title: Hypotensive effect of atorvastatin is not related to changes in inflammation and oxidative stress.
abstract: We sought to determine if atorvastatin lowers blood pressure in patients with previously diagnosed and well-controlled essential arterial hypertension and if this effect could be related to anti-inflammatory and anti-oxidative effects. Among 92 patients with essential arterial hypertension, we studied 56 non-smoking and normolipemic: 39 were randomized to receive 80 mg atorvastatin daily for 3 months (statin-treated patients, ST), and the rest continued a previous hypotensive therapy (statin-free patients, SF). Blood pressure was measured using a 24-h ambulatory blood pressure measurement device. Serum levels of high-sensitivity C-reactive protein (hs-CRP), total antioxidant status (TAS) and plasma peroxides (assessed by Oxystat) were measured in both groups. The mean change in systolic BP (SBP) for atorvastatin was -5.7 mmHg (95% confidence interval CI, -4.1 to -7.2 mmHg), and the mean change in diastolic BP (DBP) was -3.9 mmHg (95% CI, -2.7 to -5.0 mmHg). No change in BP in SF patients was observed. In the ST group, hs-CRP and peroxides did not significantly decrease. In the SF group, concentrations of hs-CRP proceeded to decrease while peroxides increased. In the ST group, changes in hs-CRP correlated with changes in total cholesterol and low-density lipoprotein cholesterol (r = 0.41, p = 0.013 and r = 0.35, p = 0.04, respectively) but did not correlate with changes in BP. The hypotensive statin effect was independent of the hypolipemic effect. During three months of observation, TAS concentrations in both groups remained stable. In this randomized study, additionally administered atorvastatin to non-smoking and normolipemic patients with well-controlled essential arterial hypertension resulted in reduction of BP. This effect was not followed by significant changes in hs-CRP, TAS or Oxystat concentrations. The hypotensive effect of atorvastatin did not depend on anti-inflammatory, anti-oxidative or hypolipemic actions.
authors.affiliation: Department of Cardiology, Medical University, M. Skłodowskiej-Curie 24A, PL15-276 Białystok, Poland. agnieszka.kuklinska@gmail.com
authors.forename: Agnieszka M
authors.initials: AM
authors.lastname: Kuklińska
authors.forename: Barbara
authors.initials: B
authors.lastname: Mroczko
authors.forename: Włodzimierz J
authors.initials: WJ
authors.lastname: Musiał
authors.forename: Robert
authors.initials: R
authors.lastname: Sawicki
authors.forename: Anna
authors.initials: A
authors.lastname: Kozieradzka
authors.forename: Monika
authors.initials: M
authors.lastname: Usowicz-Szaryńska
authors.forename: Karol
authors.initials: K
authors.lastname: Kamiński
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Knapp
authors.forename: Maciej
authors.initials: M
authors.lastname: Szmitkowski
mesh_terms: D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000378:metabolism; D000069059:Atorvastatin; D001794:Blood Pressure / Q000187:drug effects*; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D006973:Hypertension / Q000097:blood / Q000188:drug therapy*; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D000959:Antihypertensive Agents; D000975:Antioxidants; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin