Vitamin D3 Supplementation Might Improve Hypertension
By Lara C. Pullen, PhD, from Medscape
Vitamin D3 might act as an angiotensin-converting-enzyme (ACE) inhibitor in obese patients with hypertension. Chronic vitamin D3 therapy could, therefore, reduce the risk for chronic kidney disease in obese patients by reducing the activity of the renin-angiotensin system (RAS).
Anand Vaidya, MD, MMSc, from Harvard Medical School in Boston, Massachusetts, presented the research in a poster session here at the Arteriosclerosis, Thrombosis and Vascular Biology 2012 Scientific Sessions. He discussed the poster with Medscape Medical News and explained that this was “a physiology study designed as a proof-of-concept study.”
The poster described the results of the first human intervention study designed to evaluate whether vitamin D3 therapy has an effect on RAS activity in obese patients. Such patients were chosen because they are at high risk for chronic kidney disease. A follow-up study is underway with patients of normal weight.
The study involved 14 morbidly obese subjects (body mass index, 36 kg/m²) with hypertension, prediabetes, 25-hydroxyvitamin D (25[OH]D) levels below 25 ng/mL, and normal renal function. The researchers used a meticulously controlled protocol that has been demonstrated to attain reliable measures of RAS. To achieve this, they controlled for all potential modulators of RAS. For example, because many medications can affect RAS, the subjects stopped all medications for 3 months.
The duration of vitamin D3 therapy was restricted to 1 month to minimize patient dropout and confounders such as weight loss and dietary changes.
Throughout the month, patients were given 15,000 IU of vitamin D3 per day.
Their mean 25(OH)D plasma levels increased from 18 mg/dL to 52 mg/dL.
Subjects slept flat on their backs overnight in the hospital before renal plasma flow was measured. The researchers found that high-dose vitamin D3 therapy raised baseline renal plasma flow by 5% and lowered supine mean arterial pressure.
As expected, continuous infusions of angiotensin II (AngII) reduced renal blood flow. Vitamin D3 increased renal-vascular responsiveness to a continuous infusion of AngII. This was represented by a greater decline in renal plasma flow (P < .05) after vitamin D3 therapy. Dr. Vaidya explained that the effect size was small, but noted that the effect was seen after only 1 month of vitamin D therapy.
Response to AngII is inversely related to RAS level, and the results suggest a reduction in renal-vascular RAS in patients receiving vitamin D therapy.
The researchers conclude that vitamin D3 and ACE inhibitors have the same mechanism of action.
Tochi M. Okwuosa, MD, from Wayne State University in Detroit, Michigan, discussed the poster with Medscape Medical News and noted that the research was, “very interesting [and] extremely detailed.”
The findings are consistent with the researchers’ previous cross-sectional observations demonstrating a blunted vascular sensitivity to AngII in obese patients with hypertension and lower plasma levels of 25(OH)D. The current study found that vitamin D3 therapy was able to “correct” tissue responsiveness to AngII, as ACE inhibitors do. This suggests that a low vitamin D state is associated with heightened tissue RAS activity.
Obese Patients Might Benefit from More Vitamin D
Obesity and hypertension predict a higher risk for kidney disease; treatment with ACE inhibitors has been shown to diminish the risk. These findings might, therefore, support the maintenance of higher 24(OH)D levels in obese patients with hypertension. This patient-management approach might lower renal/vascular tissue RAS activity and abrogate the development of vascular and metabolic diseases associated with these conditions.
Dr. Vaidya stated clearly that the role of vitamin D therapy in abrogating the development of diseases associated with excess RAS activity has not yet been determined. He feels, however, that this area warrants investigation.
He explained that if the mechanism of action behind the intervention is not well understood, it is difficult to design a good study.
Many intervention studies allow patients to remain on their prescribed ACE inhibitors. Dr. Vaidya is concerned that the effects of vitamin D on RAS inhibition will be masked by the presence of more powerful ACE inhibitors.
Dr. Vaidya emphasized that vitamin D–induced RAS inhibition should be considered when designing future intervention studies that evaluate the influence of vitamin D3 therapy on vascular end points. He explained that “understanding the mechanism may influence how we study outcomes.”
Dr. Pinna says:
What this article demonstrates is that Vitamin D3 acts like the group of medicines used for high blood pressure: the “ACE Inhibitors.”
“ACE” stands for ANGIOTENSIN CONVERTING ENZYMES. These enzymes are valuable in controlling blood pressure. Vitamin D3 evidently substitutes for these enzymes.
If your blood pressure is high, try Vitamin D3. It does no harm. Remember, it may take a month.
Before we had medicines for high blood pressure, we had sunlight and we wore no clothes and lived outside. Think about it…