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(Hypertension. 2006;47:1052.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

Angiotensin Type 1A Receptors on Glial Cells in Rostral Ventrolateral Medulla and Hypertension

From the Department of Physiology and Institute for Biomedical Research, University of Sydney, New South Wales, Australia.

Correspondence to Prof R.A.L. Dampney, Department of Physiology, F13, The University of Sydney, NSW 2006, Australia. E-mail rogerd@physiol.usyd.edu.au

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

During the 1970s and early 1980s, all the components of the renin–angiotensin system (RAS) were identified within the brain.¹ Subsequent physiological studies have shown that angiotensin II (Ang II) can act at various sites within the brain stem and hypothalamus to regulate cardiovascular function and fluid and electrolyte balance. Further, there is increasing evidence that brain Ang II can contribute to increased sympathetic activity in hypertension and heart failure.²

In recent years, a number of investigators have studied the physiological effects of alteration of the expression of genes encoding various components of the RAS. As reviewed recently by Davisson,² early studies by Ganten and colleagues showed that transgenic rats containing the mouse renin (Ren-2) gene were hypertensive. Although there is an increased expression of Ang II in the hypothalamus and medulla oblongata of such animals, the extent to which the hypertension was caused by increased levels of central or peripheral Ang II was not clear. Later, with the development of new methods that enabled brain-selective expression of particular genes, transgenic mice in which the angiotensin type 1A (AT_1A) receptors were overexpressed in the brain but not in peripheral tissues were produced.³ These animals exhibit exaggerated pressor responses to intracerebroventricular administration of Ang II, but have a normal resting arterial blood pressure.³ Thus, this indicates that an increased density of AT_1A receptors alone is not sufficient to produce hypertension.

Other genetic models, however, have demonstrated that overactivity of the brain RAS can produce hypertension. In transgenic mice containing . . . [Full Text of this Article]

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