Related Experiment Video
Updated: Sep 1, 2025
Author Spotlight: A Pharmacodissection Approach to Uncover Mechanisms in Cardiovascular Disease Risk Populations
Published on: July 21, 2023
Seven days of statin treatment improves nitric-oxide mediated endothelial-dependent cutaneous microvascular function
Gabrielle A Dillon1, Anna E Stanhewicz2, Corinna Serviente3
1Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, PA, United States of America; Center for Healthy Aging, The Pennsylvania State University, University Park, PA, United States of America.
Insights
Endometriosis impairs blood vessel function, specifically nitric oxide (NO)-dependent dilation. Short-term atorvastatin (a statin) improved this endothelial function in women with endometriosis, suggesting a potential treatment for cardiovascular disease risk.
Area of Science:
- Cardiovascular Science
- Reproductive Endocrinology
- Vascular Biology
Background:
- Endometriosis is linked to systemic inflammation and increased cardiovascular disease (CVD) risk.
- Endothelial dysfunction, a precursor to CVD, is understudied in endometriosis.
- Statins, known for anti-inflammatory properties, are proposed for endometriosis adjunctive therapy.
Purpose of the Study:
- To investigate microvascular endothelial function in women with endometriosis.
- To determine if impaired vasodilation is mediated by reduced nitric oxide (NO) bioavailability.
- To assess the effect of short-term atorvastatin on endothelial function in these women.
Main Methods:
- Microdialysis was used to measure endothelium-dependent vasodilation via acetylcholine in 8 women with endometriosis and 8 controls.
- Nitric oxide (NO) dependency was assessed using the NO synthase inhibitor L-NAME.
- 6 women with endometriosis received 7 days of oral atorvastatin (10 mg) before repeat testing.
Main Results:
- Vasodilation was significantly blunted in women with endometriosis compared to controls (p < 0.01).
- NO-dependent vasodilation was reduced in endometriosis patients (217 vs. 88 AUC, p = 0.03).
- Atorvastatin treatment improved both Ach-induced (p < 0.01) and NO-dependent vasodilation (p = 0.05) in women with endometriosis.
Conclusions:
- Microcirculatory endothelial function is impaired in women with endometriosis, partly due to reduced NO.
- Short-term atorvastatin administration improved endothelial vasodilation.
- Statin therapy may be a viable strategy to reduce accelerated CVD risk in women with endometriosis.
Introduction:
Endometriosis is associated with systemic inflammation and increased risk of cardiovascular disease (CVD). Endothelial dysfunction is one of the first manifestations of CVD but is unexplored in women with endometriosis. HMG-CoA-reductase inhibitors (statins) exert potent anti-inflammatory effects, and have been proposed as an adjunctive therapy in women with endometriosis. We hypothesized that microvascular endothelial function would be impaired in otherwise healthy women with endometriosis mediated by reduced nitric oxide (NO)-dependent dilation and that short term statin administration would improve endothelial function.
Methods:
In 8 healthy control (HC: 33 ± 9 yr) and 8 women with endometriosis (EN: 34 ± 9 yr), laser-Doppler flux (LDF) was measured continuously during graded intradermal microdialysis perfusion of the endothelium-dependent agonist acetylcholine (Ach: 10-10-10-1 M) alone and in combination with the NO synthase inhibitor (L-NAME: 0.015 M). 6 EN repeated the microdialysis experiment following 7 days of oral atorvastatin treatment (10 mg). Cutaneous vascular conductance was calculated (CVC = LDF*mmHg-1) and normalized to site-specific maximum (28 mM sodium nitroprusside, 43 °C). The NO-dependent dilation was calculated as the difference between the areas under the dose response curves.
Results:
Ach-induced vasodilation was blunted in women with endometriosis (main effect p < 0.01), indicating impaired endothelial function. NO-dependent vasodilation was also reduced in women with endometriosis (HC: 217 ± 120.3 AUC vs. EN: 88 ± 97 AUC, p = 0.03). Oral atorvastatin improved Ach-induced (main effect p < 0.01) and NO-dependent (295 ± 153 AUC; p = 0.05) vasodilation in women with endometriosis.
Conclusion:
Microcirculatory endothelium-dependent vasodilation is impaired in women with endometriosis, mediated in part by reductions in NO. Short-term oral atorvastatin improved endothelium-dependent vasodilation, suggesting that statin therapy may be a viable intervention strategy to mitigate accelerated CVD risk in women with endometriosis.
Related Concept Videos
01:20Lipid-Lowering Drugs: Statins and Miscellaneous Agents
01:28Nitric Oxide Signaling Pathway
01:26Atherosclerosis III: Management