Differential effect of acute angiotensin II type 1 receptor blockade on the vascular and adrenal response to exogenous angiotensin II in humans |
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| Authors: | Lottermoser Katja Unger Thomas Gohlke Peter Vetter Hans Düsing Rainer |
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| Affiliation: | 1. Medizinische Universitäts-Poliklinik (KL, HV, RD), Bonn, Germany;2. Institut für Pharmakologie und Toxikologie (TU), Humboldt-Universität Berlin, Berlin, Germany;3. Institut für Pharmakologie (PG), Universität Kiel, Kiel, Germany;1. Department of Cardiology, Jichi Medical School (YH, KK, SH, KS), Tochigi, Japan;2. Department of Internal Medicine, The Zena and Michael A. Wiener Cardiovascular Center, Mount Sinai School of Medicine (KK, JES, TGP) New York, USA;3. Department of Psychiatry and Behavioral Science, State University of New York at Stony Brook (JES), Stony Brook, New York, USA;1. St. Luca Hospital (GL), Istituto Auxologico Italiano, IRCCS, Milan, Italy;2. Institute of Cardiology (BM), University of Bologna, Bologna, Italy;3. Department of Clinical and Experimental Medicine (ACP), University of Padua, Padua, Italy;4. Clinical Medicine Institute (AR), University of Ancona, Ancona, Italy;5. Department of Internal Medicine (BT), Federico II University, Naples, Italy;6. Centro Fisiologia Clinica e Ipertensione (AZ), University of Milan, Ospedale Maggiore and Istituto Auxologico Italiano, Milan, Italy;1. Department of Hypertension and Cardiorenal Medicine (JM, TN, MT, NY, HO, SH, JI, HM), Dokkyo University School of Medicine, Mibu, Tochigi, Japan;2. Department of Endocrinology and Metabolism (CK), Dokkyo University School of Medicine, Mibu, Tochigi, Japan;3. Research Institute, National Cardiovascular Center (KK), Suita, Osaka Japan;1. Department of Anatomy and Physiology (HY, MS, ZMG), Meharry Medical College, Nashville, Tennessee, USA;2. Department of Internal Medicine (ZMG), Meharry Medical College, Nashville, Tennessee, USA;3. Department of Physiology (HVR, XLC, JV, AR), University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA;4. Geriatric Research, Education and Clinical Center (HVR, JV, AR), South Texas Veterans Health Care System, Audie L. Murphy Division, San Antonio, Texas, USA |
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| Abstract: | ![]()
BACKGROUND: Aldosterone stimulation by angiotensin II may not exclusively be mediated by the angiotensin II type 1 (AT(1)) receptor. We have, therefore, investigated the vascular and adrenal response to angiotensin II infusion without and with pretreatment with the AT(1) receptor antagonist valsartan (160 mg). METHODS: In nine healthy human volunteers, angiotensin II was administered intravenously at doses of 1, 3, and 10 ng/kg/min, each over 45 min. Arterial blood pressure (BP) was measured oscillometrically at 5-min intervals. Blood for the determination of plasma renin activity and aldosterone was taken before the start of the infusion, at the end of each infusion period, and 1 h after the infusion was stopped. RESULTS: Angiotensin II increased systolic and diastolic BP from 121 +/- 3/70 +/- 2 mm Hg to a maximum of 146 +/- 2/97 +/- 1 mm Hg (P <.001) and plasma aldosterone from 39.2 +/- 9.8 to 290.7 +/- 48.3 (P <.001). The increase in BP after exogenous angiotensin II was completely abolished in volunteers pretreated with valsartan, averaging 118 +/- 3/72 +/- 1 mm Hg by the end of the maximum angiotensin infusion dose. In contrast, plasma aldosterone stimulation by angiotensin II was only partially blunted by concomitant AT(1) receptor blockade (98.9 +/- 16.3 pg/mL after the maximal dose of angiotensin II). CONCLUSIONS: These results indicate that although the vascular response to exogenous angiotensin II is exclusively mediated by the AT(1) receptor, the effects of angiotensin II on adrenal aldosterone release may involve other pathways. |
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