Search tips
Search criteria 


Logo of currcardiorevLink to Publisher's site
Curr Cardiol Rev. 2009 November; 5(4): 263–267.
PMCID: PMC2842957

Roles of Arterial Baroreceptor Reflex During Bezold-Jarisch Reflex


Among the many cardiopulmonary reflexes, this review specifically examines the roles of the arterial baroreflex during the Bezold-Jarisch reflex (BJR). Activation of cardiopulmonary vagal afferent C-fibers induces hypotension, bradycardia, and apnea, which are known collectively as the BJR; myocardial ischemia and infarction might induce the BJR. Arterial baroreflex has been established as an important negative feedback system that stabilizes arterial blood pressure against exogenous pressure perturbations. Therefore, understanding the functions of the arterial baroreflex during the BJR is crucial for elucidating its pathophysiological implications. The main central pathways of the BJR and the baroreflex are outlined herein, particularly addressing the common pathway between the reflexes. Furthermore, the pathophysiological roles of the arterial baroreflex during the BJR are described along with a brief discussion of pathophysiological merits and shortcomings of the reflexes.

Keywords: Sympathetic nerve activity, arterial pressure, cardiopulmonary reflex, central pathway, acute myocardial ischemia.


Cardiorespiratory responses showing bradycardia, hypotension, and apnea through cardiopulmonary vagal afferent C fibers are known as the Bezold-Jarisch reflex (BJR). This reflex was observed initially subsequent to intravenous injection of veratrum alkaloids [1, 2]. Activation of the cardiopulmonary vagal afferent fibers during the BJR blunts efferent sympathetic nerve activity (SNA), thereby engendering hypotension and bradycardia [3-5]. The BJR might strongly affect developing pathophysiological respon-ses or circulatory regulation, potentially activating cardiac receptors. The BJR might be observed during acute myo-cardial ischemia or infarction [6-8]. However, the pathophysiological significance of this reflex remains controvertible [9, 10].

Von Bezold and Hirt [1] initially proposed that intravenous injection of veratrum alkaloids induced hypotension and bradycardia in conjunction with apnea. Jarisch and Richter [2] reported that the powerful depressor action induced by intravenous veratridine was attributable to the cardiac branches of vagus nerves in cats. Subsequently, it has been established that this reflex originates mainly in the cardiopulmonary receptors on the unmyelinated and type C vagal afferent fibers [11-16]. Actually, the response of the BJR is abolished dramatically by bilateral vagotomy [1, 4, 17]. The vagus in the cardiopulmonary regions contains the population of chemo- and mechano-sensitive afferent C fibers, and arises from receptors located in the atria, ventricles, aorta, and lungs [18, 19]. Although the chemosensitive 5-HT3 receptors are generally known as the origin of the BJR, the mechanosensitive receptors might be also related to this reflex. Reportedly, the physiological responses to the stimulations of chemical and mechanical receptors in unmyelinated afferent C fibers are similar, respectively causing hypotension and bradycardia [20, 21]. The bradycardia and hypotension based on sympathetic vasomotor inhibition, and apnea mediated by vagal afferent C fibers from the cardiopulmonary area are today known by an extensive definition as the BJR [19, 22].

Arterial baroreflex, on the other hand, is a crucial negative feedback system that quickly stabilizes arterial blood pressure (AP) against exogenous pressure perturbations [23, 24]. For instance, moving to a standing position causes rapid hypotension in the upper body and brain because of gravity, including the risk of losing consciousness. Arterial baroreflex originates in stretch receptors (baroreceptors) distributed in the walls of carotid sinuses and aortic arches, which are the origin of afferent fibers in the glossopharyngeal and vagal nerves. Increased AP induces expansion or contraction in the baroreceptors and facilitates the arterial baroreceptors’ afferent discharge to transmit signals to the central nervous system. The baroreceptor signals inhibit the vasoconstrictor center of the medulla and excite the vagal center, ultimately causing vasodilation through the peripheral circulatory system and blunted cardiac contractility.

