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(Hypertension. 2005;46:649.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Putting the Brakes on Renin Release

Role of the A₁ Receptor

Edwin K. Jackson

From the Center for Clinical Pharmacology, Departments of Pharmacology and Medicine, University of Pittsburgh School of Medicine, Pennsylvania.

Correspondence to Edwin K. Jackson, PhD, Center for Clinical Pharmacology, 100 Technology Dr, Suite 450, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219-3130. E-mail edj@pitt.edu

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

Modulation of renin release from juxtaglomerular cells is critical for appropriate adjustments of the cardiovascular and renal systems to internal and external stresses, and dysregulation of renin release participates in the pathophysiology of hypertension, vascular disease, heart failure, and chronic renal disease. This justifies investments in research to elucidate the fundamental mechanisms regulating renin release. These investments have yielded, and continue to yield, high returns, as exemplified by Schweda et al¹ in this issue of Hypertension, showing that A₁ receptors mediate high perfusion pressure–induced inhibition of renin release, whereas prostaglandins (PGs) participate in low perfusion pressure–mediated stimulation of renin release. The purpose of this commentary is to discuss how Schweda et al’s findings confirm and challenge present-day models of renin release.

As comprehensively reviewed by Davis and Freeman² and Keeton and Campbell,³ investigators recognized early on that three systems, namely the sympathetic nervous system, the macula densa apparatus, and the intrarenal baroreceptor, are the primary physiological mechanisms regulating renin release from juxtaglomerular cells. A key development was the recognition that the two most important biochemical accelerators of renin release are catecholamines (mediating sympathetically induced renin release) and PGI₂ (mediating macula densa–induced and intrarenal baroreceptor–stimulated renin release).⁴ Subsequently, a third autocoid, adenosine (acting via A₁ receptors), was proposed to serve as a molecular brake on renin release and thereby to moderate the effects of catecholamines and PGI₂ on renin secretion.⁵ Because cAMP is a critical second messenger mediating the exocytosis of renin from juxtaglomerular cells, adenylyl cyclase unifies these concepts . . . [Full Text of this Article]

Related Article:

Blood Pressure–Dependent Inhibition of Renin Secretion Requires A1 Adenosine Receptors

Frank Schweda, Florian Segerer, Hayo Castrop, Jürgen Schnermann, and Armin Kurtz
Hypertension 2005 46: 780-786. [Abstract] [Full Text] [PDF]