Fine tuning of blood pressure by the regulator of G protein signaling (RGS) 2

Item Type:	Article
Title:	Fine tuning of blood pressure by the regulator of G protein signaling (RGS) 2
Creators Name:	da Costa Goncalves, A.C. and Luft, F.C. and Gross, V.
Abstract:	G protein–coupled receptors (GPCRs) are expressed ubiquitously and involved in a variety of physiologic and pathologic processes. One of the key steps in the GPCR signaling cascade is the phosphorylation of the Gα-subunit that triggers its dissociation from the Gβγ-subunit and from the receptor, allowing both G protein subunits to activate different downstream second messengers. Thereafter, Gα hydrolyzes the attached guanosine triphosphate (GTP) to guanosine diphosphate (GDP) by its inherent enzymatic activity and terminates signaling. Small/connecting proteins that act as GTPase activating proteins (GAP) accelerate this process. Regulator of G protein signaling (RGS) proteins play a key role in the regulation of GPCRs, by acting as GAP and increasing the rate of GPCRs deactivation. RGS2 affects GPCR-dependent and GPCR-independent pathways. RGS2 -/- displayed an increase of blood pressure (BP) mainly by an increase of total peripheral resistance. After Nω-nitro-L-arginine methyl ester (L-NAME) RGS2 -/- mice responded with a smaller BP increase during the day than RGS2 +/+, suggesting an impaired NO signaling. Infusion of angiotensin II increased BP stronger in RGS2 -/- compared with RGS2 +/+. In summary, GPCR-dependent and GPCR-independent pathways are involved in BP changes of RGS2 -/- mice. Interactions between GPCRs and RGS2 represent a regulatory mechanism for fine-tuning of BP which may be important for hypertension and may be considered as a potentially novel drug target.
Keywords:	Autonomic Nervous System, GTPase Activating Proteins, Heart Rate, Baroreflex Sensitivity, Animals, Mice
Source:	Journal of the American Society of Hypertension
ISSN:	1933-1711
Publisher:	Elsevier
Volume:	2
Number:	6
Page Range:	403-409
Date:	November 2008
Additional Information:	The original publication is available at www.sciencedirect.com
Official Publication:	https://doi.org/10.1016/j.jash.2008.05.006
PubMed:	View item in PubMed

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