In contrast, decreased AP induces contraction in the baroreceptors and inhibits arterial baroreceptors’ afferent discharge. The feedback signals minimize AP disturbances within the normal level maintaining the systemic circulation, through the autonomic nervous system [23, 25]. Consequently, excitation of the afferent fiber originating from the baroreceptors by pressure change attenuates the heart rate (HR), cardiac output, and peripheral resistance, resulting in decreased AP. Especially in cardiovascular diseases, it is crucial to assess the ability of the arterial baroreflex to regulate AP against external pressure disturbances by pharmacological agents or positional changes.

Excellent interpretations of various cardiopulmonary reflexes exist [e.g. 22, 24, 26-28]. This paper therefore specifically examines 1) the interactive roles of arterial baroreflex during the BJR, including 2) the common central pathways between the reflexes and 3) the pathophysiological roles of the BJR in acute myocardial ischemia.


In animal studies, the BJR has been chemically activated by pharmacological agents such as veratridine, nicotine, capsaicin, and a selective serotonergic 5-HT3 receptor agonist, phenyl biguanide (PBG) [29, 30]. As described herein, effects of the BJR induced by PBG were concentrated.

Changes in SNA of kidney and AP during PBG infusion are mainly mediated by the activation of vagal afferent C fibers [4, 31]. Veelken et al. [32] reported that continuous PBG infusion attenuated SNA, AP, and HR during the first minute in conscious and anesthetized rats. Sympathoinhibition was maintained for 15 min, although AP and HR reverted to baseline values. In contrast, AP and HR with SNA decreased during 20-min PBG administration (i.v.) [4, 5], indicating the disappearance of the counteraction by the arterial baroreflex under the carotid-sinus open-loop condition.

Static Property

Experimental studies have investigated the interaction between the BJR and the baroreflex. Veelken et al. [33] evaluated the baroreflex ability during the BJR by PBG infusion under the closed-loop AP response. The maximum gain of HR in the arterial baroreflex was impaired; the arterial baroreceptor control of SNA was not impaired during continuous PBG infusion, suggesting the remaining ability of the baroreflex. In contrast, the BJR attenuated the steady-state responses of SNA, AP, and HR to baroreceptor pressure input in anesthetized rabbits under the carotid-sinus open-loop condition [3, 5]. Chen [3] demonstrated that veratridine (i.v.) depressed the stepwise responses of HR to the carotid sinus pressure (CSP); the bradycardia was more prominent at lower CSP levels. In contrast, the response range of HR to CSP inputs might not be changed considerably, despite marked bradycardia [5].

Intravenous PBG [5] as well as veratridine [3] blunted stepwise responses between the CSP and AP, attenuating the response range of AP. This result was attributable mainly to the decreased gain of static responses in the sympathetic outflow reflecting the action of the central region compared to those of the peripheral region. The peripheral gain might be much lower in acute myocardial ischemia or infarction because of pump failure, indicating a further decrease in AP and the reduced static gain.

Dynamic Property

The BJR by intravenous PBG reduced the dynamic transfer gain to characterize the stability and quickness of AP regulation in the arterial baroreflex under a carotid-sinus open-loop condition in anesthetized rabbits [4, 34]. The result was due mainly to attenuating the dynamic gain in the central region [4]. Excess activation of the BJR during acute myocardial ischemia or infarction might exert inverse effects on AP regulation through attenuation of baroreflex dynamic gain as well as sympathetic suppression. Although PBG decreased the dynamic gain of the central region, the derivative characteristics were, interestingly, preserved around the operating point showing the normal AP. The dynamic gains at nonlinear CSP points such as hypertension and hypotension were attenuated during the BJR compared with that of the operating point [34].


Because of recent studies using pharmacological agents to the related receptors, the central pathways during the BJR and the arterial baroreflex have been well identified. Overall, the results seem to show a similar pathway in the two reflexes.

Main Central Pathways


The sympathetic outflow in the baroreflex mainly passes through the brainstem such as the nucleus tractus solitarius (NTS), the caudal ventrolateral medulla (CVLM), and the rostral ventrolateral medulla (RVLM) [27, 35]. First, baroreceptor afferent fibers terminate within the NTS as the crucial site of the baroreflex [36]. The NTS projects directly to the CVLM through excitatory glutamatergic chemosensitive neurons [37, 38]. Through GABAergic neurons, the CVLM inhibits sympatho-excitatory neurons in the RVLM [39, 40]. Finally, the RVLM regulates the sympathetic vasomotor tone and the barosensitive neurons projecting to the spinal cord [27, 35]. Other important pathways such as medullary raphe nuclei and the lateral tegmental field are also related to this reflex [41].


