Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.

@article{Danson2005DisruptionOI,
  title={Disruption of inhibitory G-proteins mediates a reduction in atrial beta-adrenergic signaling by enhancing eNOS expression.},
  author={Edward J. F. Danson and Yin Zhang and Claire E Sears and Angelina R Edwards and Barbara Casadei and David J. Paterson},
  journal={Cardiovascular research},
  year={2005},
  volume={67 4},
  pages={613-23}
}
OBJECTIVE Cardiac parasympathetic nerve activity is reduced in most cardiovascular disease states, and this may contribute to enhanced cardiac sympathetic responsiveness. Disruption of inhibitory G-proteins (Gi) ablates the cholinergic pathway and increases cardiac endothelial nitric oxide (NO) synthase (eNOS) expression, suggesting that NO may offset the impaired attenuation of beta-adrenergic regulation of supraventricular excitability. To test this, we investigated the role of endogenous NO… CONTINUE READING

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Disruption of inhibitory G - proteins ( Gi ) ablates the cholinergic pathway and increases cardiac endothelial nitric oxide ( NO ) synthase ( eNOS ) expression , suggesting that NO may offset the impaired attenuation of beta - adrenergic regulation of supraventricular excitability .
Disruption of inhibitory G - proteins ( Gi ) ablates the cholinergic pathway and increases cardiac endothelial nitric oxide ( NO ) synthase ( eNOS ) expression , suggesting that NO may offset the impaired attenuation of beta - adrenergic regulation of supraventricular excitability .
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