A maternal high salt diet disturbs cardiac and vascular function of offspring

High salt intake is an environmental factor that promotes increased blood pressure. We previously demonstrated that high salt diet causes aggravation of hypertension and impaired vasodilation in response to nitric oxide (NO) in young spontaneously hypertensive rats (SHR), which exhibit low sensitivity to salt in adulthood. Changes in offspring blood pressure and cardiovascular structures have been reported. However, it remains unclear to what extent a maternal high salt intake may affect cardiac and/or vascular function in offspring. Therefore, we investigated influence of exposure to a maternal high salt diet during gestation and lactation on offspring's cardiac and arterial functions in SHR.

SHR dams were fed either a high salt diet or a control diet. After weaning, the offspring were fed the high salt diet or control diet for 8weeks.

Compared with offspring of control diet-fed dams, at 12weeks of age, offspring of the high-salt diet-fed dams had lower blood pressure, heart rate, indices of both left ventricular systolic and diastolic function, and a decreased aortic vasodilation response to NO. Postnatal high salt intake did not affect blood pressure, vasodilatory response, or cardiac function in offspring of high-salt diet-fed dams. Neither maternal nor postnatal dietary salt altered levels of lipid peroxide, superoxide dismutase, or angiotensinogen mRNA in serum and ventricle of the offspring.

Exposure to high maternal dietary salt induces cardiac and vascular dysfunction in offspring. These results point to the possible importance of avoiding excess dietary salt during gestation and lactation.