Vagal afferent C fibers originating in the heart and lungs first terminate in the NTS [42]. Merahi et al. [43] demonstrated that most 5-HT3 receptors in the NTS are found on the vagal sensory afferent fibers using autoradiographic studies. Pires et al. [44] demonstrated that intracisternal or the NTS injection of the 5-HT3 receptor antagonist granisetron significantly attenuated the hypotension and bradycardia evoked by intravenous PBG, suggesting that the NTS is involved in the central pathway of the BJR.

Intravenous PBG infusion to stimulate cardiac receptors facilitates firing of CVLM neurons, resulting in the SNA inhibition [45]. Schreihofer et al. [46] showed that an intravenous PBG infusion dramatically activated the GABAergic baro-activated CVLM neuron and caused the inhibited SNA. Verberne et al. [47] demonstrated that barosensitive neurons in the RVLM were inhibited by intravenous PBG in rats. It is conceivable that PBG attenuates the dynamic gain of the neural arc transfer function by affecting baroreflex signal transduction in such brainstem areas as the NTS, the CVLM, and the RVLM through activation of the vagal afferent C fibers.

Verberne et al. [48] also showed the effects of the intravenous PBG on the neurons in rostrocaudal levels of the ventrolateral medulla (type I-VI). Cardiopulmonary receptor activation by PBG extremely suppressed the firing of barosensitive and bulbospinal neurons in the RVLM (type I), and produced excitation of the neuron in the CVLM site (type VI). These reports show direct evidence that the common sites are used for the baroreflex and the BJR. However, there might be specific differences among animals, as demonstrated in the baroreflex response in cats [41].

Common Pathway

As described above, the BJR and baroreflex signals appear to use common central pathways in brainstem regions such as the NTS, the CVLM, and the RVLM [47-49]. The glutamate receptor antagonist kynurenate into the NTS prevents the sympathoinhibition and hypotension by intravenous PBG infusion [47, 49, 50]. These results indicate that vagal afferent C fibers during the BJR use an excitatory amino acid neurotransmitter in the NTS, as shown in afferent baroreceptor fibers.

In the CVLM, the excitatory amino acid antagonist attenuates the BJR by PBG infusion [47, 51]. Bicuculine, GABA receptor antagonist, into the RVLM attenuated the response of the BJR. However, kynurenic acid did not modulate it. In addition, the BJR induced by serotonin or PBG causes a sympathoinhibition with a decrease in the firing rate of barosensitive neurons in the RVLM [47, 52]. Consequently, the central pathway of the BJR clearly correlates with the NTS, the CVLM, and the RVLM with the excitatory and inhibitory amino acid neurotransmitters in the baroreflex.


BJR Induced by Myocardial Ischemia

Actually, the BJR might strongly influence circulatory regulation during acute myocardial ischemia or infarction, when cardiac chemoreceptors are potentially activated [6, 7]. Elucidating the effects of the BJR on circulatory regulation is expected to contribute to the pathophysiological understanding in ischemic heart diseases [9, 10].

The origin of the BJR by intravenous PBG might differ from that induced by myocardial ischemia. In cardiac diseases, serotonin levels might be increased in the coronary circulation [53]. On the other hand, an increase in the myocardial acetylcholine level induced by intravenous PBG is similar to that observed in the non-ischemic myocardium during coronary artery occlusion in anesthetized cats [54, 55]. These reports imply other reasons for the induction of the BJR in myocardial ischemia. Some reports describe oxygen-derived free radicals and prostaglandins generated during ischemia and reperfusion [56, 57]. Mechanoreceptors as well as chemoreceptors might also be activated during myocardial ischemia [6].

Roles of BJR in Myocardial Ischemia

Apparently, the BJR entails both the pathophysiological merits and shortcomings. Arrhythmias by bradycardia and hypotension, which show similar responses to that of BJR, are observed more remarkably in patients with inferior and posterior walls of the heart under myocardial ischemia and infarction [6, 9, 58]. Anatomically, the population of the cardioinhibitory C fiber afferent receptors in the myocardium correlates with the site of the inferoposterior walls of the left ventricle [59].

