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(Hypertension. 2009;54:27.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
From the Institute for Surgical Research, Oslo University Hospital, Rikshospitalet and Center for Heart Failure Research, University of Oslo, Oslo, Norway.
Correspondence to Håvard Attramadal, Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, N-0027 Oslo, Norway. E-mail havard.attramadal@medisin.uio.no
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertension is a common disorder with complex etiology and particularly high prevalence among black Americans. Although the pathophysiologic mechanisms of essential hypertension are poorly understood, the disease is often associated with increased sympathetic nervous activity and elevated plasma norepinephrine levels. Such elevated plasma norepinephrine levels may, in turn, lead to increased adrenergic receptor activities in the cardiovascular system. The significance of the elevated plasma norepinephrine levels in the pathophysiologic mechanisms leading to increased blood pressure is uncertain.
In the present issue of Hypertension, Cohn et al1 report the novel findings that G protein-coupled receptor kinase 2 (βARK1/GRK2) levels and activities correlate with both blood pressure and plasma norepinephrine levels in a cohort of black Americans with normal blood pressure or with essential hypertension and metabolic syndrome but without other known chronic disease. Although a minority of the patients in the cohort actually had hypertension according to the current clinical definition, the study convincingly demonstrates that GRK2 expression correlates with systolic blood pressure. No correlation with blood pressure was found for any of the other common members of the GRK family. It will be interesting to see in the future to what extent increased GRK2 activities pertain only to black Americans with essential hypertension or to what extent the reported findings are pathophysiological responses common to hypertension among all races.
GRKs are enzymes that catalyze phosphorylation and desensitization of agonist-activated G protein-coupled receptors, now preferably denoted as 7 transmembrane segment receptors. Thus, the authors contend that increased GRK2 levels cause
Related Article:
Hypertension 2009 54: 71-76.
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