Vitamin D3 Therapy Corrects the Tissue Sensitivity to Angiotensin II Akin to the Action of a Converting Enzyme Inhibitor in Obese Hypertensives: An Interventional Study
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Context: Vitamin D deficiency and obesity are associated with increased tissue renin-angiotensin system (RAS) activity. Objective: The objective of the study was to evaluate whether vitamin D3 therapy in obesity reduces tissue-RAS activity, as indicated by an increase in tissue sensitivity to angiotensin II (AngII). Participants: Participants included obese subjects with hypertension and 25-hydroxyvitamin D less than 25 ng/ml. Design: Subjects were studied before and after 1 month of vitamin D3 15,000 IU/d, while in dietary sodium balance, and off all interfering medications. Fourteen subjects successfully completed all study procedures. Setting: The study was conducted at a clinical research center. Outcome Measures: At each study visit, tissue sensitivity to AngII was assessed by measuring renal plasma flow (RPF), mean arterial pressure (MAP), and adrenal secretion of aldosterone during an infusion of AngII. Subjects were then given captopril, and a second AngII infusion to evaluate the effect of captopril on tissue-RAS activity. Results: Vitamin D3 therapy increased 25-hydroxyvitamin D (18 to 52 ng/ml) and basal RPF (+5%) and lowered supine MAP (−3%) (all P < 0.01). There was a greater decline in RPF and higher stimulation of aldosterone with AngII infusion after vitamin D3 therapy (both P < 0.05). As anticipated, captopril increased the renal-vascular, MAP, and adrenal sensitivity to AngII, but this effect was much smaller after vitamin D3 therapy, indicating that vitamin D3 therapy corrected the tissue sensitivity to AngII akin to captopril. Conclusions: Vitamin D3 therapy in obese hypertensives modified RPF, MAP, and tissue sensitivity to AngII similar to converting enzyme inhibition. Whether chronic vitamin D3 therapy abrogates the development of diseases associated with excess RAS activity warrants investigation.
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The PTH response to angiotensin II was further enhanced in the same subjects following vitamin D3 therapy, which also marginalized the influence of captopril on subsequent angiotensin II infusions.
“The PTH-response to AngII was further enhanced in the same subjects following vitamin D3 therapy, which also marginalized the influence of captopril on subsequent AngII infusions (presumptively due to maximal suppression of the endogenous tissue-RAAS with vitamin D3 therapy)4.”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
Infusion of angiotensin II at 1 ng/kg/min in a vitamin D deficient state acutely increased serum aldosterone by 148% and PTH by 10.3% from baseline.
“Infusion of AngII (1 ng/kg/min) in a vitamin D deficient state resulted in an expected rise in serum aldosterone (+148%) (as previously described)4, but also a +10.3% increase in PTH from baseline (Figure 1a).”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
Vitamin D deficiency blunts tissue-responsiveness to exogenous angiotensin II by inducing a state of high tissue-RAAS activity.
“We previously showed that vitamin D deficiency blunts tissue-responsiveness to exogenous AngII by inducing a state of high tissue-RAAS activity4,6,31; this blunted sensitivity to AngII could be corrected by lowering the tissue-RAAS with an ACE inhibitor or vitamin D3 therapy4,33.”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
When integrated with Study 1, an incremental relationship between the RAAS and PTH was observed, modulated by angiotensin II dose, ACE inhibition, and vitamin D status.
“When integrated with the findings from Study 1 (Figure 1a–c), an incremental relationship between the RAAS and PTH was observed, which was modulated by AngII dose, as well as by ACE inhibition and vitamin D status (both of which sensitize the tissue responsiveness to AngII infusion)4,6,31–33.”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
The blunted sensitivity to angiotensin II could be corrected by lowering the tissue-RAAS with an ACE inhibitor or vitamin D3 therapy.
“We previously showed that vitamin D deficiency blunts tissue-responsiveness to exogenous AngII by inducing a state of high tissue-RAAS activity4,6,31; this blunted sensitivity to AngII could be corrected by lowering the tissue-RAAS with an ACE inhibitor or vitamin D3 therapy4,33.”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
Both ACE inhibition and vitamin D3 therapy independently enhanced the PTH response to angiotensin II infusion.
“The role of AngII as the mediator of these effects was further supported by the fact that the regulation of PTH was influenced by interventions known to sensitize tissue-responsiveness to AngII4,33: both ACE inhibition and vitamin D3 therapy independently enhanced the PTH-response to AngII infusion.”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
The subjects in all four studies were overweight or obese, as previously reported, but had comparable 25-hydroxyvitamin D concentrations.
“The subjects in all four studies were overweight or obese, as previously reported4, but had comparable 25-hydroxyvitamin D (25[OH]D) concentrations (Table 1).”
From Human Interventions to Characterize Novel Relationships Between the Renin–Angiotensin–Aldosterone System and Parathyroid Hormone (2014) · cites this paper as [4]
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- Authors
- Vaidya, A., Sun, B., Larson, C., Forman, J. P., & Williams, J. S.
- Affiliations
- Brigham and Women's Hospital (US)
- Division of Endocrinology, Diabetes, and Hypertension (A.V., B.S., C.L., J.S.W.), Boston, Massachusetts 02115
- Corresponding author
- Vaidya, Anand
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2012-07-01
- Volume
- 97
- Issue
- 7
- Pages
- 2456-2465
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC3387405
- OpenAlex
- W2061737727
- Cited by
- 68
- References
- 51
- Citations by year
- 2025: 4 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 2 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 4 · 2015: 5 · 2014: 6 · 2013: 14 · 2012: 1
- FWCI
- 5.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Brigham and Women's Hospital (M01 RR02635)
- Harvard Catalyst (UL1-RR025758, RR025758)
- National Institutes of Health (RR‐02635)
- American Medical Association Foundation
- National Heart, Lung, and Blood Institute (K23HL08236-03, F32HL104776, T32HL007609, P50HL055000, K23HL111771)
- U.S. National Library of Medicine (U54LM008748)
- National Center for Research Resources (UL1RR025758, M01RR002635)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Keywords
- vitamin D3 supplementation, angiotensin II sensitivity, tissue renin-angiotensin system, obesity, hypertension, 25-hydroxyvitamin D, captopril, aldosterone secretion, renal plasma flow, mean arterial pressure, ACE inhibitors
- MeSH terms
- Adult, Angiotensin II, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Captopril, Cholecalciferol, Drug Resistance, Drug Synergism, Female, Humans, Hypertension, Male, Middle Aged, Obesity, Vitamin D Deficiency, Renal Plasma Flow
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