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Quantifying Acute Changes in Renal Sympathetic Nerve Activity in Response to Central Nervous System Manipulations in Anesthetized Rats
Published on: September 11, 2018
S100B modulates the hemodynamic response to norepinephrine stimulation.
James N Tsoporis1, Christopher B Overgaard, Shehla Izhar
1Division of Cardiology, Department of Medicine, Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.
American Journal of Hypertension
|August 29, 2009
Summary
The absence of S100B protein attenuates hemodynamic responses to norepinephrine (NE), while its overexpression prevents NE-induced cardiac hypertrophy and smooth muscle cell proliferation.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Biochemistry
Background:
- S100B protein is a known intrinsic negative regulator of myocardial hypertrophy.
- Previous studies indicated S100B's role in the heart's response to norepinephrine (NE).
Purpose of the Study:
- To investigate the role of S100B in acute and chronic hemodynamic responses to NE.
- To determine S100B's influence on NE-induced cardiac hypertrophy and smooth muscle cell proliferation.
Main Methods:
- Utilized S100B knockout (KO), transgenic (TG), and control (CD1) mice.
- Administered daily subcutaneous injections of NE (1.5 mg/kg) or vehicle for 28 days.
- Assessed hemodynamic parameters, myocyte hypertrophy, smooth muscle proliferation, and intracellular calcium concentrations.
Main Results:
- S100B KO mice showed attenuated blood pressure responses to NE.
- NE-induced cardiac hypertrophy and smooth muscle proliferation were augmented in KO mice.
- S100B overexpression in TG mice prevented NE-induced hypertrophy and proliferation, and reduced cytosolic calcium.
Conclusions:
- Absence of S100B attenuates hemodynamic responses to catecholamines.
- S100B plays a critical role in preventing cardiac hypertrophy and smooth muscle proliferation.
- S100B interacts with AHNAK in response to NE in cardiac and vascular tissues.
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