| Increased renovascular response to angiotensin II in persons genetically predisposed to arterial hypertension disappears after chronic angiotensin-converting enzyme inhibition. | |
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MedLine Citation:
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PMID: 15106809 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE AND METHODS: Functional changes in the kidneys of healthy men with (FH+) (n = 15) and without (FH-) (n = 15) family history of primary arterial hypertension were examined during administration of low-dose exogenous angiotensin II (A2) (1 ng/kg per min) before and after acute (1 mg intravenous enalaprilat) and chronic (7 days oral enalapril, 30 mg/day) angiotensin-converting enzyme (ACE) inhibition. RESULTS: Before chronic ACE inhibition, A2 increased mean arterial blood pressure (FH+, 8.7 +/- 0.8 mmHg; FH-, 8.9 +/- 0.9 mmHg), plasma immunoreactive A2 (FH+, 21 +/- 2 pg/ml; FH-, 18 +/- 3 pg/ml) and plasma aldosterone (FH+, 64 +/- 7 pg/ml; FH-, 56 +/- 6 pg/ml) to a similar degree in both groups. Chronic ACE inhibition had no impact on A2 blood pressure, plasma A2, or plasma aldosterone effects. A2 significantly increased renal vascular resistance in both groups (FH+, 3956 +/- 462 dyne s cm(-5); FH-, 2219 +/- 550 dyne s cm(-5)), but the effect was more pronounced in FH+ (P = 0.02). Glomerular hemodynamics, estimated by a modified Gomez model, revealed increased afferent and efferent responsiveness to A2 in FH+ subjects. These differences disappeared after chronic ACE inhibition when total, afferent and efferent sensitivities to A2 were similar in both groups. CONCLUSIONS: Systemic blood pressure and plasma aldosterone responses to A2 were similar in men with or without a genetic disposition to primary arterial hypertension. However, our data demonstrate that men with a family history of hypertension have increased renovascular sensitivity to A2, and that chronic ACE inhibition normalizes their sensitivity. |
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Authors:
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Hartmut Schächinger; Thomas Dieterle; Benedict Martina; Christoph Haberthür; Peter R Huber; Andreas Bock; Jürgen Drewe; Klaus Gyr |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of hypertension Volume: 22 ISSN: 0263-6352 ISO Abbreviation: J. Hypertens. Publication Date: 2004 Jan |
Date Detail:
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Created Date: 2004-04-26 Completed Date: 2004-11-06 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: England |
Other Details:
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Languages: eng Pagination: 175-80 Citation Subset: IM |
Affiliation:
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Medical Outpatient Clinic, Department of Internal Medicine, University Hospital Basel, Switzerland. hartmut.schaechinger@unibas.ch |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Aldosterone / blood Angiotensin II / administration & dosage*, metabolism Angiotensin-Converting Enzyme Inhibitors / therapeutic use* Biological Markers / blood Blood Pressure / drug effects Diastole / drug effects Dose-Response Relationship, Drug Genetic Predisposition to Disease / genetics* Glomerular Filtration Rate / drug effects Humans Hypertension / drug therapy*, genetics* Kidney / blood supply, drug effects*, metabolism Male Reference Values Regional Blood Flow / drug effects Renin / drug effects, metabolism Systole / drug effects Time Factors Treatment Outcome Vascular Resistance / drug effects Vasoconstrictor Agents / administration & dosage*, metabolism |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin-Converting Enzyme Inhibitors; 0/Biological Markers; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II; 52-39-1/Aldosterone; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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