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(Hypertension. 2006;47:1062.)
© 2006 American Heart Association, Inc.

Original Articles

Angiotensin II Decreases the Renal MRI Blood Oxygenation Level–Dependent Signal

Hartmut Schachinger; Markus Klarhöfer; Lilly Linder; Jürgen Drewe; Klaus Scheffler

From the Division of Clinical Physiology (H.S.), Graduate School of Psychobiology, University of Trier, Trier, Germany; and Clinical Research Center (H.S., L.L., J.D.), Department of Internal Medicine and Magnetic Resonance Physics (M.K., K.S.), Department of Medical Radiology, University Hospital Basel, Basel, Switzerland.

Correspondence to Hartmut Schachinger, Clinical Physiology, FB I, University of Trier, Johanniterufer 15, 54290 Trier, Germany. E-mail schaechi{at}uni-trier.de

Acute experimental reduction of renal blood flow decreases the renal blood oxygenation level–dependent (BOLD) MRI signal in animals. Angiotensin II also reduces renal blood flow, but the ability of BOLD MRI to dynamically detect this response has not yet been investigated in humans. Six healthy male volunteers underwent an individual dose-finding study to identify the intravenous doses of angiotensin II, norepinephrine, and sodium nitroprusside necessary to induce a 15-mm Hg peak mean arterial blood pressure change. MRI studies followed within 3 weeks, when angiotensin II (8.8±1.4 ng/kg), norepinephrine (52±12 ng/kg), and sodium nitroprusside (2.0±0.3 µg/kg) were given twice in an unblocked, randomized sequence while imaging experiments were performed on a 1.5-T Siemens Sonata. A multiecho echo-planar imaging sequence was used to acquire T2* maps with a temporal resolution of 1 respiratory cycle. Averaged over a renal cortex dominated region of interest, angiotensin II caused a shortening of T2* between 6% and 10%. Sodium nitroprusside and norepinephrine, although of equal potency concerning blood pressure responses, did not alter the renal BOLD signal. The renal BOLD response to angiotensin II appeared with short onset latency (as early as 10 seconds after peripheral intravenous angiotensin II bolus administration) suggesting that this response is a consequence of altered perfusion rather than increased renal oxygen consumption. The methods described here are suitable to assess renal responsiveness to angiotensin II and may, thus, be of great value in human hypertension research.

Key Words: kidney • magnetic resonance imaging • blood pressure • angiotensin II • norepinephrine • nitroprusside

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