Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION

Hackett, James G.; Abboud, François M.; Mark, Allyn L.; Schmid, Phillip G.; Heistad, Donald D.; Bollard, Dennis; Brooks, Leonard

doi:10.1161/01.res.31.1.8

Cited by 88 publications

(40 citation statements)

References 19 publications

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“…29 ' 30 Electrical stimulation of the carotid sinus nerve, which mimics increased carotid sinus pressure, produces inhibition of coronary sympathetic constrictor tone. 31 ' 32 In the present experiments a restriction of flow and oxygen delivery was observed before a-receptor blockade but not afterwards; the most probable interpretation of these results is that an a-receptor vasoconstrictor mechanism limits coronary blood flow during reflex sympathetic activation from the carotid sinus baroreceptors.…”

Section: Neural Controlsupporting

confidence: 48%

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Mohrman¹,

Feigl²

1978

Circulation Research

248

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Before a-receptor blockade, either intracoronary norepinephrine infusion or reflex sympathetic activation from the carotid sinus resulted in an increase of only 0.85 ml/100 g mirr' in oxygen delivery for each increase of 1 ml/100 g min" 1 in cardiac oxygen consumption. Under these circumstances, myocardial oxygen extraction increased and coronary venous oxygen content fell. After a-receptor blockade, either intracoronary norepinephrine infusion or a carotid sinus reflex resulted in an increase of 1.23 ml/100 g min ' in oxygen delivery for each increase of 1 ml/100 g min' 1 in cardiac oxygen consumption. Myocardial oxygen extraction and coronary venous oxygen content changed only slightly after a-receptor blockade. The greater coronary vasodilation and lesser change in cardiac oxygen extraction after a-receptor blockade were significantly different (P < 0.001) from the values before blockade. It is concluded that the coronary a-receptor constrictor mechanism competes with metabolic vasodilation during sympathetic activation even when there are large increases in myocardial metabolism. The net effect of the a-receptor constrictor influence is to restrict the metabolically related flow increase by about 30%, thus increasing oxygen extraction and decreasing coronary venous oxygen content.IT HAS LONG been known that stimulation of the sympathetic innervation of the heart results in tachycardia and augmented contractility, accompanied by increased myocardial oxygen consumption, increased coronary blood flow, and decreased coronary sinus oxygen content. A previous study in this laboratory demonstrated that sympathetic a-receptor coronary vasoconstriction is capable of competing with local metabolic control and lowering coronary sinus oxygen tension after adrenergic /3-receptor blockade. 17 In that study the positive inotropic and chron-

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Section: Neural Controlsupporting

confidence: 48%

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Mohrman¹,

Feigl²

1978

Circulation Research

248

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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%

“…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. Hackett et al (1972) stimulated the carotid sinus nerve in animals whose hearts were paced, and observed a reflex coronary vasodilatation that was diminished by the administration of atropine. Similarly, Vatner (1983) has shown that the coronary vasodilatation associated with stimulation of peripheral chemoreceptors is mediated by both an increase in cholinergic activity and a decrease in a-adrenergic tone.…”

Section: G a Ord Wa Y And K H Pitettimentioning

confidence: 99%

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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“…First of all, in the present investigation the cerebral circulation was left intact and the carotid chemoreceptor reflex was stimulated without inducing cerebral hypoxia. It has been shown by Jacobs et al (3) and Hackett et al (23), that intracarotid nicotine or cyanide stimulates primarily the carotid chemoreceptor reflex. It is also felt that central nervous system stimulation did not occur, because after ipsilateral carotid sinus nerve section, no change in systemic or LV function was observed with intracarotid nicotine or cyanide.…”

Section: * Discussionmentioning

confidence: 97%

Control of the Myocardial Contractile State by Carotid Chemo- and Baroreceptor and Pulmonary Inflation Reflexes in Conscious Dogs

Vatner¹,

Rutherford²

1978

J. Clin. Invest.

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A B S T R A C T The effects of carotid chemoreceptor stimulation with intracarotid injections of either nicotine, 0.2 ug/kg, or cyanide, 2 ,ug/kg, were compared with the effects ofbilateral carotid occlusion on left ventricular (LV) pressure, dPldt, and diameter in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. With heart rate maintained constant, carotid chemoreceptor stimulation increased mean arterial pressure by 27+3%, LV end diastolic diameter by 4±0.9% and LV dP/dt by 21+2%. With ventilation controlled during succinylcholine infusion, carotid chemoreceptor stimulation increased mean arterial pressure by 43+2% and dP/dt by 37+5%, values significantly greater, P < 0.01, than were observed in dogs with spontaneous ventilation. Similarly, in dogs with spontaneous ventilation after vagotomy, carotid chemoreceptor stimulation also increased dPldt by a greater amount, i.e., by 48±9%. The increases in LV end diastolic diameter were not affected significantly by either cholinergic blockade with atropine or beta adrenergic blockade with propranolol. Although cholinergic blockade did not affect the inotropic or pressor responses significantly, beta adrenergic blockade attenuated the pressor response and essentially abolished the inotropic response. Bilateral carotid occlusion increased mean arterial pressure and LV end diastolic diameter by similar amounts to those observed with chemoreceptor stimulation, but increased dP/dt significantly less, P < 0.02, i.e., by 13±2%. As was

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Coronary Vascular Responses to Stimulation of Chemoreceptors and Baroreceptors: EVIDENCE FOR REFLEX ACTIVATION OF VAGAL CHOLINERGIC INNERVATION

Cited by 88 publications

References 19 publications

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

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

Control of the Myocardial Contractile State by Carotid Chemo- and Baroreceptor and Pulmonary Inflation Reflexes in Conscious Dogs

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