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Central and peripheral renin-angiotensin systems in ouabain-induced hypertension

Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Submitted 31 October 2005 ; accepted in final form 24 February 2006

Chronic subcutaneous infusion of ouabain causes hypertension via central pathways involving angiotensin type 1 (AT₁) receptor stimulation. The present study assessed plasma and tissue ANG I and II levels as well as AT₁ receptor and angiotensin-converting enzyme (ACE) mRNA levels and binding densities by real-time PCR and in vitro autoradiography in relevant brain nuclei and peripheral tissues (heart and kidney) in rats at 1 and/or 2 wk after start of ouabain infusion at 50 µg/day. After 2 wk (but not after 1 wk), blood pressures significantly increased (+15 mmHg). At 2 wk, plasma ANG I and II levels were markedly suppressed by ouabain. In contrast, in the heart and kidneys, ANG I levels were not affected, and ANG II levels tended to decrease, whereas in the hypothalamus ANG II content clearly increased. At 1 wk, no changes in ACE and AT₁ receptor densities were seen. After 2 wk, there were significant decreases in AT₁ receptor mRNA and densities in the organum vasculosum of the lamina terminalis (OVLT), subfornical organ (SFO), and paraventricular nucleus (PVN). ACE densities decreased only in the OVLT and SFO, but ACE mRNA showed more variable responses (decrease in OVLT vs. increase in PVN). In the kidneys, at 2 wk both AT₁ receptor and ACE densities were decreased, but mRNA abundance did not change. The heart showed no significant changes. The increase in hypothalamic ANG II content and associated decreases in central AT₁ receptor and ACE densities support the involvement of the brain renin-angiotensin system in the central hypertensive mechanism of action of ouabain.

angiotensin II; angiotensin type 1 receptors; angiotensin-converting enzyme; brain; kidneys

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