Carotid baroceptor influence on coronary vascular resistance in the anesthetized dog

DiSalvo, Joseph; Parker, PE; Jb, Scott; Fj, Haddy

doi:10.1152/ajplegacy.1971.221.1.156

Cited by 38 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent evidence also indicates that a-adrenergic activation can reduce the diameter of large coronary arteries (Gerova et al, 1979;Vatner et al, 1980a). Carotid sinus hypotension (Feigl, 1968;Bond and Green, 1969;DiSalvo et al, 1971;Mohrman and Feigl, 1978;Powell and Feigl, 1979) has also been shown to result in sympathetic a-adrenergic-mediated changes in left coronary resistance in the presence of )3-adrenergic receptor blockade. Whereas reflex a-adrenergic constriction of the right coronary circulation in conscious dogs has been demonstrated with autonomic nervous system activity intact (Murray and Vatner, 1981b), an absolute reduction in right coronary blood flow was not observed during carotid sinus hypotension.…”

Section: Discussionmentioning

confidence: 99%

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

Murray

Lavallée

Vatner

1984

Circulation Research

View full text Add to dashboard Cite

SUMMARY. We examined the late coronary vascular response to carotid chemoreceptor reflex activation in normal, conscious dogs instrumented for the measurement of right main and left circumflex coronary artery blood flows, arterial and right ventricular pressures, and arterial and coronary sinus blood gases and O 2 contents. With heart rate held constant by electrical stimulation, and with respiration controlled or allowed to vary spontaneously, carotid chemoreceptor reflex activation (induced by intracarotid nicotine) elicited a striking biphasic coronary vascular response characterized by an early dilation (previously described) and a late constriction. For example, with respiration controlled and with the autonomic nervous system intact, carotid chemoreceptor reflex activation resulted in a late increase in arterial pressure (19 ± 4%; P < 0.002), absolute reductions in right main (24 ± 4%; P < 0.002), and left circumflex (12 ± 2%; P < 0.004) coronary blood flows, and increases in right (62 ± 13%; P < 0.002) and left (26 ± 3%; P < 0.0001) coronary resistances. This carotid chemoreceptor reflex activation-induced late coronary constriction was also associated with a concomitant increase in myocardial oxygen extraction, i.e., arterial oxygen content remained constant, while coronary sinus oxygen content decreased (19 ± 6%; P < 0.04). Neither propranolol nor atropine had any significant effect on the magnitude of the right coronary constriction. However, both the absolute reduction in right coronary blood flow and increase in right coronary resistance were abolished by phentolamine. Furthermore, either total cardiac denervation or adrenalectomy significantly attenuated (P < 0.01) carotid chemoreceptor reflex activation-induced reductions in right coronary blood flow and increase in right coronary resistance. We conclude that, with autonomic nervous system activity intact, carotid chemoreceptor reflex activation can elicit an absolute reflexly mediated reduction in coronary blood flow in the normal, conscious dog, despite an increase in arterial pressure. The mechanism of this vasoconstriction involves a-adrenergic receptor stimulation mediated by both cardiac sympathetic nerves and circulating catecholamines. {Circ Res 54: 96-106, 1984) THERE NOW exists a relatively large body of experimental evidence which supports the concept that sympathetic activation can result in a-adrenergic coronary vasoconstriction. This concept is based primarily on experiments in which sympathetic activation has resulted in increases in arterial pressure which have been greater than concomitant increases in coronary blood flow, with a consequent increase in coronary resistance. It is somewhat surprising that despite recent interest in the role of coronary vasoconstriction in the pathogenesis of coronary artery vasospasm (Hillis and Braunwald, 1978;Maseri et al., 1978), there is little compelling evidence that aadrenergic vasoconstriction can mediate an absolute reduction in coronary blood flow in the presence of an intact autonomic n...

show abstract

Section: Discussionmentioning

confidence: 99%

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

Murray

Lavallée

Vatner

1984

Circulation Research

View full text Add to dashboard Cite

show abstract

“…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%

“…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).…”

mentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Carotid baroreceptor reflex coronary vasodilation in the dog.

Ito

Feigl²

1985

Circulation Research

View full text Add to dashboard Cite

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...

show abstract

“…The increase in myocardial metabolism leads to an increase in coronary blood flow, but there is a concomitant α-adrenoceptor-mediated coronary vasoconstriction that restrains the increase in coronary blood flow and increases myocardial oxygen extraction [15, 18, 52, 58, 64]. …”

Section: Sympathetic Controlmentioning

confidence: 99%

Neural Control of Coronary Blood Flow

Feigl

1998

J Vasc Res

View full text Add to dashboard Cite

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.

show abstract

Carotid baroceptor influence on coronary vascular resistance in the anesthetized dog

Cited by 38 publications

References 0 publications

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

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

Carotid baroreceptor reflex coronary vasodilation in the dog.

Neural Control of Coronary Blood Flow

Contact Info

Product

Resources

About