Does blood pressure reduction necessarily compromise cardiac function or renal hemodynamics? Effects of the angiotensin-converting enzyme inhibitor quinapril
dc.contributor.author | Kjeldsen, Sverre E. | en_US |
dc.contributor.author | Gupta, Rakesh K. | en_US |
dc.contributor.author | Krause, Lisa C. | en_US |
dc.contributor.author | Weder, Alan B. | en_US |
dc.contributor.author | Julius, Stevo | en_US |
dc.date.accessioned | 2006-04-10T15:15:22Z | |
dc.date.available | 2006-04-10T15:15:22Z | |
dc.date.issued | 1992-05 | en_US |
dc.identifier.citation | Kjeldsen, 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.uri | http://www.sciencedirect.com/science/article/B6W9H-4BV46C8-J1/2/014543fb1c410afdd61ec8b113815db7 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/30095 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1575171&dopt=citation | en_US |
dc.description.abstract | Clinical 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.extent | 677324 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Does blood pressure reduction necessarily compromise cardiac function or renal hemodynamics? Effects of the angiotensin-converting enzyme inhibitor quinapril | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department 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.affiliationum | Division 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.affiliationum | Division 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.affiliationum | Division 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.affiliationum | Division 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.pmid | 1575171 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/30095/1/0000467.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1016/0002-8703(92)91066-A | en_US |
dc.identifier.source | American Heart Journal | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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