Key result
Under both acute and chronic conditions, hyperglycemia enhanced the relaxation response of rat aorta vessels mediated by perivascular adipose tissue.
Why the study?
Does hyperglycemia alter perivascular adipose tissue (PVAT) modulation of vascular function in rat aorta?
Does hyperglycemia alter perivascular adipose tissue (PVAT) modulation of vascular function in rat aorta?
Hyperglycemia enhances PVAT-mediated vascular relaxation, providing a potential mechanism for postprandial blood pressure changes and hypotension in chronic type-1 diabetes models.
Caution against clinical extrapolation; extends preclinical PVAT data in hyperglycemia but leaves open human relevance.
OBJECTIVE: To study the acute and chronic effect of hyperglycemia on perivascular adipose tissue (PVAT) function in rat aorta. METHOD: Alterations in PVAT function in rat aorta incubated with 22 mmol/l D-glucose for 30 min and in aorta from streptozotocin (STZ)-induced diabetic rats were studied. RESULTS: Incubation with D-glucose caused an attenuation of contraction in response to phenylephrine, both in the presence and absence of endothelium, whereas removal of PVAT eliminated this attenuation effect. The presence of PVAT did not affect concentration-related relaxation response of the aorta to carbamylcholine in STZ rats. There was also no difference in the relaxation response of the aorta to carbamylcholine between STZ and control rats. The presence of PVAT, however, caused a higher attenuation of the concentration-dependent contraction to phenylephrine in aorta from STZ rats with intact endothelium as compared with that from control rats. Incubation of the aorta from control rats with Nomega-nitro-L-arginine or carboxy-2-phenyl-4,4,5,5-tetra-methyl-imidazoline-1-oxyl-3-oxide potentiated the contraction of the vessels to phenylephrine, and this potentiation effect was higher in the vessels from STZ rats than control rats when N-nitro-L-arginine was used. Removal of PVAT reduced this potentiation effect and eliminated the difference between the vessels from control and STZ rats. CONCLUSION: Under both acute and chronic conditions, hyperglycemia enhanced the relaxation response of the vessels mediated by PVAT. These new findings provide important information on the mechanism underlying the postprandial effect of hyperglycemia on blood pressure control and the presence of hypotension under chronic hyperglycemia in a type-1 model of diabetes.
No takes yet. Share an insight, caveat, or question.
Lee et al. (2008) studied Hyperglycemia and Type-1 Diabetes. Hyperglycemia (D-glucose incubation and STZ-induced diabetes) vs. Control rats and absence of D-glucose was evaluated on Alterations in PVAT function (contraction to phenylephrine and relaxation to carbamylcholine). Under both acute and chronic conditions, hyperglycemia enhanced the relaxation response of rat aorta vessels mediated by perivascular adipose tissue.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: