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Study Objective: To assess the effects of ibuprofen on blood pressure control in patients being treated with antihypertensive drugs.Design: Randomized, blinded, placebo-controlled, parallel trial of ibuprofen compared with acetaminophen and with placebo in 3-week treatment periods.Setting: A general internal medicine clinic at a university hospital.Patients: Forty-five patients with essential hypertension controlled by treatment with at least two antihypertensive drugs were enrolled. Of these, 41 completed the study; treatment was discontinued in 3 of the 15 patients in the ibuprofen group due to breakage of the drug capsules, and after randomization in 1 of the 14 patients in the placebo group due to unstable angina. All 15 patients in the acetaminophen group completed the study.Interventions: All previous antihypertensive regimens were continued. During the 3-week treatment, ibuprofen, 400 mg, was administered orally every 8 hours; acetaminophen, 1 g, orally every 8 hours; or placebo, 2 capsules, orally every 8 hours.Measurements and Main Results: In the ibuprofen group, the mean increase from baseline after 3 weeks of treatment was significant in the average supine diastolic blood pressure (6.4 mm Hg; 95% confidence interval [CI], 1.05 to 11.75; p = 0.0239); supine mean arterial pressure (6.6 mm Hg; 95% CI, 1.25 to 11.95; p = 0.0205); and sitting mean arterial pressure (5.8 mm Hg; 95% CI, 1.57 to 10.04; p = 0.0123). The mean increase in blood pressure variables in the ibuprofen group was significantly different compared with the mean increase in the variables in the placebo group after 3 weeks of treatment: supine systolic blood pressure (7.1 mm Hg compared with -4.5 mm Hg; 95% CI for the difference in means, 2.5 to 20.6; p = 0.0133); supine diastolic pressure (6.4 mm Hg compared with 0.0; 95% CI for difference in means, 0.87 to 12.4; p = 0.0250); supine mean arterial pressure (6.6 mm Hg compared with -1.5; 95% CI for difference in means, 2.0 to 14.2; p = 0.0110); sitting systolic pressure (6.8 mm Hg compared with -3.7; 95% CI for difference in means, 2.0 to 19.0; p = 0.0169); sitting diastolic pressure (5.3 mm Hg compared with -1.1; 95% CI for difference in means, 0.76 to 12.1; p = 0.0273); and sitting mean arterial pressure (5.8 mm Hg compared with -2.0; 95% CI for difference in means, 1.5 to 14.1; p = 0.0169).(ABSTRACT TRUNCATED AT 400 WORDS) [ABSTRACT FROM AUTHOR]

We wished to determine whether enhanced bioavailability of bradykinin (BK) and vasodilatory prostaglandins contribute to renovascular and sodium-handling effects of angiotensin-converting enzyme (ACE) inhibition after myocardial infarction (MI). We studied rats after coronary artery ligation treated for 3 weeks with captopril or losartan (2 g/L drinking water for each agent). Hemodynamic and renal function studies were performed in conscious rats before and after sequential infusion BK inhibitor (BKI, 0.02 ng/kg/min) and indomethacin (1 mg/kg). Myocardial infarction increased filtration fraction (FF) 20% (p < .004) but did not change glomerular filtration rate (GFR), urine flow (UF), renal blood flow (RBF), renal vascular resistance (RVR), urine sodium (UNa), or fractional excretion of sodium (FENa). Captopril decreased (p < 0.001) mean arterial pressure (MAP) 25%, UF 61%, RVR 65%, and FENa 75% and increased (p < 0.05) GFR 22%, and RBF 34%. Losartan decreased (p < 0.05) MAP 27%, UF 52%, RVR 21%, and FENa 44%. In captopril-treated MI rats, BKI decreased (p < 0.05) GFR 22% and RBF 25% and increased (p < 0.05) RVR 32%, UNa 43%, and FENa 28%, whereas indomethacin decreased (p < 0.05) GFR 24% and increased (p < 0.05) UNa 86% and FENa 112%. In losartan-treated MI rats, BKI increased (p < 0.05) UNa 42% and FENa 60%, whereas indomethacin increased (p < 0.05) UNa 79% and FENa 85%. Activation of the BK and prostaglandin systems may play an important role in regulating renal function during chronic ACE inhibition, primarily by enhancing the renal vasodilatory effects of angiotensin II (AII) blockade.

Although the hypotriglyceridemic effect of large doses of n-3 fatty acids (n-3 FAs) is well established, the effects of prolonged use of very low doses on lipids, lipoproteins, and apolipoproteins have not been clearly defined. This investigation compares the relative effects of very low, clinically practical doses of n-3 FAs on lipids, lipoproteins, and apolipoproteins in hypertriglyceridemic subjects. Ten subjects received 2.2 g n-3 FAs/d (group 1), seven received 1.1 g n-3 FAs/d (group 2), and eight received olive oil (group 3, placebo control) for 20-wk treatment period. In group 1, both low-density-lipoprotein cholesterol (LDL-C) and LDL-apolipoprotein B concentrations increased significantly from baseline values (28% and 23%, respectively; p less than 0.05) after treatment. Compared with the placebo group, the increase in LDL apolipoprotein B in both fish oil groups was statistically and clinically significant (p less than 0.05). Only minor changes in plasma triglyceride concentrations occurred. The data suggest that very low doses of n-3 FAs may cause potentially adverse increases in LDL-C and LDL-apolipoprotein B concentrations.

The safety of sympathomimetic decongestants (SMDs) in patients with hypertension remains controversial. Little experimental evidence exists for making proper recommendations regarding their use in hypertensive subjects. In order to determine the correct role of SMDs in such patients, physicians will need criteria with which to assess new data and reevaluate the existing literature. Using standardized methodologic criteria to judge clinical trials, we critically appraised the published evidence of the effects of SMDs on blood pressure control in hypertensive patients. A search of the English literature from 1966 to 1984 revealed 12 prospective clinical studies out of 37 articles that specifically addressed the potential adverse pressor effect of SMDs. Of these, only one study evaluated hypertensive patients in a double-blind randomized fashion. Despite few threats to generalizability, the results of that investigation suggest that intranasal phenylephrine is safe in patients with controlled hypertension. The effects of phenylpropanolamine and pseudoephedrine in hypertensive patients are unclear since only small numbers of unrepresentative normotensive subjects have been studied; thus, the evidence to support the widespread belief that SMDs are unsafe in hypertensive patients is weak and circumstantial. Recommendations for treatment and methods to improve future study designs are suggested.