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Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion
Published on: May 26, 2022
Cholecalciferol treatment downregulates renin-angiotensin system and improves endothelial function in essential
Davide Carrara1, Rosa Maria Bruno, Alessandra Bacca
1aDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy *Davide Carrara and Rosa Maria Bruno contributed equally to the study.
Insights
Vitamin D deficiency is linked to cardiovascular disease. Supplementing with vitamin D (cholecalciferol) normalized levels, reduced the renin-angiotensin system, and improved vascular function in hypertensive patients.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Nutritional Science
Background:
- Vitamin D deficiency is associated with increased cardiovascular disease risk.
- Mechanisms may involve the renin-angiotensin-aldosterone system (RAAS) and vascular dysfunction.
- Interventional studies on vitamin D's effects on RAAS and vascular function are limited.
Purpose of the Study:
- To investigate whether vitamin D (cholecalciferol) supplementation can suppress the RAAS and improve vascular function in patients with essential hypertension and hypovitaminosis D.
Main Methods:
- Thirty-three patients with essential hypertension and low vitamin D received 50,000 IU/week cholecalciferol for 8 weeks.
- Control groups included hypertensive patients with normal vitamin D and normotensive individuals.
- Evaluated plasma vitamin D, RAAS components (renin activity, renin, angiotensin II, aldosterone), and vascular function (flow-mediated dilation, pulse wave velocity).
Main Results:
- Vitamin D levels normalized in treated patients.
- Significant reductions were observed in plasma renin activity, renin, and angiotensin II levels.
- Flow-mediated dilation (FMD) significantly improved, indicating enhanced endothelial function.
Conclusions:
- Restoring normal vitamin D levels via cholecalciferol treatment effectively inhibits the peripheral renin-angiotensin system.
- This intervention improves endothelial function in essential hypertensive patients with vitamin D deficiency.
Background:
Vitamin D deficiency is related to an increased prevalence of cardiovascular disease. Renin-angiotensin-aldosterone system suppression and vascular dysfunction are considered among the main mechanisms implicated in this association. However, interventional studies demonstrating that vitamin D replacement reduces circulating renin-angiotensin-aldosterone components and improves vascular function in humans are still lacking.
Methods:
Thirty-three consecutive patients with essential hypertension and hypovitaminosis D underwent therapy with cholecalciferol 50 000 IU/week orally for 8 weeks. Thirty-three hypertensive patients with normal vitamin D levels and 20 normotensive individuals were also enrolled as control groups. At baseline and at the end of the study, we evaluated plasma renin activity, circulating renin, angiotensin II, aldosterone and plasma vitamin D levels. Endothelial function [flow-mediated dilation (FMD)], carotid-femoral pulse wave velocity and augmentation index, peripheral and central blood pressure were also acquired.
Results:
After 8-week cholecalciferol administration, all treated patients normalized plasma 25(OH)D values. Furthermore, a reduction in plasma levels of plasma renin activity (1.17 ± 0.3 vs 1.51 ± 0.4 ng/ml per h, P = 0.02), renin (13.4 ± 1.7 vs 19.2 ± 2.9 pg/ml, P < 0.001), angiotensin II (11.6 ± 1.6 vs 15.8 ± 2.7 pg/ml, P = 0.02) was observed at the end of the study. FMD was significantly increased after cholecalciferol treatment (4.4 ± 2.6 vs 3.3 ± 2.1%, P < 0.05), in the absence of changes of brachial artery diameter and endothelium-independent vasodilation. Carotid-femoral pulse wave velocity and augmentation index were not modified, as well peripheral and central blood pressure.
Conclusion:
The restoration of normal vitamin D levels after 8-week cholecalciferol treatment is able to inhibit peripheral renin-angiotensin system and improve FMD in essential hypertensive patients with hypovitaminosis D.
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