G-protein-coupled receptor kinase activity is increased in hypertension - PubMed (original) (raw)

G-protein-coupled receptor kinase activity is increased in hypertension

R Gros et al. J Clin Invest. 1997.

Abstract

Impaired vascular beta-adrenergic responsiveness may play an important role in the development and/or maintenance of hypertension. This defect has been associated with an alteration in receptor/guanine nucleotide regulatory protein (G-protein) interactions. However, the locus of this defect remains unclear. G-Protein-coupled receptor kinases (GRKs) phosphorylate serine/threonine residues on G-protein-linked receptors in an agonist-dependent manner. GRK activation mediates reduced receptor responsiveness and impaired receptor/G-protein coupling. To determine whether the impairment in beta-adrenergic response in human hypertension might be associated with altered GRK activity, we studied lymphocytes from younger hypertensive subjects as compared with older and younger normotensive subjects. We assessed GRK activity by rhodopsin phosphorylation and GRK expression by immunoblot. GRK activity was significantly increased in lymphocytes from younger hypertensive subjects and paralleled an increase in GRK-2 (beta ARK-1) protein expression. In contrast, no alterations in cAMP-dependent kinase (A-kinase) activity or GRK-5/6 expression were noted. GRK activity was not increased in lymphocytes from older normotensive subjects who demonstrated a similar impairment in beta-adrenergic-mediated adenylyl cyclase activation. These studies indicate that GRK activity is selectively increased in lymphocytes from hypertensive subjects. The increase in GRK activity may underlie the reduction in beta-adrenergic responsiveness characteristic of the hypertensive state.

PubMed Disclaimer

Comment in

Similar articles

Cited by

References

    1. J Clin Invest. 1990 Mar;85(3):647-52 - PubMed
    1. Curr Eye Res. 1990 Apr;9(4):343-55 - PubMed
    1. Trends Pharmacol Sci. 1990 May;11(5):190-4 - PubMed
    1. Clin Pharmacol Ther. 1990 Jul;48(1):87-95 - PubMed
    1. FASEB J. 1990 Aug;4(11):2881-9 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources