Angiotensin type 2 receptors: blood pressure regulation and end organ damage. (April 2015)

• Record Type: Journal Article
• Authors: Sumners, Colin; de Kloet, Annette D; Krause, Eric G; Unger, Thomas; Steckelings, Ulrike Muscha
• Is Part Of: Current opinion in pharmacology. Volume 21(2015)
• Page Start: 115
• Page End: 121
• Publication Date: 2015-04
• Subjects: Pharmacology -- Periodicals; Pharmaceutical Preparations -- Periodicals; Drug Therapy -- Periodicals; Biopharmaceutics -- Periodicals; Pharmacologie -- Périodiques; Pharmacology; Periodicals; 615.105
• DOI: 10.1016/j.coph.2015.01.004
• Languages: English
• ISSNs: 1471-4892

Abstract

Highlights: The AT2-receptor (AT2R) mediates vasodilation. Systemic application of AT2R-agonists does not lower blood pressure. Low-dose blockade of AT1-receptors unmasks the BP lowering effects of AT2Rs. Intracerebroventricular or intrarenal application of AT2R-agonists reduces BP. AT2R-stimulation protects from hypertensive end-organ damage without BP lowering. Abstract : In most situations, the angiotensin AT2-receptor (AT2R) mediates physiological actions opposing those mediated by the AT1-receptor (AT1R), including a vasorelaxant effect. Nevertheless, experimental evidence vastly supports that systemic application of AT2R-agonists is blood pressure neutral. However, stimulation of AT2R locally within the brain or the kidney apparently elicits a systemic blood pressure lowering effect. A systemic effect of AT2R stimulation on blood pressure can also be achieved, when the prevailing effect of continuous background AT1R-stimulation is attenuated by low-dose AT1R blockade. Despite a lack of effect on blood pressure, AT2R stimulation still protects from hypertensive end-organ damage. Current data and evidence therefore suggest that AT2R agonists will not be suitable as future anti-hypertensive drugs, but that they may well be useful for end-organ protection in combination with established anti-hypertensives.