Preserved Left Ventricular Performance In Spontaneously Hypertensive Rats Following Preload And Afterload Challenges

Abstract

Hypertension‐induced left ventricular (LV) hypertrophy is an independent risk factor for heart failure. We studied LV performance and myocardial nitric oxide (NO) signaling and reactive oxygen species (ROS) in 6‐month‐old SHRs and age‐matched Wistar‐Kyoto rats (WKY) subjected to preload and afterload challenges. Under basal conditions, LV nNOS, but not eNOS, expression and nitrite/nitrate (NOx) were higher in SHR than in WKY rats. SHRs also exhibited higher LV weight, LV developed pressure (LVDP), LV end‐systolic pressure (LVESP), rate of rise (LV dp/dtmax) and fall (LV dp/dtmin) in LV pressure. In the acute volume overload model (dextrose infusion), SHRs showed significantly smaller reductions in LV dp/dtmax and LVDP and greater increases in LVEDP and isovolumic relaxation constant (Tau, τ), compared with WKY rats, suggesting enhanced systolic and depressed diastolic functions in SHRs. We also report improved LV performance in SHRs during pressure overload (phenylephrine infusion) as reflected by the increases in LVDP, LVESP, LV dp/dtmin, and LV dp/dtmax. LV ROS was increased by the two overload challenges in WKY, but not SHR, rats. The results suggest that despite evidence of early LV hypertrophy, the ability of the SHR to curtail myocardial oxidative stress may accounts, at least partly, for the preservation of the left ventricular performance during pressure or volume overload challenge in SHRs.