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


Scheffler,  K
Department High-Field Magnetic Resonance, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Schächinger, H., Klarhöfer M, Linder L, Drewe, J., & Scheffler, K. (2006). Angiotensin II Decreases the Renal MRI Blood Oxygenation Level–Dependent Signal. Hypertension, 47(6), 1062-1066. doi:10.1161/​01.HYP.0000220109.98142.a3.

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.