Blockade of brain mineralocorticoid receptors or Na+ channels prevents sympathetic hyperactivity and improves cardiac function in rats post-MI.

@article{Huang2005BlockadeOB,
  title={Blockade of brain mineralocorticoid receptors or Na+ channels prevents sympathetic hyperactivity and improves cardiac function in rats post-MI.},
  author={Bing S. Huang and Frans H H Leenen},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2005},
  volume={288 5},
  pages={
          H2491-7
        }
}
  • Bing S. Huang, F. Leenen
  • Published 1 May 2005
  • Biology, Medicine
  • American journal of physiology. Heart and circulatory physiology
In rats post-myocardial infarction (MI), sympathetic hyperactivity can be prevented by blockade of brain mineralocorticoid receptors (MR). Stimulatory responses to central infusion of aldosterone can be blocked by benzamil and therefore appear to be mediated via Na+ channels, presumably epithelial Na+ channels (ENaC), in the brain. To evaluate this concept of endogenous mineralocorticoids in Wistar rats post-MI, we examined effects of blockade of MR and Na+ channels in the brain. At 3 days… 
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61 Citations
Background Citations
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61 Citations

Citation Type

Citation Type

Central infusion of aldosterone synthase inhibitor attenuates left ventricular dysfunction and remodelling in rats after myocardial infarction.
TLDR
The data suggest that aldosterone produced locally in the brain acts as the main agonist of mineralocorticoid receptors in the CNS and contributes substantially to the progressive heart failure post MI.
Inhibition of brain angiotensin III attenuates sympathetic hyperactivity and cardiac dysfunction in rats post-myocardial infarction.
TLDR
Results indicate that brain APA and Ang III appear to play a pivotal role in the sympathetic hyperactivity and LV dysfunction in rats post-MI and RB150 may be a potential candidate for central nervous system-targeted therapy post- MI.
Blockade of mineralocorticoid receptors improves salt-induced left-ventricular systolic dysfunction through attenuation of enhanced sympathetic drive in mice with pressure overload
TLDR
Findings indicate that activation of brain αENaC and AT1R through mineralocorticoid receptors contributes to the acquisition of Na sensitivity to induce sympathoexcitation and high salt intake accelerates sympathetic activation and LV systolic dysfunction in a pressure overload model.
Activation of mineralocorticoid receptors in the rostral ventrolateral medulla is involved in hypertensive mechanisms in stroke-prone spontaneously hypertensive rats
TLDR
It is suggested that activation of MRs in the RVLM enhances sympathetic activity, thereby contributing to the neural mechanism of hypertension in the SHRSP.
Sympathetic hyperactivity and cardiac dysfunction post-MI: different impact of specific CNS versus general AT1 receptor blockade.
Hypothalamic Activation in Rats With Ischemia-Induced Heart Failure Novel Effect of Mineralocorticoid Receptor Antagonism to Reduce Proinflammatory
TLDR
This study reveals a previously unrecognized effect of MR antagonism to minimize cytokine-induced central neural excitation in rats with HF, and results show no improvement in left ventricular function.
Novel Effect of Mineralocorticoid Receptor Antagonism to Reduce Proinflammatory Cytokines and Hypothalamic Activation in Rats With Ischemia-Induced Heart Failure
TLDR
A previously unrecognized effect of MR antagonism is revealed to minimize cytokine-induced central neural excitation in rats with HF and reduce hypothalamic COX-2 expression and PVN neuronal activation.
Regulation of hypothalamic renin–angiotensin system and oxidative stress by aldosterone
TLDR
Data indicate that aldosterone, via ‘ouabain’, increases in the PVN angiotensin‐converting enzyme, AT1R and oxidative stress, but decreases nNOS, and suggest that endogenous ald testosterone may cause the similar pattern of changes observed in salt‐sensitive hypertension and heart failure postmyocardial infarction.
Aldosterone Contributes to Sympathoexcitation in Renovascular Hypertension.
TLDR
Aldosterone contributes to autonomic dysfunction and intrarenal injury in 2K1C, these effects are mediated by the CNS.
Epithelial sodium channel inhibition in cardiovascular disease. A potential role for amiloride.
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