Hyper-responsiveness to angiotensin II is related to cardiac structural adaptation in hypertensive subjects
Autor: | Karl F. Hilgers, Roland E. Schmieder, Matthias R.W. Langenfeld, Hans P. Schobel, Tim Schäufele, Arnfried U. Klingbeil |
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Rok vydání: | 1999 |
Předmět: |
Adult
Male Mean arterial pressure medicine.medical_specialty Physiology Heart Ventricles Radioimmunoassay Hemodynamics Blood Pressure Essential hypertension Renal Circulation Drug Hypersensitivity chemistry.chemical_compound Predictive Value of Tests Internal medicine Renin–angiotensin system Internal Medicine medicine Humans Vasoconstrictor Agents Aldosterone business.industry Angiotensin II Blood Pressure Monitoring Ambulatory medicine.disease Blood pressure Endocrinology chemistry Echocardiography Renal blood flow Hypertension Injections Intravenous Cardiology and Cardiovascular Medicine business Follow-Up Studies Glomerular Filtration Rate |
Zdroj: | Journal of Hypertension. 17:825-833 |
ISSN: | 0263-6352 |
Popis: | Background Angiotensin II has been found to be a growt stimulating factor for myocardial cells. In humans, angiotensin II infusion causes vasoconstriction in systemic and renal vasculature and leads to aldosterone secretion. Our hypothesis was that hyper-responsiveness to angiotensin II is related to left ventricular mass in human essential hypertension. Methods and results In 30 normotensive individuals and 30 subjects with mild essential hypertension (white men, mean age 26 ± 3 years), the responsiveness to angiotensin II was assessed by measuring changes in mean arterial pressure, renal blood flow, glomerular filtration rate and aldosterone secretion in response to i.v. angiotensin II infusion (0.5 and 3.0 ng/kg per min). The provoked changes to angiotensin II infusion were similar ir the normotensive and hypertensive group with the exception of an exaggerated increase in mean arterial pressure in hypertensives (14 ± 5 versus 10 ± 5 mmHg, P< 0.001 at 3.0 ng/kg per min angiotensin II). The increase in mean arterial pressure was correlated with left ventricular mass in hypertensive subjects (angiotensin II 0.5 ng/kg per min: r= 0.49, P< 0.005; angiotensin II 3.0 ng/kg per min: r= 0.35, P< 0.05); no such correlation was found in the normotensive group. After taking into account baseline mean arterial pressure and body mass index, the increase in mean arterial pressure to angiotensin II 0.5 ng/kg per min was still correlated with left ventricular mass (partial r = 0.50, P< 0.01). Similarly, the change of glomerular filtration rate but not of renal blood flow in response to angiotensin II 0.5 ng/kg per min was correlated with left ventricular mass, (r= 0.42, P |
Databáze: | OpenAIRE |
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