Related Experiment Videos
Elevated sympathetic nervous activity in mice deficient in alphaCGRP
Y Oh-hashi1, T Shindo, Y Kurihara
1Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
Circulation Research
|November 22, 2001
Summary
Alpha-Calcitonin gene-related peptide (alphaCGRP) deficiency increases blood pressure and sympathetic activity. This study reveals alphaCGRP
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Genetics
Background:
- Alpha-Calcitonin gene-related peptide (alphaCGRP) is a neuropeptide involved in numerous physiological functions.
- Understanding alphaCGRP's role in cardiovascular regulation is crucial for identifying potential therapeutic targets.
Purpose of the Study:
- To investigate the physiological functions of alphaCGRP in cardiovascular regulation.
- To elucidate the role of alphaCGRP in modulating sympathetic nervous system activity.
Main Methods:
- Development of an alphaCGRP-null mouse model using gene targeting.
- Measurement of mean arterial pressure (MAP) and heart rate (HR) in anesthetized and conscious mice.
- Assessment of autonomic nervous system activity via pharmacological blockade and baroreceptor reflex analysis.
- Analysis of urinary catecholamine metabolites and heart rate variability.
Main Results:
- AlphaCGRP-null mice exhibited significantly higher basal MAP and HR compared to wild-type mice.
- Elevated MAP in null mice was attributed to increased peripheral vascular resistance, not altered cardiac output.
- Increased sympathetic nervous activity was evidenced by elevated urinary catecholamine metabolites and reduced HR variability in null mice.
Conclusions:
- AlphaCGRP plays a significant role in regulating cardiovascular function.
- The findings suggest alphaCGRP exerts an inhibitory influence on sympathetic nervous system activity.
- Deficiency in alphaCGRP leads to heightened sympathetic tone and elevated blood pressure.