with physiological saline. Contraction of aorta from the 2 groups of rats in response to phenylephrine or serotonin was significantly attenuated by the presence of PVAT in both the presence and absence of endothelium. This attenuation effect on contraction to phenylephrine was higher, however, in vessels from control rats than in vessels from hypertensive rats in the absence of endothelium. In the mesenteric resistance arteries, lumen diameter was larger in both hypertensive and control vessels with intact PVAT than in vessels with PVAT removed. The medial wall was thicker in arteries from hypertensive rats. The presence of PVAT potentiated the contraction induced by KCl in mesenteric arteries from control rats, but not in hypertensive rats. PVAT also attenuated the contraction of mesenteric arteries in response to phenylephrine or serotonin in both hypertensive and control groups. Mesenteric arteries from hypertensive rats were more responsive to stimulation by serotonin than those from control rats. We conclude that the increased blood pressure of Wistar rats that occurred after infusion with angiotensin II was associated with changes in the functions of PVAT in the aorta and mesenteric arteries and in the structure and function of resistance arteries.