Reflex Vascular Responses to Stimulation of Chemoreceptors with Nicotine and Cyanide

Calvelo, Manuel G.; Abboud, François M.; Bollard, Dennis; Abdel-Sayed, Wadie

doi:10.1161/01.res.27.2.259

Cited by 66 publications

(16 citation statements)

References 19 publications

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“…The work of Berne et al (13) Differential reflex activation of the components of the autonomic system is evident in these and in previous studies (4). Stimulation of chemoreceptors has been shown to activate sympathetic adrenergic constrictor fibers to the gracilis muscle and simultaneously to activate sympathetic noncholinergic vasodilator fibers in the paw (4).…”

Section: Discussionmentioning

confidence: 78%

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

Hackett

Abboud

Mark

et al. 1972

Circulation Research

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Coronary vascular responses to stimulation of chemoreceptors were studied in anesthetized, artificially ventilated dogs. The circumflex coronary artery was perfused at constant flow so that changes in perfusion pressure reflected changes in coronary resistance. Practolol, a myocardioselective beta-receptor antagonist, and pacing were used to minimize indirect effects of myocardial responses on coronary resistance. Carotid and aortic injections of nicotine produced decreases in coronary perfusion pressure averaging -21 mm Hg and -22 mm Hg, respectively. Decreases with carotid and aortic injections of cyanide averaged -8 mm Hg and -17 mm Hg, respectively. These coronary dilator responses were abolished by bilateral vagotomy or atropine. Changes in perfusion pressure with carotid injections of nicotine averaged +3 mm Hg after vagotomy and +2 mm Hg after administration of atropine. The coronary dilator responses to carotid chemoreceptor stimulation were accompanied by increases in coronary sinus Po 2 in five studies and no change in two studies. Carotid sinus nerve stimulation caused abrupt and sustained coronary vasodilatation. After vagotomy or administration of atropine, the response to carotid sinus nerve stimulation was no longer abrupt but occurred gradually, suggesting that a component of the reflex response was blocked. These studies indicate that stimulation of chemoreceptors activates a vagal cholinergic vasodilator pathway to coronary vessels in the dog. Activation of this pathway appears also to contribute to reflex coronary responses to stimulation of baroreceptors.

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Section: Discussionmentioning

confidence: 78%

“…These differential responses represent reflex activation of different autonomic sympathetic pathways to skeletal muscle and skin (4). The lack of information concerning effects of stimulation of chemoreceptors on coronary vascular resistance prompted this study.…”

Section: Reflex Coronary Responsesmentioning

confidence: 99%

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

Hackett

Abboud

Mark

et al. 1972

Circulation Research

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“…Stimulation ofarterial chemoreceptors by excess carbon dioxide and lack of oxygen affects systemic arterial blood pressure and respiratory drive (de Burgh Daly & Scott, 1962;de Burgh Daly & Hazzledine, 1963;Calvelo, Abboud, Ballard & Abdel-Sayed, 1970). Such systemic effects during hypercapnia or hypoxia may alter the arterial blood flow to the nasal mucosa and hence the nasal airway resistance.…”

Section: Discussionmentioning

confidence: 99%

“…As mentioned in a previous study (Lung et al 1984), a decrease in airway resistance may be caused by (1) an increase in arterial resistance to inflow via active constriction of the arterioles; (2) an opening of the arteriovenous anastomoses; or (3) a decrease in vascular outflow resistance by dilatation of the thick-walled veins. The effect of chemoreceptor stimulation on the venous segment ofdifferent vascular beds is not uniform; there is vascoconstriction in the splenic veins (Pelletier & Shepherd, 1972) but vasodilatation of the large veins of the cutaneous vascular bed (Calvelo et al 1970;Shepherd & Pelletier, 1975). All arteries, veins and arteriovenous anastomoses in the nasal mucosa have a rich autonomic nerve supply in the form of an adventitial plexus of non-myelinated nerve fibres (Cauna, 1970a, b).…”

Section: Discussionmentioning

confidence: 99%

Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog.

