Abstract
A maternal low-protein diet (MLP) fed during pregnancy leads to hypertension in adult rat offspring. Hypertension is a major risk factor for ischaemic heart disease. This study examined the capacity of hearts from MLP-exposed offspring to recover from myocardial ischaemia-reperfusion (IR) and related this to cardiac expression of β-adrenergic receptors (β-AR) and their associated G proteins. Pregnant rats were fed control (CON) or MLP diets (n = 12 each group) throughout pregnancy. When aged 6 months, hearts from offspring underwent Langendorff cannulation to assess contractile function during baseline perfusion, 30 min ischemia and 60 min reperfusion. CON male hearts demonstrated impaired recovery in left ventricular pressure (LVP) and dP/dt max (P < 0.01) during reperfusion when compared to MLP male hearts. Maternal diet had no effect on female hearts to recover from IR. MLP males exhibited greater membrane expression of β 2-AR following reperfusion and urinary excretion of noradrenaline and dopamine was lower in MLP and CON female rats versus CON males. In conclusion, the improved cardiac recovery in MLP male offspring following IR was attributed to greater membrane expression of β 2-AR and reduced noradrenaline and dopamine levels. In contrast, females exhibiting both decreased membrane expression of β 2-AR and catecholamine levels were protected from IR injury.
Highlights
Adult cardiovascular disease is associated with metabolic and physiological aberrations that occur during fetal development
There was no significant effect of maternal diet on the recovery of female indices of cardiac function (LVP, dP/dtmax, heart rate (HR)) to ischemiareperfusion insult (Table 1)
The key finding from the present study is that hearts from maternal low-protein diet (MLP) male offspring demonstrated improved recovery in cardiac function following IR when compared to CON males, whereas IR recovery in females was unaffected by maternal diet
Summary
Adult cardiovascular disease is associated with metabolic and physiological aberrations that occur during fetal development. Epidemiological studies provide evidence that intrauterine growth retardation increases the risk of hypertension and cardiovascular disease in adult life [1]. Such findings led to the fetal programming hypothesis that exposure to a suboptimal intrauterine environment can predispose to adult noncommunicable disease [2]. Protein restriction had no effect on recovery of the female heart [10] This sexspecific effect concurs with previous findings in rats in which intrauterine growth restriction as a result of either hypoxia or undernutrition caused cardiac remodelling and impaired recovery to IR in adult male offspring [11]
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