The induction of the BJR might prevent overexertion of the cardiac muscle by bradycardia and hypotension [10]. The reduction of energy consumption might be beneficial for hampering ischemic insult and salvaging tissues in the ischemic border zone, indicating a heart-protective effect [9, 60, 61].

The BJR attenuates the ability of AP regulation by the arterial baroreflex. Excess activation of the BJR might cause severe bradycardia and hypotension, placing the patient's life at risk because the magnitude of sympathetic inhibition and vagal activation during the BJR is not regulated in terms of AP regulation. Therefore, for patients with acute cardiac ischemia or infarction, clinicians should consider drug treatments causing a pressure change or change of a position with caution because of the blunted ability of the baroreflex during the BJR. Furthermore, the BJR might cause sudden cardiac death during ischemic injury [6] because severe hypotension eliminates the buffering function in the baroreflex regulation.


This report reviewed the baroreflex capability during the BJR that might be induced in myocardial ischemia or infarction. Through a vagal afferent pathway from the cardiac receptors, the BJR inhibited SNA, AP, and HR; the ability of the baroreflex was blunted especially in the central region such as the brainstem. Both the BJR and the baroreflex share similar central pathways-the NTS, the CVLM, and the RVLM-causing the reduction of dynamic and static gains.

In acute myocardial ischemia or infarction, preventing severe hypotension during the BJR is necessary for stabilization of AP by the baroreflex system because, apparently, the natural property of life-the heart protection to prevent the local death of myocardium-is dominantly selected under such risky conditions, irrespective of blunting of the baroreflex ability and the possibility of sudden cardiac death. Further investigations related to central and peripheral regions are necessary to establish the pathophysiological mechanisms of the baroreflex and the BJR.


