Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

Murray, Paul A.; Lavallée, Michel; Vatner, Stephen F.

doi:10.1161/01.res.54.1.96

Cited by 30 publications

(13 citation statements)

References 68 publications

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“…The coronary vasodilatation seen in the present study is similar to that which has PULMONARY CHEMOREFLEX AND CORONAR Y RESISTANCE 287 been observed previously during carotid sinus nerve stimulation (Hackett, Abboud, Mark, Schmid & Heistad, 1972), peripheral chemoreceptor stimulation (Hashimoto, Igarashi, Uei & Kumakura, 1964;Vatner & McRitchie, 1975;Vatner, 1983;Murray, Lavallee & Vatner, 1984), carotid sinus baroreceptor stimulation (Ito & Feigl, 1985), and the Bezold-Jarish reflex (Feigl, 1975). Further, the neurohumoral basis for the changes in coronary resistance evoked by capsaicin in the present study is comparable to that seen in previous studies.…”

Section: G a Ord Wa Y And K H Pitettisupporting

confidence: 91%

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

Ordway¹,

Pitetti²

1986

The Journal of Physiology

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SUMMARY1. A constant-flow preparation was used to assess coronary arterial resistance while activating pulmonary C fibres in chloralose-anaesthetized dogs.2. A Gregg cannula was passed through the left common carotid artery until the tip fitted snugly in the left circumflex coronary artery. The cannula was perfused with blood from the left femoral artery and blood flow through the cannula was maintained constant with a perfusion pump. Perfusion pressure in the coronary artery was measured from a side arm in the cannula, and resistance in that vessel was calculated as the ratio of pressure to blood flow.3. Capsaicin (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) ,ug/kg), injected into the right jugular vein, produced significant (P<0-05) decreases in heart rate, systemic arterial pressure, coronary arterial pressure and coronary arterial resistance. These responses were abolished by bilateral vagotomy. Neither left atrial injections of capsaicin nor acutely decreasing the systemic arterial pressure by occluding the inferior vena cava had a significant effect on the coronary arterial pressure or resistance. Additionally, overdrive pacing of the heart had no effect on the reflex decreases in coronary arterial pressure and resistance that were evoked when capsaicin was injected into the jugular vein.4. a-Adrenergic blockade reduced the reflex decrease in coronary arterial pressure and resistance evoked by capsaicin by 31 and 38 %, respectively. Combined z-adrenergic and cholinergic blockade reduced the reflex decreases in both coronary arterial pressure and resistance by approximately 89 %.5. These results indicate that activation of pulmonary C fibres produces a reflex decrease in coronary arterial resistance, and that this response is due to the combined effects of increased parasympathetic cholinergic activity and withdrawal of oz-adrenergic tone.

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Section: G a Ord Wa Y And K H Pitettisupporting

confidence: 91%

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

Ordway¹,

Pitetti²

1986

The Journal of Physiology

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“…Although a carotid body chemoreceptor reflex influence on coronary vessels has been demonstrated (Hackett et al, 1972;Vatner and McRitchie, 1975;Murray and Vatner, 1983;Murray et al, 1984), these receptors have been shown to be relatively insensitive to arterial pressure in the range of 60-220 mm Hg (Biscoe et al, 1970;Mancia, 1975). Thus, the reflex observed in the present study most likely originated from carotid sinus baroreceptors.…”

Section: Neural Controlmentioning

confidence: 48%

“…These neural pathways can be reflexly activated by several stimuli. Parasympathetic coronary vasodilation is part of the BezoldJarisch reflex (Feigl, 1975) and the carotid body chemoreflex (Hackett et al, 1972;Vatner and McRitchie, 1975;Murray and Vatner, 1983;Murray et al, 1984). Reflex sympathetic a-receptor coronary 493 vasoconstriction in response to carotid sinus hypotension has been reported in preparations with fireceptor blockade (Feigl, 1968;DiSalvo et al, 1971;Powell and Feigl, 1979) and without /3-receptor blockade (Mohrman and Feigl, 1978).…”

Section: Neural Controlmentioning

confidence: 99%

Carotid baroreceptor reflex coronary vasodilation in the dog.

