C‐Reactive Protein‐Related Endothelial Vasodilator Dysfunction in Healthy Adults

Elevated plasma concentrations of C‐reactive protein (CRP) are associated with an increased risk of cardiovascular (CV) disease. The underlying mechanisms for this increased risk, however, remain unclear. We determined whether elevation in plasma CRP is associated with endothelial vasodilator dysfunction, independent of other CV risk factors. To address this aim, 54 healthy, sedentary adults (35M/19F; age 56±2 yr) were stratified based on plasma CRP concentrations according to AHA/CDC guidelines: CRP < 1.0 mg/L (low CRP; n=22), CRP 1.0–3.0 mg/L (moderate CRP; n=16), and CRP > 3.0 mg/L (high CRP; n=16). Forearm blood flow (FBF; plethysmography) was assessed in response to incremental intrabrachial doses of acetylcholine (ACh) and sodium nitroprusside (SNP). FBF responses to ACh were ~25% lower (P<0.05) in the moderate (4.2±0.3 to 10.9±0.9 mL/100 mL tissue/min) and high (4.1±0.2 to 10.7±0.8) compared with the low (4.2±0.2 to 14.4±0.9) CRP group. Furthermore, there was an inverse relation between CRP and peak FBF to ACh (r=−0.31; P<0.05). There were no gender interactions or CRP‐related differences in FBF to SNP. Elevations in plasma CRP are associated with impaired endothelium‐dependent vasodilation in otherwise healthy adults. Endothelial vasodilator dysfunction may contribute mechanistically to the increased risk of CV disease with elevated CRP concentrations.