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Background: Microvascular function plays an important role in ARVD (atherosclerotic renovascular disease). RFR (renal flow reserve), the capacity of renal vasculature to dilate, is known to reflect renal microvascular function. In this pilot study, we assessed PET (positron emission tomography)-based RFR values of healthy persons and renal artery stenosis patients.Seventeen patients with ARVD and eight healthy subjects were included in the study. Intravenous enalapril 1 mg was used as a vasodilatant, and the maximum response (blood pressure and RFR) to it was measured at 40 min. Renal perfusion was measured by means of oxygen-15-labeled water PET. RFR was calculated as a difference of stress flow and basal flow and was expressed as percent [(stress blood flow − basal blood flow)/basal blood flow] × 100%.Results: RFR of the healthy was 22%. RFR of the stenosed kidneys of bilateral stenosis patients (27%) was higher than that of the stenosed kidneys of unilateral stenosis patients (15%). RFR of the contralateral kidneys of unilateral stenosis patients was 21%. There was no difference of statistical significance between RFR values of ARVD subgroups or between ARVD subgroups and the healthy. In the stenosed kidneys of unilateral ARVD patients, stenosis grade of the renal artery correlated negatively with basal (p = 0.04) and stress flow (p = 0.02). Dispersion of RFR values was high.Conclusions: This study is the first to report [15O]H2O PET-based RFR values of healthy subjects and ARVD patients in humans. The difference between RFR values of ARVD patients and the healthy did not reach statistical significance perhaps because of high dispersion of RFR values. [15O]H2O PET is a valuable non-invasive and quantitative method to evaluate renal blood flow though high dispersion makes imaging challenging. Larger studies are needed to get more information about [15O]H2O PET method in evaluation of renal blood flow. [ABSTRACT FROM AUTHOR]

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) may increase blood pressure (BP) and potentially reduce the efficacy of several antihypertensive drugs. We evaluated the effect of low-dose acetylsalicylic acid (ASA) on BP control in drug-treated hypertensive patients in a primary care population., Design/methods: Nine hundred and five successive patients aged 25–91 years (mean 65.5 years) from 15 health centers in south-west Finland were studied. The patients were on antihypertensive monotherapy (45.7%) or on combination therapy (54.3%). Office BP was measured twice with a 2-min interval after at least a 10-min rest using an ordinary sphygmomanometer., Results: Patients receiving ASA (n = 246) showed lower diastolic BP (83.9 ± 9.0 vs. 87.0 ± 9.6 mmHg; P < 0.001) compared with those who were not using any NSAIDs (n = 659). No significant difference in systolic BP was observed between the groups. As a result, pulse pressure was slightly higher in the ASA group (66.9 ± 18.9 vs. 63.3 ± 17.7 mmHg, P = 0.01). Mean arterial pressure was lower in the ASA group (106.2 ± 10.6 vs. 108.1 ± 10.4 mmHg, P = 0.02). In a stepwise linear multivariate model, ASA remained a significant predictor of lower diastolic BP even after the adjustment with the confounding effects of age and sex., Conclusion: According to our population-based study low-dose ASA does not have deleterious effects on BP control in drug-treated hypertensive patients.