Ito

Feigl²

1985

Circulation Research

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SUMMARY. The hypothesis that neurally mediated coronary vasodilation occurs as part of the carotid baroreceptor reflex was investigated. The left main coronary artery was cannulated and perfused at constant pressure (100 mm Hg) in closed-chest, chloralose-anesthetized dogs. The heart was paced at a constant rate between 60 and 70 beats/min after atrioventricular heart block. Propranolol (1 mg/kg) was given to prevent j3-receptor-mediated alterations in contractility. Aortic blood pressure was stabilized with a blood reservoir. The aortic depressor nerves were cut bilaterally to prevent the buffering influence of aortic arch baroreceptors on the carotid baroreceptor reflex. The carotid sinuses were vascularly isolated and perfused with arterial blood at controlled pressures. Under these conditions, a step change in carotid sinus pressure from 70 to 210 mm Hg produced a 0.29 ml/min per g increase in coronary flow above control and a 10 mm Hg increase in coronary sinus blood oxygen tension. A step in carotid sinus pressure from 70 to 150 mm Hg resulted in a flow increase of 0.13 ml/min per g and a coronary sinus oxygen tension increase of 5.3 mm Hg relative to prestimulation values. Atropine (0.5 mg/kg, iv) blocked most of the reflex coronary vasodilation, indicating a parasympathetic component, and the addition of adrenergic a-receptor blockade with phenoxybenzamine (0.25 mg/kg, ic) abolished the remaining response, demonstrating sympathetic participation. The reflex nature of the coronary response was confirmed with carotid sinus denervation and vagotomy. It is concluded that carotid sinus hypertension results in a graded reflex neural coronary vasodilation independent of myocardial metabolic factors. The major component is due to activation of parasympathetic coronary vasodilator fibers, but there is also inhibition of sympathetic vasoconstrictor fibers. (Circ Res 56: 486-495, 1985) PREVIOUS studies have demonstrated that adrenergic a-receptor coronary vasoconstriction can be reflexly elicited by carotid sinus hypotension (Feigl, 1968(Feigl, , 1983DiSalvo et al., 1971;Limet et al., 1975;Powell and Feigl, 1979;Ely et al., 1981). However, the reflex response to carotid sinus hypertension is less clear. Both coronary vasoconstriction (DiSalvo et al., 1971) and coronary vasodilation (Limet et al., 1975) have been observed during acute elevations in carotid sinus pressure. Coronary vasodilation during the elevation of aortic pressure has also been attributed to the carotid baroreflex (White et al., 1976). Electrical stimulation of the afferent carotid sinus nerve has been employed to mimic carotid sinus hypertension, and either coronary vasoconstriction (Falicov et al., 1970) or vasodilation (Vatner et al., 1970;Hackett et al., 1972;Religa et al., 1972;Solti et al., 1975) has been observed. However, it is difficult to equate a given nerve stimulation frequency with a carotid sinus pressure stimulus that physiologically activates baroreceptors. Furthermore, electrical stimulation of carotid sinus baroreceptor affe...

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“…84 With controlled ventilation, a significant a-adrenoceptormediated coronary constrictor response is apparent in conscious dogs during carotid chemoreceptor activation. 85 Several central nervous sites from which aadrenergic coronary constriction can be elicited have been identified in anesthetized cats.86 However, a physiological or pathological role for these central nervous sites in regulating coronary blood flow remains to be established. a-Adrenergic coronary constriction during exercise.…”

mentioning

confidence: 99%

Alpha-adrenergic mechanisms in myocardial ischemia.

Heusch¹

1990

Circulation

239

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Dedicated to Prof Dr. Franz Loogen on the occasion of his 70th birthday c-Adrenoceptor-mediated effects of sympathetic activation on the heart and coronary circulation are reviewed with emphasis on the pathophysiology of myocardial ischemia. A classification of a-adrenoceptor subtypes is presented, and the effects of a-adrenoceptor activation on presynaptic sympathetic nerve terminals, cardiomyocytes, endothelium, platelets, and coronary smooth muscle cells are discussed. av-Adrenergic coronary vasoconstriction at rest and during situations of sympathetic activation such as exercise and excitement is analyzed for the segmental, transmural, and regional distribution of coronary blood flow. Evidence for a significant contribution of av-adrenergic coronary vasoconstriction to experimental and clinical myocardial ischemia is provided. Cardiomyocyte a-adrenoceptor activation may be involved in ischemic and reperfusion arrhythmias. The participation of presynaptic and postsynaptic aadrenoceptors, as well as of ael-and a2-adrenoceptors, in experimental and clinical myocardial ischemia will require further investigation. (Circulation 1990;81:1-13) D uring the sympathetic activation induced by exercise or excitement, the activity of cardiac sympathetic nerves, as well as the release of circulating catecholamines, is enhanced. The resultant activation of cardiac 83-adrenoceptors by neuronal and humoral catecholamines mediates an increase in heart rate and myocardial inotropic state, thereby increasing myocardial oxygen demand. Increased oxygen demand is adequately matched by an augmented oxygen supply after metabolic dilation of the coronary vasculature under normal conditions.' However, the direct effect of the sympathetic neurotransmitter norepinephrine on coronary vascular smooth muscle cells is vasoconstriction through activation of a-adrenoceptors. Even when under normal conditions a substantial coronary dilator reserve is present, a-adrenergic constriction acts to limit metabolic coronary dilation by about 30%, such that myocardial oxygen extraction increases together with coronary blood flow during sympathetic activation to match oxygen supply to the increased myocardial oxygen demand.2-4

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Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

Cited by 30 publications

References 68 publications

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

Stimulation of pulmonary C fibres decreases coronary arterial resistance in dogs.

Carotid baroreceptor reflex coronary vasodilation in the dog.

Alpha-adrenergic mechanisms in myocardial ischemia.

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