Abstract
C-Reactive Protein (CRP) levels correlate with systolic and diastolic blood in normotensive subjects. We evaluated the hypothesis that hypertensives will have a higher CRP level compared to normotensives and variability in activity of the renin angiotensin system and degree of insulin resistance may modulate these levels. CRP levels were measured in 18 normotensive and 222 hypertensive subjects. All anti-hypertensive medications were discontinued two weeks before the study and subjects were placed on a controlled low salt (10 mmol sodium) diet for one week. Blood was drawn for CRP, plasma renin activity (PRA), glucose, insulin and aldosterone at 8AM with the subjects fasting and lying in a supine position. Hypertensives had approximately a five fold greater CRP levels compared to normotensives (2.46 ± 0.34 and 0.50 ± 0.14 mg/l respectively, mean ± SEM p<0.0001). The low renin and normal/high renin hypertensive subgroups had almost identical levels (2.4 ± 0.79 and 2.47 ± 0.37, p=0.97). In hypertensive subjects there was no racial difference in CRP levels (blacks 2.1 ± 0.64 and whites 2.5 ± 0.37, p=0.49) but females had higher levels compared to males (3.29 ± 0.6 and 1.7 ± 0.36, p<0.001). Using a multivariate analysis the following factors significantly influenced CRP levels: PRA (p<0.001), BMI (p=0.001), cholesterol (p=0.001), aldosterone (p=0.007), insulin resistance (p=0.024) and gender (p<0.001) (R-squared for the model 0.30). All had a positive influence except aldosterone, which decreased CRP levels. Hypertensives have a significantly higher underlying inflammatory state compared to normotensives, particularly in women, that could contribute to their increased cardiovascular risk. Multiple factors contribute to the increased CRP levels seen in hypertensives with variations in PRA, BMI, cholesterol, insulin resistance, gender and aldosterone explaining about 30% of its variation.