Transmural regulation of myocardial perfusion by neuropeptide Y

Gutterman, David D.; Morgan, Donald A.

doi:10.1007/bf00797913

Cited by 8 publications

(4 citation statements)

References 31 publications

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“…These authors conclude that ␣ 1 -adrenoceptor-mediated coronary constriction limits oxygen delivery to the subendocardium and compromises myocardial contraction. Although the experimental conditions in Gwirtz et al's study differ from the present investigation, the detrimental effects of ␣-adrenoceptor vasoconstriction found by Gwirtz et al are not supported by the present results or the literature discussed above (2,12,16,17). The reason for the discrepancy is not apparent at this time.…”

Section: H2753contrasting

confidence: 93%

“…The difference may be due to neuropeptide Y, which is coreleased with norepinephrine from sympathetic nerves. Gutterman and Morgan(12) observed that the coinfusion of neuropeptide Y with norepinephrine potentiated the norepinephrine effect of augmenting inner layer flow compared with outer layer flow in a preparation with adenosine-induced vasodilation. Norepinephrine infusion was used in the present experiment because it is not practical to obtain a long steady effect with electrical stimulation of sympathetic nerves while adjusting the aortic snare to match systolic blood pressure before and after ␣-adrenoceptor blockade.Adrenergic activation has been shown to decrease arterial compliance in vivo(3).…”

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confidence: 99%

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α-Adrenergic vasoconstriction reduces systolic retrograde coronary blood flow

Morita

Mori

Tsujioka

et al. 1997

American Journal of Physiology-Heart and Circulatory Physiology

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There is a paradoxical α-adrenoceptor-mediated coronary vasoconstriction whenever there is adrenergic activation of the heart, as during cardiovascular reflexes or exercise. A previous study demonstrated that this paradoxical vasoconstriction helps maintain blood flow to the vulnerable inner layer of the left ventricular wall during exercise, but the mechanism for this effect was not elucidated. The purpose of the present investigation was to test the hypothesis that α-adrenoceptor-mediated vasoconstriction lessens the to-and-fro oscillation of blood flow that occurs in the coronary arterial tree during systole and diastole. Septal coronary artery blood velocity was measured in anesthetized open-chest dogs with a 20-MHz pulsed Doppler velocimeter. Systolic retrograde velocity and diastolic forward velocity were compared during norepinephrine infusion before and after α-adrenoceptor blockade with phenoxybenzamine. Systolic aortic pressure was held constant by aortic banding; heart rate was controlled by pacing at 80, 140, and 200 beats/min; and maximum left ventricular dP/d t was unchanged by α-blockade. At each pacing rate, systolic retrograde velocity was significantly greater after α-blockade, indicating that α-vasoconstriction reduced systolic retrograde flow by changing coronary vascular impedance. Transmural blood flow was measured with microspheres in a second group of dogs during the same experimental conditions, and flow to the inner layer of the left ventricle was diminished by α-adrenoceptor blockade at a heart rate of 250 beats/min, demonstrating a beneficial effect of α-vasoconstriction. In conclusion, adrenergic α-adrenoceptor-mediated coronary vasoconstriction reduces systolic retrograde coronary flow during norepinephrine infusion. This lessens to-and-fro flow oscillation in the coronary circulation and probably is the mechanism whereby α-vasoconstriction helps maintain blood flow to the inner layer of the left ventricle during exercise.

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Section: H2753contrasting

confidence: 93%

mentioning

confidence: 99%

α-Adrenergic vasoconstriction reduces systolic retrograde coronary blood flow

Morita

Mori

Tsujioka

et al. 1997

American Journal of Physiology-Heart and Circulatory Physiology

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“…Regional interruption of autonomic innervation occurs after myocardial infarction and may predispose the heart to arrhythmias and/or alterations in coronary flow, depending on the location and the overall extent of injury (1023). In general, sympathetic nerves release norepinephrine, neuropeptide Y, and ATP, while parasympathetic nerves release acetylcholine and vasoactive intestinal polypeptide (237, 351, 413, 422, 478, 817, 818). Studies by Brody and colleagues also provide seminal evidence of a role for central neural pathways in the regulation of coronary blood flow.…”

Section: Neural Controlmentioning

confidence: 99%

Regulation of Coronary Blood Flow

Goodwill

Dick

Kiel

et al. 2017

Comprehensive Physiology

244

248

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The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery.

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“…During resting conditions α-adrenoceptor activation has little effect on transmural flow distribution, because there is an adequately long diastolic period to fill intramyocardial capacitance and there is ample vasodilator reserve in the subendocardium [2, 6, 40]. However, when tachycardia is combined with high coronary flow caused by adenosine infusion [27, 40], dipyridamole [2], or exercise [37] α-adrenoceptor activation has a favorable effect on transmural flow distribution. These observations may explain the well-documented paradoxical α-adrenoceptor-mediated coronary vasoconstriction during exercise.…”

Section: Transmural Blood Flowmentioning

confidence: 99%

Neural Control of Coronary Blood Flow

Feigl

1998

J Vasc Res

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Parasympathetic control of coronary blood flow has been extensively studied in dogs, and a clear vasodilator effect not dependent on changes in myocardial metabolism was observed. Parasympathetic vasodilatation is mediated via nitric oxide (EDRF) and is activated during carotid baroreceptor and chemoreceptor reflexes. Intracoronary infusions of acetylcholine in humans results in increased coronary blood flow and epicardial coronary artery dilatation except in atherosclerotic epicardial coronary vessels, which show a paradoxical vasoconstriction. Sympathetic α-adrenoceptor-mediated coronary vasoconstriction has been repeatedly demonstrated whenever there is adrenergic activation of the heart, as during exercise or a carotid sinus baroreceptor reflex in dogs or during a cold pressor reflex in humans. Recent evidence indicates that there is a beneficial effect of this paradoxical vasoconstrictor influence in that it helps preserve flow to the vulnerable inner layer of the left ventricle, but only when both heart rate and coronary flow are high. β-Adrenoceptor-mediated coronary vasodilatation also occurs during adrenergic activation of the heart. The dominant site for β-vasodilatation is in small arterioles, while the dominant site for α-vasoconstriction is in microvessels larger than ∼100 µm diameter. The β-adrenoceptor coronary vasodilatation is an example of feedforward open-loop control that complements the closed-loop negative feedback control by local metabolic factors. The combined feedback and feedforward control mechanism has the advantage of an excellent match between coronary blood flow and myocardial oxygen consumption with a rapid response time but without the instability inherent in high gain feedback systems.

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Transmural regulation of myocardial perfusion by neuropeptide Y

Cited by 8 publications

References 31 publications

α-Adrenergic vasoconstriction reduces systolic retrograde coronary blood flow

α-Adrenergic vasoconstriction reduces systolic retrograde coronary blood flow

Regulation of Coronary Blood Flow

Neural Control of Coronary Blood Flow

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