1. Bezold A, Hirt L. Uber die physiologischen Wirkungen des essingsauren Veratrins. Unters Physiol Lab Wurtzburg. 1867;1:75–6.
2. Jarisch A, Richter H. Die afferenten Bahnen des Veratrineeffekts in den Herznerven. Arch Exp Pathol Pharmakol. 1939;193:355–71.
3. Chen HI. Interaction between the baroreceptor and Bezold-Jarisch reflexes. Am J Physiol Heart Circ Physiol. 1979;237:H655–61. [PubMed]
4. Kashihara K, Kawada T, Yanagiya Y, et al. Bezold-Jarisch reflex attenuates dynamic gain of baroreflex neural arc. Am J Physiol Heart Circ Physiol. 2003;285:H833–40. [PubMed]
5. Kashihara K, Kawada T, Li M, Sugimachi M, Sunagawa K. Bezold-Jarisch reflex blunts arterial baroreflex via the shift of neural arc toward lower sympathetic nerve activity. Jpn J Physiol. 2004;54:395–404. [PubMed]
6. Robertson D, Hollister AS, Forman MB, Robertson RM. Reflexes unique to myocardial ischemia and infarction. J Am Coll Cardiol. 1985;5:99B–104B. [PubMed]
7. Meyrelles SS, Mill JG, Cabral AM, Vasquez EC. Cardiac baroreflex properties in myocardial infarcted rats. J Auton Nerv Syst. 1996;60:163–8. [PubMed]
8. Meyrelles SS, Bernardes CF, Modolo RP, Mill JG, Vasquez EC. Bezold-Jarisch reflex in myocardial infarcted rats. J Auton Nerv Syst. 1997;63:144–52. [PubMed]
9. Mark AL. The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am Coll Cardiol. 1983;1:90–102. [PubMed]
10. Schultz HD. Cardiac vagal chemosensory afferents. Function in pathophysiological states. Ann N Y Acad Sci. 2001;940:59–73. [PubMed]
11. Frink RJ, James TN. Intracardiac route of the Bezold-Jarisch reflex. Am J Physiol. 1971;221:1464–9. [PubMed]
12. Lee TM, Kuo JS, Chai CY. Central integrating mechanism of the Bezold-Jarisch and baroceptor reflexes. Am J Physiol. 1972;222:713–20. [PubMed]
13. Thorén PN, Mancia G, Shepherd JT. Vasomotor inhibition in rabbits by vagal nonmedullated fibers from cardiopulmonary area. Am J Physiol. 1975;229:1410–3. [PubMed]
14. Oberg B, Thorén P. Circulatory responses to stimulation of medullated and non-medullated afferents in the cardiac nerve in the cat. Acta Physiol Scand. 1973;87:121–32. [PubMed]
15. Donald DE, Shepherd JT. Reflexes from the heart and lungs: physiological curiosities or important regulatory mechanisms. Cardiovasc Res. 1978;12:446–69. [PubMed]
16. Zucker IH, Cornish KG. The Bezold-Jarisch in the conscious dog. Circ Res. 1981;49:940–8. [PubMed]
17. Higuchi S, Morgan DA, Mark AL. Contrasting reflex effects of chemosensitive and mechanosensitive vagal afferents. Hypertension. 1988;11:674–9. [PubMed]
18. Coleridge HM, Coleridge JC. Cardiovascular afferents involved in regulation of peripheral vessels. Annu Rev Physiol. 1980;42:413–27. [PubMed]
19. Verberne AJ, Saita M, Sartor DM. Chemical stimulation of vagal afferent neurons and sympathetic vasomotor tone. Brain Res Brain Res Rev. 2003;41:288–305. [PubMed]
20. Fox IJ, Gerasch DA, Leonard JJ. Left ventricular mechano-receptors: a haemodynamic study. J Physiol. 1977;273:405–25. [PubMed]
21. Gillis RA, Quest JA. Neural actions of digitalis. Annu Rev Med. 1978;29:73–9. [PubMed]
22. Campagna JA, Carter C. Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology. 2003;98:1250–60. [PubMed]
23. Guyton AC, Coleman TG, Granger HJ. Circulation: overall regulation. Annu Rev Physiol. 1972;34:13–46. [PubMed]
24. Sagawa K. Handbook of Physiology. The Cardiovascular System. Peripheral Circulation and Organ Blood Flow. pt 2. Vol. 3. Bethesda, MD: American Phyisiology Society, sect. 2; 1983. Baroreflex control of systemic arterial pressure and vascular bed; pp. 453–96. chapt. 14.
25. Lanfranchi PA, Somers VK. Arterial baroreflex function and cardiovascular variability: interactions and implications. Am J Physiol Regul Integr Comp Physiol. 2002;283:R815–26. [PubMed]
26. Hainsworth R. Reflexes from the heart. Physiol Rev. 1991;71:617–58. [PubMed]
27. Dampney RA. Functional organization of central pathways regulating the cardiovascular system. Physiol Rev. 1994;74:323–64. [PubMed]
28. Aviado DM, Guevara Aviado D. The Bezold-Jarisch reflex. A historical perspective of cardiopulmonary reflexes. Ann N Y Acad Sci. 2001;940:48–58. [PubMed]
29. Hardcastle J, Hardcastle PT. 5-Hydroxytryptamine-induced secretion by rat jejunum in-vitro involves several 5-hydroxytryptamine receptor subtypes. J Pharm Pharmacol. 1998;50:539–47. [PubMed]
