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Hypertension. 2005;45:845-846
Published online before print March 21, 2005, doi: 10.1161/01.HYP.0000161868.75872.e6
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(Hypertension. 2005;45:845.)
© 2005 American Heart Association, Inc.


Editorial Commentaries

Microvascular Effects of Aldosterone and Angiotensin Type 2 Receptors

Thomas L. Pallone

From the Division of Nephrology, Departments of Medicine and Physiology, University of Maryland at Baltimore.

Correspondence to Thomas L. Pallone, MD, Division of Nephrology, N3W143, 22 S Greene St, University of Maryland Medical System, Baltimore, MD 21201. E-mail tpallone@medicine.umaryland.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

In the current issue of Hypertension, Gonzalez et al describe the modulation of mesenteric vascular angiotensin type 2 receptor (AT2R) expression by aldosterone.1 The principal findings are as follows: (1) AT2R activation dilates phenylephrine preconstricted mesenteric arterioles; (2) 4 days of oral salt loading eliminates AT2R-mediated dilation and reduces expression of AT2R mRNA and protein; (3) an adrenal hormone is implicated because the effects of salt loading are mimicked by adrenalectomy; (4) of the candidate adrenal hormones, aldosterone is identified because mineralocorticoid replacement prevents the effects of adrenalectomy; and (5) aldosterone upregulates AT2R expression in explanted mesenteric arterioles. These well designed series of experiments strongly support a role for aldosterone to stimulate expression of AT2R and adds to the growing repertoire of roles that aldosterone plays in vasculature physiology.

The AT2R-mediated vasodilation observed by Gonzalez et al1 elegantly reproduces similar effects reported in the mesentery and other vascular preparations.2–5 AT2R induced vasodilation of mesenteric arterioles appears as endothelium-dependent,6 acts through kinin and nitric oxide (NO) generation,7 and involves myocyte hyperpolarization through stimulation of large-conductance Ca2+-dependent potassium channels.8 Such AT2R-mediated reduction of vascular resistance generalizes beyond the mesenteric vascular bed. Systemic AT2R activation through infusion of angiotensin II plus AT1 receptor blockers lowers blood pressure9 and AT2-null mice have mild hypertension with an exaggerated blood pressure response to deoxycorticosterone acetate plus salt.10,11 Carotid arteries,12 coronary arterioles,13 renal afferent arterioles,14–16 and descending vasa recta17 are dilated by AT2R activation. The participation of bradykinin B2 receptor activation and NO generation in . . . [Full Text of this Article]


Related Article:

High-Salt Diet Inhibits Expression of Angiotensin Type 2 Receptor in Resistance Arteries
Magdalena Gonzalez, Lorena Lobos, Felipe Castillo, Lorna Galleguillos, Nandy C. Lopez, and Luis Michea
Hypertension 2005 45: 853-859. [Abstract] [Full Text] [PDF]