Gq-Coupled Receptor Agonists Mediate Cardiac Hypertrophy Via the Vasculature

DOI Web Site 被引用文献2件
  • Janelle R. Keys
    From the Department of Surgery, Duke University Medical Center, Durham, NC.
  • Emily A. Greene
    From the Department of Surgery, Duke University Medical Center, Durham, NC.
  • Walter J. Koch
    From the Department of Surgery, Duke University Medical Center, Durham, NC.
  • Andrea D. Eckhart
    From the Department of Surgery, Duke University Medical Center, Durham, NC.

抄録

<jats:p>The Gq-coupled receptor-signaling pathway has been implicated in the cardiac hypertrophic response to stress, but little is actually known about the contributions of Gq signaling in either the heart or the vasculature. Therefore, we developed a line of transgenic mice that express a peptide inhibitor of Gq (GqI) in vascular smooth muscle to determine if vascular Gq signaling was important in the cardiac hypertrophic response. After chronic administration of the Gq agonists phenylephrine, serotonin, and angiotensin II, we observed an attenuation of mean arterial blood pressure and an inhibition of cardiac hypertrophy in the transgenic mice with vascular-specific GqI expression. In contrast, cardiac GqI peptide expression did not attenuate the hypertension or the cardiac hypertrophy. Importantly, all mice were capable of cardiac hypertrophy, because direct β-adrenergic receptor stimulation induced a similar level of hypertrophy in both lines of transgenic mice. This clearly suggests that after chronic Gq-coupled receptor agonist administration, it is the hypertensive state induced by vascular Gq activation that mediates remodeling of the heart, rather than direct stimulation of cardiac Gq-coupled receptors. Thus, the contribution of vascular Gq-coupled signaling to the development of cardiac hypertrophy is significant and suggests that expression of the GqI peptide is a novel therapeutic strategy to lower Gq-mediated hypertension and cardiac hypertrophy.</jats:p>

収録刊行物

  • Hypertension

    Hypertension 40 (5), 660-666, 2002-11

    Ovid Technologies (Wolters Kluwer Health)

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