Abstract
Statin use is associated with lower aldosterone levels. We hypothesized that caveolin-1 may be important for the uptake of statins into the adrenal gland and would affect statin’s aldosterone-lowering effects. The aim of this study was to test whether the caveolin-1 risk allele (rs926198) would affect aldosterone levels associated with statin use. The Hypertensive Pathotype database includes healthy and hypertensive individuals who have undergone assessment of adrenal hormones. Individuals were studied off antihypertensive medications but were maintained on statins if prescribed by their personal physician. Adrenal hormones were measured at baseline and after 1 hour of angiotensin II stimulation on both high- and low-sodium diets. A mixed-model repeated-measures analysis was employed with a priori selected covariates of age, sex, body mass index, and protocol (low versus high sodium, baseline versus angiotensin II stimulated aldosterone). A total of 250 individuals were included in the study; 31 individuals were taking statins (12.4%) and 219 were not. Among statin users, carrying a caveolin-1 risk allele resulted in a 25% (95% CI, 1–43.2) lower aldosterone level (P=0.04). However, among nonstatin users, carrying a caveolin-1 risk allele resulted in no significant effect on aldosterone levels (P=0.38). Additionally, the interaction between caveolin-1 risk allele and statin use on aldosterone levels was significant (P=0.03). These findings suggest caveolin-1 risk allele carrying individuals are likely to receive the most benefit from statin’s aldosterone-lowering properties; however, due to the observational nature of this study, these findings need further investigation.
Highlights
Statin use is associated with lower aldosterone levels
These findings are significant because renin-angiotensin-aldosterone system (RAAS) dysregulation and mineralocorticoid receptor activation are involved in the pathogenesis of coronary artery disease, myocardial infarction, hypertension, atrial fibrillation, renal disease, and heart failure.[5,6,7]
Statins may exert their effects on eNOS through Cav[1] as endocytosis of caveolae has been shown to mediate the activation of eNOS.[10,12]
Summary
Statin use is associated with lower aldosterone levels. We hypothesized that caveolin-1 may be important for the uptake of statins into the adrenal gland and would affect statin’s aldosterone-lowering effects. Cav[1], a scaffolding protein, is the main component of caveolae and is important in transmembrane cholesterol transportation, cholesterol accumulation, and cholesterol efflux.[10] simvastatin treatment decreased Cav[1] expression and increased eNOS (endothelial nitric oxide synthase) expression in patients who underwent abdominal aortic aneurysm repair.[11] The study highlighted a potential link between statins and Cav[1] and suggested a possible pleiotropic benefit of statins outside of lipid reduction Statins may exert their effects on eNOS through Cav[1] as endocytosis of caveolae has been shown to mediate the activation of eNOS.[10,12] The interplay between Cav[1], statin use, and aldosterone levels has yet to be determined. We hypothesized that Cav[1] may be important for the uptake of statins by the Hypertension is available at https://www.ahajournals.org/journal/hyp
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