Abstract P059: Carotid Artery Stiffness Is Elevated In Young Hypertensive Rats Relative To Age-matched Normotensive Rats

Abstract

Hypertension has a bidirectional relationship with arterial stiffening, a hallmark feature that reduces vascular compliance, resulting in increased blood velocity, disruptions to laminar flow, and target organ injury. Our prior studies in transgenic hypertensive (mRen2)27 rats document age-related sex differences in cardiac dysfunction associated with cerebrovascular changes that develop earlier in males than females. Both sexes develop cardiac dysfunction and cerebrovascular damage by 1 year of age. The current objective was to determine systolic blood pressure (SBP) and arterial stiffness (AS) in both the carotid artery and aortic arch in young adult male and female (mRen2)27 versus normotensive Sprague Dawley (SD) rats. SBP was measured at 20 weeks of age via tail-cuff, to which rats were acclimated prior to measurements. AS data was obtained from transthoracic echocardiograms using the Vevo 2100 LAZR ultrasound. Data are presented as mean ± SEM; t- tests were conducted using GraphPad Prism 8 (p<0.05 considered significant). SBP was higher in both male (182 ± 3 mm Hg) and female (184 ± 7 mm Hg) (mRen2)27 rats compared with male (136 ± 5 mm Hg) and female (121 ± 5 mm Hg) SD rats. AS was significantly higher in the aortic arch of female (mRen2)27 rats: 5.9 ± 0.6 mm/ms compared with 2.8 ± 0.6 mm/ms for SD female rats. In male (mRen2)27 rats, aortic arch stiffness was 5.1 ± 0.5 compared with 3.5 ± 0.1 for SD male rats. The carotid artery was significantly stiffer in both male and female (mRen2)27 rats versus the SD control rats: female (mRen2)27, 6.9 ± 0.6 mm/ms, versus female SD, 2.6 ± 0.5 mm/ms; male (mRen2)27, 4.1 ± 0.2 mm/ms, versus male SD rats, 3.0 ± 0.2 mm/ms. Our findings suggest that young adult hypertensive rats, regardless of sex, exhibit greater AS relative to normotensive rats. While the increased carotid stiffness could contribute to cerebrovascular damage, further studies at different time points in both sexes are necessary to understand the mechanisms involved in the development of AS and the relationship, if any, to the sex differences in progression of cerebrovascular disease.