Effect of the HMG-CoA Reductase Inhibitors on Blood Pressure in Patients With Essential Hypertension and Primary Hypercholesterolemia

Certain hydroxymethylglutaryl coenzyme A reductase inhibitors, ie, statins, may cause vasodilation by restoring the endothelial dysfunction that frequently accompanies hypertension and hypercholesterolemia. Several studies have found that a blood pressure reduction is associated with the use of stat...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1999-12, Vol.34 (6), p.1281-1281
Main Authors: Glorioso, Nicola, Troffa, Chiara, Filigheddu, Fabiana, Dettori, Francesco, Soro, Aldo, Parpaglia, Paolo Pinna, Collatina, Stefano, Pahor, Marco
Format: Article
Language:English
Subjects:
Adult
Aged
Biological and medical sciences
Blood Pressure - drug effects
Cholesterol - blood
Cholesterol, HDL - blood
Cholesterol, HDL - drug effects
Cholesterol, LDL - blood
Cholesterol, LDL - drug effects
Cold Temperature
Cross-Over Studies
Double-Blind Method
Endothelins - blood
Female
General and cellular metabolism. Vitamins
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - adverse effects
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Hypercholesterolemia - complications
Hypertension - complications
Hypertension - diagnosis
Hypertension - drug therapy
Male
Medical sciences
Middle Aged
Pharmacology. Drug treatments
Pravastatin - adverse effects
Pravastatin - pharmacology
Pravastatin - therapeutic use
Treatment Outcome
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Summary:Certain hydroxymethylglutaryl coenzyme A reductase inhibitors, ie, statins, may cause vasodilation by restoring the endothelial dysfunction that frequently accompanies hypertension and hypercholesterolemia. Several studies have found that a blood pressure reduction is associated with the use of statins, but conclusive evidence from controlled trials is lacking. After an 8-week placebo and diet run-in period, 30 persons with moderate hypercholesterolemia and untreated hypertension (total cholesterol 6.29±0.52 mmol/L, systolic and diastolic blood pressure 149±6 and 97±2 mm Hg) were randomized in a double-blind manner to placebo or pravastatin (20 to 40 mg/d) in a crossover design. In 25 participants who completed the 32-week trial, pravastatin decreased total and LDL cholesterol (both −1.09 mmol/L, P =0.001), systolic and diastolic blood pressure (−8 and −5 mm Hg, both P =0.001), and pulse pressure (−3 mm Hg, P =0.011) and blunted the blood pressure increase caused by the cold pressor test (−4 mm Hg, P =0.005) compared with placebo. It also reduced the level of circulating endothelin-1 (P =0.001). The blood pressure results were virtually unchanged in stratified analyses according to gender and age and in intention-to-treat analyses that included the 5 patients who dropped out of the study. When the participants were taking either placebo or pravastatin, blood pressure was not significantly correlated with total or LDL cholesterol or with circulating endothelin-1. Pravastatin decreases systolic, diastolic, and pulse pressures in persons with moderate hypercholesterolemia and hypertension. This antihypertensive effect may contribute to the documented health benefits of certain statins.
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.34.6.1281