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Does blood pressure reduction necessarily compromise cardiac function or renal hemodynamics? Effects of the angiotensin-converting enzyme inhibitor quinapril

dc.contributor.authorKjeldsen, Sverre E.en_US
dc.contributor.authorGupta, Rakesh K.en_US
dc.contributor.authorKrause, Lisa C.en_US
dc.contributor.authorWeder, Alan B.en_US
dc.contributor.authorJulius, Stevoen_US
dc.date.accessioned2006-04-10T15:15:22Z
dc.date.available2006-04-10T15:15:22Z
dc.date.issued1992-05en_US
dc.identifier.citationKjeldsen, Sverre E., Gupta, Rakesh K., Krause, Lisa, Weder, Alan B., Julius, Stevo (1992/05)."Does blood pressure reduction necessarily compromise cardiac function or renal hemodynamics? Effects of the angiotensin-converting enzyme inhibitor quinapril." American Heart Journal 123(5): 1433-1438. <http://hdl.handle.net/2027.42/30095>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6W9H-4BV46C8-J1/2/014543fb1c410afdd61ec8b113815db7en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/30095
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1575171&dopt=citationen_US
dc.description.abstractClinical studies indicate that the angiotensin-converting enzyme inhibitor quinapril is an effective antihypertensive agent when administered once daily. At the end of a 4-week, double-blind crossover trial comparing quinapril and placebo, patients were admitted for a hemodynamic profile study 12 hours after taking the previous dose. A final 20 mg dose of quinapril had no additional effect on blood pressure. This is interesting inasmuch as the plasma half-life of the active metabolite quinaprilat is approximately 2 hours and the effective accumulation half-life is approximately 3 hours. The blood pressure reduction in patients with mild hypertension receiving long-term quinapril therapy may be more closely related to prolonged angiotensin-converting enzyme inhibition or to an effect on tissue angiotensin II concentration than to the plasma half-life. This may be the case particularly for cardiac output and renal circulation, because quinapril lowers total vascular resistance without increasing cardiac output or disturbing autoregulation of renal blood flow. Reduced ventricular wall stress, improved diastolic function, and lower renal perfusion pressure may spare cardiac function and glomeruli from hypertensive vascular damage.en_US
dc.format.extent677324 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleDoes blood pressure reduction necessarily compromise cardiac function or renal hemodynamics? Effects of the angiotensin-converting enzyme inhibitor quinaprilen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Internal Medicine, Ullevaal University Hospital, Oslo, Norway; Division of Hypertension, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Mich., USA.en_US
dc.contributor.affiliationumDivision of Hypertension, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Mich., USA; Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.en_US
dc.contributor.affiliationumDivision of Hypertension, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Mich., USA; Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.en_US
dc.contributor.affiliationumDivision of Hypertension, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Mich., USA; Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.en_US
dc.contributor.affiliationumDivision of Hypertension, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Mich., USA; Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.en_US
dc.identifier.pmid1575171en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/30095/1/0000467.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0002-8703(92)91066-Aen_US
dc.identifier.sourceAmerican Heart Journalen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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