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Studies with an antimouse PlGF antibody showed no effect on fetal development, hypertension, regression of healthy vessels, or increased risk of thrombosis in mice; thus, it is assumed that targeting PlGF will be devoid of the side effects associated with VEGF(R) inhibitors (Eskens and Verweij, 2006; Fischer et al, 2007).
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Overexpression of P450 epoxygenases attenuates the development of hypertension and improves cardiac function in spontaneous hypertensive rats [ 12].
Insulin resistance and compensatory hyperinsulinemia often coexist in hypertensive patients, which may play a role in the development of hypertension.
The hyperuricemic rats developed subtle renal injury associated with activation of the reninangiotensin system and development of hypertension.
Furthermore, a new study by heart and kidney specialists in South Korea suggests that C-reactive protein is "an independent risk factor for the development of hypertension," which in turn increases the chances of suffering a heart attack or stroke.
Subsequent experiments indicated a role of fumarase insufficiency in the development of hypertension in SS rats.
This elevation of sympathetic activity contributes to the development of hypertension.
Dietary factors play an important role in the development of hypertension (HTN).
This defect may contribute to the development of hypertension in later life.
These results implicate adrenaline-containing neurons in the brainstem in the development of hypertension.
In this model, the development of hypertension, proteinuria, and progressive renal fibrosis eventually leads to end-stage renal disease [1 3].
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