Key result
ICV infusion of MAPK inhibitors (PD98059 or SP600125) or losartan decreased AT(1)-R protein and mRNA in the hypothalamus of rats with heart failure, indicating MAPKs mediate AT(1)-R upregulation.
Population
Rats with ischemia-induced heart failure (coronary ligation) and sham-operated controls
Comparison
4-week or 3-hour intracerebroventricular… vs Sham-operated controls and untreated HF rats
Design
Preclinical
Follow-up
4 weeks
Authors
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May implicate hypothalamic MAPKs in HF-related AT1-R upregulation; leaves open clinical translation to sympathetic modulation.
MAPKs p44/42 and c-Jun N-terminal kinase mediate the upregulation of hypothalamic AT1 receptors in rats with heart failure, suggesting Ang II upregulates its own receptor via this pathway.
Wei et al. (2008) studied Heart failure. ICV infusion of losartan, PD98059, or SP600125 vs. Sham-operated controls or untreated HF rats was evaluated on AT(1)-R protein, mRNA, and immunoreactivity in the paraventricular nucleus and subfornical organ. ICV infusion of MAPK inhibitors (PD98059 or SP600125) or losartan decreased AT(1)-R protein and mRNA in the hypothalamus of rats with heart failure, indicating MAPKs mediate AT(1)-R upregulation.
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