Does Rosuvastatin Lower Blood Pressure?

Rosuvastatin is primarily prescribed to lower cholesterol, but research suggests it may also influence blood pressure. This potential effect is of interest because high cholesterol and hypertension often coexist, increasing cardiovascular risk. Understanding whether rosuvastatin helps regulate blood pressure could inform treatment strategies.

Researchers have examined how the drug interacts with arterial function and studied its impact in different populations.

Pathways Affecting Arterial Tone

Arterial tone is regulated by endothelial function, vascular smooth muscle activity, and neurohormonal signaling. Rosuvastatin, an HMG-CoA reductase inhibitor, may influence these mechanisms beyond its lipid-lowering effects. One key pathway involves nitric oxide (NO) bioavailability. NO, synthesized by endothelial nitric oxide synthase (eNOS), promotes vasodilation. Studies indicate statins, including rosuvastatin, enhance eNOS expression and activity, improving endothelial function and reducing vascular resistance. A clinical trial in Hypertension (2019) found rosuvastatin increased flow-mediated dilation (FMD) in patients with dyslipidemia, supporting its role in endothelial-dependent vasodilation.

Rosuvastatin also reduces oxidative stress and inflammation, both of which contribute to arterial stiffness and hypertension. Reactive oxygen species (ROS) degrade NO, diminishing its vasodilatory effects. By upregulating antioxidant enzymes and suppressing NADPH oxidase activity, rosuvastatin helps preserve NO availability. Additionally, it lowers pro-inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which impair endothelial function and promote vasoconstriction. A meta-analysis in The American Journal of Cardiology (2021) found statin therapy, particularly with high-potency agents like rosuvastatin, significantly reduced arterial stiffness markers such as pulse wave velocity (PWV).

Another pathway involves calcium channel regulation in vascular smooth muscle cells. Intracellular calcium levels dictate smooth muscle contraction, and excessive calcium influx increases vascular resistance. Research suggests statins modulate calcium signaling by inhibiting Rho-kinase activity, reducing myosin light chain phosphorylation, and promoting vasorelaxation. A study in Circulation Research (2020) found rosuvastatin attenuated vasoconstriction in hypertensive animal models by downregulating Rho-associated kinase expression, reinforcing its vascular effects.

Clinical Data in Elevated Pressure

Several studies have examined rosuvastatin’s effect on blood pressure in hypertensive individuals. While primarily prescribed for cholesterol reduction, research suggests it may contribute to modest reductions in systolic and diastolic pressure, particularly in patients with additional cardiovascular risk factors. A randomized controlled trial in The Journal of Clinical Hypertension (2020) assessed hypertensive patients with hyperlipidemia taking rosuvastatin. Over 12 months, participants saw an average systolic blood pressure reduction of 4–6 mmHg and a diastolic decrease of 2–3 mmHg compared to a placebo group. While not as significant as antihypertensive medications, these reductions suggest an ancillary benefit.

The observed blood pressure reductions appear linked to improved endothelial function and arterial compliance. A study in Hypertension Research (2021) found PWV, a marker of arterial stiffness, declined after six months of rosuvastatin therapy, correlating with better vascular elasticity. These benefits were more pronounced in individuals with elevated inflammation markers, reinforcing the hypothesis that statins mitigate hypertension through anti-inflammatory and vasodilatory pathways.

Meta-analyses provide broader insights into rosuvastatin’s potential antihypertensive effects. A systematic review in The American Journal of Hypertension (2022) analyzed 15 randomized controlled trials involving over 10,000 patients. Statin therapy, particularly with high-potency agents like rosuvastatin, was associated with an average systolic blood pressure reduction of 3.8 mmHg and a diastolic decrease of 2.2 mmHg. These effects were more pronounced in older adults and those with metabolic syndrome, suggesting patient characteristics influence the drug’s impact on blood pressure.

Effects in Normotensive Adults

In normotensive adults, rosuvastatin’s impact on blood pressure is less pronounced. Since key mechanisms regulating vascular tone function optimally in these individuals, external interventions, including statins, have a limited effect. However, some studies suggest rosuvastatin may still contribute to subtle hemodynamic changes, particularly in those with endothelial dysfunction or metabolic abnormalities.

One area of interest is arterial stiffness, which affects long-term cardiovascular health even without elevated blood pressure. A study in Atherosclerosis (2021) examined normotensive participants with high low-density lipoprotein (LDL) cholesterol on rosuvastatin therapy for six months. While resting blood pressure remained unchanged, arterial compliance improved, as indicated by reductions in augmentation index (AIx), a marker of wave reflection in arteries. These findings suggest that while rosuvastatin may not lower blood pressure outright in normotensive individuals, it could enhance vascular function and overall cardiovascular resilience.

Some research also indicates rosuvastatin may influence autonomic regulation of blood pressure. A trial in Clinical Science (2022) examined heart rate variability (HRV) in normotensive adults on statin therapy, revealing modest shifts toward enhanced parasympathetic tone. While these changes did not significantly lower average blood pressure, they suggest rosuvastatin may contribute to improved autonomic stability, potentially reducing the risk of future dysregulation.

Variation by Individual Factors

Rosuvastatin’s effect on blood pressure varies based on genetic predisposition, metabolic health, and baseline cardiovascular status. Genetic polymorphisms affecting lipid metabolism and vascular responsiveness may determine whether an individual experiences meaningful blood pressure changes. Variants in the endothelial nitric oxide synthase (eNOS) gene influence vascular reactivity, potentially amplifying or diminishing the drug’s vasodilatory effects. Similarly, polymorphisms in the SLCO1B1 gene, which encodes a transporter involved in statin uptake, can affect drug bioavailability and subsequent physiological responses.

Metabolic health also plays a role. Individuals with insulin resistance or metabolic syndrome often exhibit endothelial dysfunction and increased arterial stiffness—conditions that statins may help mitigate. A retrospective analysis of electronic health records found patients with metabolic syndrome were more likely to experience modest systolic pressure reductions on rosuvastatin compared to those without metabolic abnormalities. This suggests that while the drug may not significantly affect normotensive individuals with optimal vascular function, those with preexisting metabolic disturbances may see greater benefits.