Recent evidence suggests vitamin D has a critical role in maintaining heart health through activation of the vitamin D receptor expressed in cardiomyocytes, and vitamin D deficiency may be implicated in the pathophysiology of HFrEF through activation of the renin-angiotensin system, impaired calcium handling, exaggerated inflammation, secondary hyperparathyroidism, pro-fibrotic properties, and proatherogenic potential.
Because vitamin D deficiency activates the renin-angiotensin-aldosterone system (RAAS), we hypothesized that this vitamin would interact with the RAAS to influence blood pressure (BP) in nondipper hypertensive patients.
Our data suggest that even short-term severe vitamin D deficiency may directly promote hypertension and impacts on renin-angiotensin system components that could contribute to target-organ damage.
Mice with diet-induced vitamin D deficiency showed increased systolic and diastolic blood pressure, high plasma renin, and decreased urinary sodium excretion.