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Hypertension-induced left ventricular (LV) hypertrophy is an independent risk factor for heart failure. To understand the impact of LV hypertrophy on cardiac hemodynamic before heart failure development, we studied LV performance and nitric oxide (NO) and reactive oxygen species (ROS) signaling in 6-month-old SHRs and age-matched Wistar-Kyoto rats (WKY) subjected to preload and afterload challenges. SHRs 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. Further, LV nNOS, but not eNOS, expression and nitrite/nitrate (NOx) were higher in SHRs than WKYs. Acute volume overload (dextrose infusion) caused smaller reductions in LV dp/dtmax and LVDP and greater increases in LVEDP and isovolumic relaxation constant (Tau, τ) in SHRs, compared with WKYs, suggesting a better preserved systolic and depressed diastolic functions in SHRs. SHRs exhibited improved LV performance during pressure overload (phenylephrine infusion) as reflected by the greater increases in LVDP, LVESP, LV dp/dtmin, and LV dp/dtmax. LV ROS was increased by overload challenges in WKYs but not in SHRs. Overall, the blunted increase in LV ROS may account for the betterpreserved ventricular performance during volume or pressure overload in SHRs despite evidence of early LV hypertrophy.

Preserved Left Ventricular Performance in Spontaneously Hypertensive Rats Following Preload and Afterload Challenges