Endothelium-dependent coronary dilation in response to norepinephrine in conscious dogs

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Abstract

The coronary vascular response to norepinephrine (NE) in conscious dogs is biphasic: a functional hyperemia followed by an α-receptor mediated vasoconstriction. This study examined the role of nitric oxide (NO) in mediating the dilatory response to NE. Four dogs were chronically instrumented to measure left ventricular systolic and diastolic pressures (LVSP, LVEDP), maximal rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (MAP), and circumflex flow velocity (CFV). Resting control values were: LVSP 118 ±1.5 (SEM) mmHg, LVEDP 6±1.5 mmHg, dP/dtmax 2550±428 mmHg/sec, MAP 83±6 mmHg, HR 80±5 bpm, and CFV 3.4±1.4 kHz. Intracoronary (i.e.) injection of 03 μg NE caused a 53±17% increase in CFV followed by a 15±4% decrease. After blockade of NO synthesis using Nω-nitro-L-arginine (E-NA. 75 mg, i.e.), resting hemodynamic values were unchanged, but the coronary dilatory response to 20 μg acetylcholine, i.c., was reduced by 58±4%. After NO blockade the coronary flow increased only 28±11% in response to NE. The vasoconstriction was unchanged. These data indicate that the coronary response to NE in the conscious dog involves both endothelium independent and dependent components.

Original languageEnglish
JournalFASEB Journal
Volume11
Issue number3
StatePublished - 1 Dec 1997

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norepinephrine
endothelium
Endothelium
Dilatation
Norepinephrine
Dogs
Flow velocity
dogs
nitric oxide
Nitric Oxide
vasoconstriction
Vasoconstriction
heart rate
Arterial Pressure
Heart Rate
Blood Pressure
Hyperemia
Hemodynamics
acetylcholine
Ventricular Pressure

Cite this

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title = "Endothelium-dependent coronary dilation in response to norepinephrine in conscious dogs",
abstract = "The coronary vascular response to norepinephrine (NE) in conscious dogs is biphasic: a functional hyperemia followed by an α-receptor mediated vasoconstriction. This study examined the role of nitric oxide (NO) in mediating the dilatory response to NE. Four dogs were chronically instrumented to measure left ventricular systolic and diastolic pressures (LVSP, LVEDP), maximal rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (MAP), and circumflex flow velocity (CFV). Resting control values were: LVSP 118 ±1.5 (SEM) mmHg, LVEDP 6±1.5 mmHg, dP/dtmax 2550±428 mmHg/sec, MAP 83±6 mmHg, HR 80±5 bpm, and CFV 3.4±1.4 kHz. Intracoronary (i.e.) injection of 03 μg NE caused a 53±17{\%} increase in CFV followed by a 15±4{\%} decrease. After blockade of NO synthesis using Nω-nitro-L-arginine (E-NA. 75 mg, i.e.), resting hemodynamic values were unchanged, but the coronary dilatory response to 20 μg acetylcholine, i.c., was reduced by 58±4{\%}. After NO blockade the coronary flow increased only 28±11{\%} in response to NE. The vasoconstriction was unchanged. These data indicate that the coronary response to NE in the conscious dog involves both endothelium independent and dependent components.",
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N2 - The coronary vascular response to norepinephrine (NE) in conscious dogs is biphasic: a functional hyperemia followed by an α-receptor mediated vasoconstriction. This study examined the role of nitric oxide (NO) in mediating the dilatory response to NE. Four dogs were chronically instrumented to measure left ventricular systolic and diastolic pressures (LVSP, LVEDP), maximal rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (MAP), and circumflex flow velocity (CFV). Resting control values were: LVSP 118 ±1.5 (SEM) mmHg, LVEDP 6±1.5 mmHg, dP/dtmax 2550±428 mmHg/sec, MAP 83±6 mmHg, HR 80±5 bpm, and CFV 3.4±1.4 kHz. Intracoronary (i.e.) injection of 03 μg NE caused a 53±17% increase in CFV followed by a 15±4% decrease. After blockade of NO synthesis using Nω-nitro-L-arginine (E-NA. 75 mg, i.e.), resting hemodynamic values were unchanged, but the coronary dilatory response to 20 μg acetylcholine, i.c., was reduced by 58±4%. After NO blockade the coronary flow increased only 28±11% in response to NE. The vasoconstriction was unchanged. These data indicate that the coronary response to NE in the conscious dog involves both endothelium independent and dependent components.

AB - The coronary vascular response to norepinephrine (NE) in conscious dogs is biphasic: a functional hyperemia followed by an α-receptor mediated vasoconstriction. This study examined the role of nitric oxide (NO) in mediating the dilatory response to NE. Four dogs were chronically instrumented to measure left ventricular systolic and diastolic pressures (LVSP, LVEDP), maximal rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (MAP), and circumflex flow velocity (CFV). Resting control values were: LVSP 118 ±1.5 (SEM) mmHg, LVEDP 6±1.5 mmHg, dP/dtmax 2550±428 mmHg/sec, MAP 83±6 mmHg, HR 80±5 bpm, and CFV 3.4±1.4 kHz. Intracoronary (i.e.) injection of 03 μg NE caused a 53±17% increase in CFV followed by a 15±4% decrease. After blockade of NO synthesis using Nω-nitro-L-arginine (E-NA. 75 mg, i.e.), resting hemodynamic values were unchanged, but the coronary dilatory response to 20 μg acetylcholine, i.c., was reduced by 58±4%. After NO blockade the coronary flow increased only 28±11% in response to NE. The vasoconstriction was unchanged. These data indicate that the coronary response to NE in the conscious dog involves both endothelium independent and dependent components.

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