Omental Arteries from Diabetic Hypertensive Subjects are Larger and Stiffer than those from Non‐Diabetic Normotensives

Abstract

Diabetes and hypertension are associated with structural and mechanical changes of the resistance vasculature that contribute to cardiovascular disease development and progression. We have previously reported that in mouse isolated resistance arteries prolonged vasoconstriction leads to vascular inward remodeling and stiffening, through a process that requires smooth muscle actin polymerization. We hypothesized that human arteries from diabetic hypertensive subjects would be inwardly remodeled and stiffer than those from non‐diabetic normotensives. We also hypothesized that actin stress fiber disruption would dilate and soften the arteries from diabetic hypertensives. To test these hypotheses, omental samples were obtained from patients undergoing abdominal surgery at The University of Missouri Hospital. Small arteries were isolated, cannulated and analyzed using pressure myography. Vascular luminal diameters and wall‐thicknesses were monitored by videomicroscopy at different levels of intraluminal pressure (5–120mmHg) under passive conditions (calcium‐free buffer with 100μM adenosine and 2mM EGTA) in the absence or presence of Mycalolide‐B (2uM) to disrupt the actin cytoskeleton. Investigators were blinded to the subject condition throughout the experimental procedures. Data were used for assessment of vascular remodeling and characterization of vascular wall mechanical properties. Subsequently, the arterial parameters obtained were compared across groups according to diabetic and hypertensive status retrieved from medical records. Results indicate that small omental arteries from diabetic hypertensive (N=10) subjects have larger diameters and are stiffer than those from non‐diabetic normotensives (N=22, P<0.05). Data also show that disruption of the actin cytoskeleton had no significant effects on their mechanical properties. We conclude that small omental arteries from diabetic and hypertensive subjects undergo a process of outward remodeling that results in them becoming larger and stiffer and that, at the single time point of our sampling, this is not dependent on vascular cell actin stress fibers.Support or Funding InformationNational Institutes of Health grants: R01 HL137769 (JP), R01 HL088105 (LM‐L).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.