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| |  Unique Mechanism of Action of Omapatrilat May Offer Benefit Over Antihypertensive Lisinopril NEW YORK, NY -- May 19, 2000 -- Data presented at the American Society of Hypertension's 15th Scientific Meeting indicate that omapatrilat, a novel cardiovascular drug, has a mechanism of action that differs importantly from angiotensin-converting enzyme (ACE) inhibitors, and may offer significant benefit in patients with hypertension. Omapatrilat demonstrated greater reduction in blood pressure than the ACE inhibitor lisinopril in individuals with salt-sensitive hypertension who typically do not respond well to ACE inhibitors. The research was conducted at a total of eight U.S. sites, led by The Keck School of Medicine of the University of Southern California, Los Angeles. "Hypertensive patients differ in how well they respond to various types of blood pressure-lowering medication, and salt sensitivity is an important variable," said V.M. Campese, M.D., Professor of Medicine and Chief, Division of Nephrology at The Keck School of Medicine of the University of Southern California, Los Angeles and lead investigator of the study. "This study suggests that vasopeptidase inhibition with omapatrilat may offer advantages for patients who typically don't respond well to ACE inhibitors, such as African Americans and the elderly." Omapatrilat is the most clinically advanced member of the new class of cardiovascular drugs known as vasopeptidase inhibitors (VPIs) that produce simultaneous inhibition of two key enzymes -- neutral endopeptidase (NEP) and ACE -- which help regulate blood pressure. In the clinical study, both omapatrilat (a VPI) and lisinopril (an ACE inhibitor) suppressed ACE activity, but differed markedly in their impact on atrial natriuretic peptide (ANP). ANP is a vasoactive peptide that helps lower blood pressure. By inhibiting NEP, omapatrilat significantly increased the levels of ANP in study patients, enhancing the body's own natural vasodilator peptides. "In this study, increases in ANP were seen with omapatrilat, but not lisinopril," said Campese. "This may explain the greater efficacy with omapatrilat in people who typically don't respond well to ACE inhibition alone." The blood pressure-lowering effects of omapatrilat were compared with those of lisinopril in 61 salt-sensitive hypertensive men and women. Twenty- eight of the salt-sensitive patients were randomized to receive a one week starting dose of 10 mg of omapatrilat titrated to 40 mg and 33 patients received a starting dose of 10 mg of lisinopril titrated to 20 mg for 3 weeks. Characteristic of a VPI, omapatrilat significantly increased (P<0.001) urinary excretion of ANP and significantly increased (P<0.05) plasma ANP levels. Lisinopril had no effect on urinary ANP and reduced plasma ANP. Both treatments reduced the average ambulatory systolic (top number) and diastolic (bottom number) blood pressure levels as measured over 24 hours. However, compared with lisinopril, omapatrilat produced significantly greater reductions in both systolic and diastolic pressure. The average drop in systolic pressure was 15.4 mm Hg (millimeters of mercury) for omapatrilat versus 7.2 mm Hg for lisinopril (P = 0.004). The average drop in diastolic blood pressure was 9.3 mm Hg for omapatrilat versus 5.1 mm Hg for lisinopril (P = 0.008).
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