Lung¹,

Wang²

1986

The Journal of Physiology

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SUMMARY1. The experiments were performed on anaesthetized dogs which breathed spontaneously or were artificially ventilated and paralysed.2. The spontaneous nasal arterial blood flow was measured on one side of the nose while nasal vascular resistance was determined on the other side simultaneously.3. Nasal arterial blood flow was measured by means of an electromagnetic flow sensor placed around the terminal branch of the internal maxillary artery, the main arterial supply to the nasal mucosa.4. Nasal vascular resistance was measured by constant-flow perfusion of the terminal branch of the internal maxillary artery.5. Nasal airway resistance was assessed by monitoring the transnasal pressure at constant airflow through each side of the nose simultaneously.6. Hypercapnic gas challenge (8 % C02, 30 % 02 in N2) to the lungs increased nasal vascular resistance and decreased nasal airway resistance. Similar gas challenge to the nose did not affect nasal vascular resistance but decreased nasal airway resistance.7. Hypoxic gas challenge (6 % 02 in N2) to the lungs did not affect the nasal vascular resistance but decreased nasal airway resistance only when the nasal vascular bed was under controlled perfusion. Similar gas challenge to the nose did not affect either nasal vascular or airway resistance.8. Arterial chemoreceptor stimulation by intracarotid injection of sodium cyanide increased nasal vascular resistance and decreased nasal airway resistance.9. The nasal vascular response to hypercapnia and arterial chemoreceptor stimulation was reflex in nature, being abolished by nasal sympathectomy.10. The nasal airway response to hypercapnia, hypoxia and arterial chemoreceptor stimulation was reflex in nature, being partially or completely abolished by nasal sympathectomy.11. Hypercapnia probably induced a local vasodilatatory effect on the capacitance vessels whereas hypoxia had no direct action on the vasculature.

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“…20 ' 21 In contrast, a vasodilator response to stimulation of the carotid bodies has been shown in some tissues. 23 Therefore, it is possible that the hypercapnic reflex elicited by the carotid bodies can differentially induce either constriction or dilatation in various vascular beds. The cerebrovascular response to hypercapnia is to dilate.…”

Section: Discussionmentioning

confidence: 99%

Role of the carotid body in speeding the cerebrovascular response to altered PaCO2 in baboons.

McCalden¹,

Rosendorff²

1977

Stroke

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SUMMARYThe alterations in cerebral perfusion with graded hypercapnia were measured in the baboon using the intra-carotid 1M xenon clearance technique. In addition, the tidal percent of COj and the blood flow in the common carotid artery were measured using a capnograph and an electromagnetic flowmeter respectively. The delay times between the induced increments in tidal respiratory percent of CO] and the beginning of the blood flow increments were assessed, together with the rate of increment of the blood flow at each level of hypercapnia. The changes in cerebral perfusion, delay time and rate of blood flow increase with hypercapnia were measured before and after bilateral denervation and destruction of the carotid bifurcation receptors.Hypercapnia normally caused an increased cerebral perfusion which was attenuated when carotid receptor function was destroyed. This change was only significantly different from normal with the highest value of Pco a . Before removal of carotid receptor function the mean delay time was 13.7 ± 1.2 seconds and the rate of increment in carotid flow was 29.7 ± 8.4 ml/min per min. These values were similar at all levels of hypercapnia. After carotid receptor removal the mean delay time was significantly increased at 35.8 ± 9.0 seconds while the rate of flow increment was unchanged at 36.0 ± 5.2 ml/min per min. These results in the baboon suggest that the carotid bifurcation receptors provide a quantitatively small but fast mechanism mediating the cerebrovascular dilator response to hypercapnia. IN 1974, Ponte and Purves1 suggested that the cerebral vasodilator response to a raised arterial Pco 2 is mediated, at least in part, by carotid and aortic chemoreceptors. Since then many workers have investigated the role of a neural reflex in cerebral hypercapnic vasodilatation. Hoff, Mackenzie and Harper 2 showed that, in the baboon, section of the seventh cranial nerve had no effect on the cerebral response to either hypercapnia or hypoxia. Similarly, Linton, Miller and Cameron 3 found in the rabbit that the carotid sinus had no influence on the response to hypercapnia. Other recent studies also failed to demonstrate any role for the carotid chemoreceptors in the control of cerebral blood flow in the dog* or cat. 6 On the other hand, James and MacDonell 6 have shown in the dog that stimulation of the vascularly isolated carotid bifurcation with hypercapnic or hypertensive blood caused alteration in cerebral blood flow. We have recently shown that the carotid body chemoreceptors do play a quantitatively small role in the cerebrovascular dilator response to hypercapnia.7 However, this role became apparent only at high Paco 2 values and was quantitatively smaller than that reported previously by Ponte and Purves.1 Also, we have suggested that the hypercapnic cerebral vasodilatation is mediated by a quantitatively small but fast reflex arising in the peripheral chemoreceptors.7 If this is true, it may explain some of the variation in the literature as different authors may have made their measur...

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Reflex Vascular Responses to Stimulation of Chemoreceptors with Nicotine and Cyanide

Cited by 66 publications

References 19 publications

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

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

Effects of hypercapnia and hypoxia on nasal vasculature and airflow resistance in the anaesthetized dog.

Role of the carotid body in speeding the cerebrovascular response to altered PaCO2 in baboons.

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