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The effect of norepinephrine on the coronary microcirculation
J Quillen1, F Sellke, P Banitt
1Cardiovascular Center, Veterans Administration Medical Center, Iowa City, Iowa.
Journal of Vascular Research
|January 1, 1992
Summary
Norepinephrine (NE) primarily dilates coronary microvessels through beta-adrenoceptor activation and endothelium-derived relaxing factor (EDRF) release. Alpha-adrenoceptor-mediated constriction of these vessels by NE is minimal.
Area of Science:
- Cardiovascular Physiology
- Adrenergic Signaling
- Microcirculation Research
Background:
- Sympathetic nervous system's role in large coronary arteries is known.
- Adrenergic regulation of coronary resistance vessels often relies on indirect flow measurements.
- Direct in vitro studies of microvessel responses to adrenergic agents are limited.
Purpose of the Study:
- To investigate the direct effects of norepinephrine (NE) on coronary microcirculation.
- To elucidate the mechanisms underlying NE's action on these vessels in vitro.
Main Methods:
- Pressurization of isolated porcine coronary microvessels (80-200 microns).
- Measurement of vessel diameters using a Halpern microvessel imaging apparatus.
- Assessment of NE effects with and without preconstriction, and in the presence of propranolol, LY83583 (cGMP depletion), and hemoglobin (EDRF inhibition).
Main Results:
- Norepinephrine (NE) induced complete relaxation in preconstricted microvessels.
- Relaxation responses to NE were attenuated by propranolol and LY83583.
- Inhibition of endothelium-derived relaxing factor (EDRF) also reduced NE-induced relaxation.
- NE caused minimal constriction, even with alpha-adrenoceptor blockade or EDRF inhibition.
Conclusions:
- Norepinephrine (NE) predominantly causes vasodilation in porcine coronary microvessels.
- Vasodilation is mediated by both beta-adrenoceptor activation and EDRF release.
- Alpha-adrenoceptor-mediated constriction by NE in coronary microvessels is negligible.