Key result
Central AT1 receptor mRNA antisense decreased resting renal sympathetic nerve activity and normalized the enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.
Why the study?
Does central administration of AT1R mRNA antisense reduce enhanced cardiac sympathetic afferent reflex and resting renal sympathetic nerve activity in rats with chronic heart failure?
Population
Rats with coronary ligation-induced chronic heart failure (CHF) and sham-operated rats
Comparison
Intracerebroventricular administration or… vs Scrambled oligonucleotides
Design
Preclinical
Follow-up
5 hours
Authors
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AT1R antisense normalizes enhanced CSAR in rat CHF; leaves open whether central RAS targeting modulates sympathetic drive in human heart failure.
Does central administration of AT1R mRNA antisense reduce enhanced cardiac sympathetic afferent reflex and resting renal sympathetic nerve activity in rats with chronic heart failure?
Central AT1R mRNA antisense reduces AT1R protein expression and normalizes enhanced sympathetic reflexes in a rat model of chronic heart failure.
Zhu et al. (2004) studied chronic heart failure. AT1 receptor mRNA antisense oligodeoxynucleotides vs. scrambled oligonucleotides was evaluated on cardiac sympathetic afferent reflex (CSAR) and resting renal sympathetic nerve activity (RSNA). Central AT1 receptor mRNA antisense decreased resting renal sympathetic nerve activity and normalized the enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.
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