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1 Kinesiology, Temple University, Philadelphia, Pennsylvania, United States
2 Cardiovascular Research Center, Temple University, Philadelphia, Pennsylvania, United States
3 Physiology, Temple University, Philadelphia, Pennsylvania, United States
4 Physiology, Temple University, Philadelphia, Pennsylvania, United States; Cardiovascular Research Center, Temple University, Philadelphia, Pennsylvania, United States
5 Kinesiology, Temple University, Philadelphia, Pennsylvania, United States; Cardiovascular Research Center, Temple University, Philadelphia, Pennsylvania, United States; Physiology, Temple University, Philadelphia, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: jlibonat{at}temple.edu.
-adrenergic receptor (AR) responsiveness is down-regulated in LVH induced by chronic hypertension. While exercise training in hypertension enhances AR responsiveness, the role of adenylyl cyclase remains unclear. The purpose of the present study was to test whether treadmill running in the spontaneous hypertension rat (SHR) model improves LV responsiveness to forskolin (FOR) or the combination of FOR + isoproterenol (FOR+ISO). Female SHR (16-wks) were placed into sedentary (SHR-SED, n=7) or treadmill trained (SHR-TRD, n=8) groups. Wistar-Kyoto (WKY, n=7) animals acted as controls. Langendorff LV performance was established at baseline and with FOR infusion (1 and 5 µmol/L) and FOR+ISO (5 µmol/L + 1*10-8 mol/L, respectively). Heart rate (HR), systolic blood pressure, and heart to body weight ratio were lower in WKY relative to both SHR groups (p<0.05). LV performance and HR similarly increased in all groups with FOR infusion. In the presence of 5 µmol/L FOR, ISO increased LV developed pressure (LVDevP), +dP/Dt and -dP/DT to a greater extent in SHR-TRD than SHR-SED (p<0.05). Phospholamban phosphorylation at the Thr17 was greater in SHR-TRD relative to SHR-SED and WKY (p<0.05). LVDevP was moderately correlated with phospholamban phosphorylation at both the Ser16 (r=0.64; p<0.05) and Thr17 (r=0.52; p<0.05). The adenylyl cyclase step in the AR cascade is not down-regulated in the early course of hypertension and the enhanced AR responsiveness with training is mediated at levels other than adenylyl cyclase. AR inotropic responsiveness in the presence of direct adenylyl cyclase agonism is improved in trained compared to sedentary SHR hearts.
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