Molecular Mechanism of Aggravation of Hypertensive Organ Damages by Short-Term Blood Pressure Variability
There is increasing evidence that not only the elevation of systolic and diastolic blood pressure (BP) but also
the increase in BP variability (or fluctuation) are associated with hypertensive organ damages and the morbidity and
mortality of cerebrovascular and cardiovascular events. However, the molecular mechanism whereby the increase in BP
variability aggravates hypertensive organ damages remains unknown. Thus, we created a rat chronic model of a
combination of hypertension and large BP variability by performing bilateral sino-aortic denervation in spontaneously
hypertensive rat. A series of our studies using this model revealed that large BP variability induces chronic myocardial
inflammation by activating local angiotensin II and mineralocorticoid receptor systems and thereby aggravates cardiac
hypertrophy and myocardial fibrosis, leading to systolic dysfunction, in hypertensive hearts. In addition, large BP
variability induces the aggravation of arteriolosclerotic changes and ischemic cortical fibrosis in hypertensive kidney via
local angiotensin II system.
Keywords: Angiotensin II, cardiac hypertrophy, fibrosis, inflammation, mineralocorticoid receptor, statins.
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