Abstracts Category : Other

Effects of a Chronic Mental Stress Intervention Protocol on Vasomotor Function in Common Carotid Artery from Wistar-Kyoto and Spontaneously- Hypertensive Rats

by Laura Bennett

ABSTRACTChronic mental stress is emerging as a cardiovascular disease (CVD) risk factor;however, the underlying physiological mechanisms to explain how chronic mental stress may becausing CVD are still under investigation. Previous literature has demonstrated that chronicmental stress can induce endothelial dysfunction, which is a well-known independent risk factorfor CVD. The purpose of this study was to further investigate the underlying pathophysiologicalmechanisms that may be contributing to this endothelial dysfunction, in the normotensiveWistar-Kyoto (WKY) and Spontaneously Hypertensive (SHR) rat models. A chronic mentalstress protocol, known as the Unpredictable Chronic Mild Stress (UCMS) protocol, was used toinduce chronic mental stress in the animals in order to determine its effects on endothelialfunction. Animals were divided up into four groups: WKY CON, WKY UCMS, SHR CON, andSHR UCMS. To test the efficacy of the UCMS protocol, behavioural tests were performed toconfirm the presence of mental stress in the animals in the UCMS groups compared to thecontrol groups (Coat status: WKY: p<0.0001, SHR: p<0.0006; Splash test (GroomingFrequency): WKY: p=0.5581, SHR: p=0.0050). Unexpectedly, compared to WKY CONendothelium-dependent, acetylcholine (ACh)-stimulated vasocontraction (Maximum Amp(MAX): 27.255.95, Area Under the Curve (AUC): 54.2210.98, EC50: 2.580.79), UCMS wasfound to significantly attenuate endothelium-dependent, ACh-stimulated MAX (11.862.91;p=0.043) and AUC (24.875.43; p=0.037), but not EC50 (2.481.20; p=0.913). Likewise,compared to SHR CON endothelium-dependent, ACh-stimulated vasocontraction (MAX:48.59.0, AUC: 84.315.4, EC50: 2.440.70), UCMS was found to attenuate endotheliumdependent,ACh-stimulated MAX (33.406.51; p=0.083), AUC (65.4212.76; p=0.170), andEC50 (1.620.43; p=0.202), however this attenuation did not reach significance. Furthermore,compared to WKY CON endothelium-dependent, ACh-stimulated vasorelaxation MAX:92.433.08, AUC: 300.617.84, EC50: 95.2532.16), UCMS was found to significantly augmentendothelium-dependent, ACh-stimulated AUC (349.913.42; p=0.040), and insignificantlyaugment endothelium-dependent, ACh-stimulated MAX (101.01.35; p=0.241) and EC50(41.08.44; p=0.120). Likewise, compared to SHR CON endothelium-dependent, AChstimulatedvasorelaxation (MAX: 83.813.19, AUC: 282.412.19, EC50: 69.4125.53), UCMSwas found to augment endothelium-dependent, ACh-stimulated MAX (88.652.63; p=0.250),AUC (287.011.09; p=0.781), and EC50 (87.8332.3; p=0.669), however this augmentation didnot reach significance. Dose-dependent response curves to sodium nitroprusside (SNP) andU46619 were similar across all groups, suggesting that the attenuated vasocontraction andenhanced vasorelaxation was not due to UCMS having an effect on vascular smooth muscle(VSM) sensitivity, but is more likely due to a reduction in endothelium-derived contractingfactor (EDCF) production/bioavailability and/or an increase in