30. Whalen EJ, Johnson AK, Lewis SJ. Functional evidence for the rapid desensitization of 5-HT(3) receptors on vagal afferents mediating the Bezold-Jarisch reflex. Brain Res. 2000;873:302–5. [PubMed]
31. Veelken R, Leonard M, Stetter A, et al. Pulmonary serotonin 5-HT3-sensitive afferent fibers modulate renal sympathetic nerve activity in rats. Am J Physiol Heart Circ Physiol. 1997;272:H979–86. [PubMed]
32. Veelken R, Hilgers KF, Leonard M, et al. A highly selective cardiorenal serotonergic 5-HT3-mediated reflex in rats. Am J Physiol Heart Circ Physiol. 1993;264:H1871–7. [PubMed]
33. Veelken R, Hilgers KF, Ditting T, Fierlbeck W, Geiger H, Schmieder RE. Subthreshold stimulation of a serotonin 5-HT3 reflex attenuates cardiovascular reflexes. Am J Physiol. 1996;271:R1500–6. [PubMed]
34. Kashihara K. Dynamic baroreflex properties at various carotid sinus pressures during vagal afferent activation. Proceedings of the 2008 IEEE International Conference on Systems, Man, and Cybernetics (in press).
35. Pilowsky PM, Goodchild AK. Baroreceptor reflex pathways and neurotransmitters: 10 years on. J Hypertens. 2002;20:1675–88. [PubMed]
36. Gebber GL, Barman SM, Zviman M. Sympathetic activity remains synchronized in presence of a glutamate antagonist. Am J Physiol. 1989;256:R722–32. [PubMed]
37. Guyenet PG, Filtz TM, Donaldson SR. Role of excitatory amino acids in rat vagal and sympathetic baroreflexes. Brain Res. 1987;407:272–84. [PubMed]
38. Koshiya N, Guyenet PG. NTS neurons with carotid chemoreceptor inputs arborize in the rostral ventrolateral medulla. Am J Physiol Regul Integr Comp Physiol. 1996;39:R1273–8. [PubMed]
39. Sun MK, Guyenet PG. GABA-mediated baroreceptor inhibition of reticulospinal neurons. Am J Physiol. 1985;249:R672–80. [PubMed]
40. Blessing WW. Depressor neurons in rabbit caudal medulla act via GABA receptors in rostral medulla. Am J Physiol. 1988;254:H686–92. [PubMed]
41. Barman SM, Phillips SW, Gebber GL. Medullary lateral tegmental field mediates the cardiovascular but not respiratory component of the Bezold-Jarisch reflex in the cat. Am J Physiol Regul Integr Comp Physiol. 2005;289:R1693–702. [PubMed]
42. Kalia M, Mesulam MM. Brain stem projections of sensory and motor components of the vagus complex in the cat: I. The cervical vagus and nodose ganglion. J Comp Neurol. 1980;193:435–65. [PubMed]
43. Merahi N, Orer HS, Laporte AM, Gozlan H, Hamon M, Laguzzi R. Baroreceptor reflex inhibition induced by the stimulation of serotonin3 receptors in the nucleus tractus solitarius of the rat. Neuroscience. 1992;46:91–100. [PubMed]
44. Pires JG, Silva SR, Ramage AG, Futuro-Neto HA. Evidence that 5-HT3 receptors in the nucleus tractus solitarius and other brainstem areas modulate the vagal bradycardia evoked by activation of the von Bezold-Jarisch reflex in the anesthetized rat. Brain Res. 1998;791:229–34. [PubMed]
45. Schreihofer AM, Guyenet PG. The baroreflex and beyond: control of sympathetic vasomotor tone by GABAergic neurons in the ventrolateral medulla. Clin Exp Pharmacol Physiol. 2002;29:514–21. [PubMed]
46. Schreihofer AM, Guyenet PG. Baro-activated neurons with pulse-modulated activity in the rat caudal ventrolateral medulla express GAD67 mRNA. J Neurophysiol. 2003;89:1265–77. [PubMed]
47. Verberne AJ, Guyenet PG. Medullary pathway of the Bezold-Jarisch reflex in the rat. Am J Physiol Regul Integr Comp Physiol. 1992;263:R1195–202. [PubMed]
48. Verberne AJ, Stornetta RL, Guyenet PG. Properties of C1 and other ventrolateral medullary neurones with hypothalamic projections in the rat. J Physiol. 1999;517:477–94. [PubMed]
49. Vayssettes-Courchay C, Bouysset F, Laubie M, Verbeuren TJ. Central integration of the Bezold-Jarish reflex in the cat. Brain Res. 1997;744:272–8. [PubMed]
50. Vardhan A, Kachroo A, Sapru HN. Excitatory amino acid receptors in the nucleus tractus solitarius mediate the responses to the stimulation of cardiopulmonary vagal afferent C fiber endings. Brain Res. 1993;618:23–31. [PubMed]
51. Verberne AJ, Beart PM, Louis WJ. Excitatory amino acid receptors in the caudal ventrolateral medulla mediate a vagal cardiopulmonary reflex in the rat. Exp Brain Res. 1989;78:185–92. [PubMed]
52. Saita M, Verberne AJ. Roles for CCK1 and 5-HT3 receptors in the effects of CCK on presympathetic vasomotor neuronal discharge in the rat. Br J Pharmacol. 2003;139:415–23. [PMC free article] [PubMed]
53. Vikenes K, Farstad M, Nordrehaug JE. Serotonin is associated with coronary artery disease and cardiac events. Circulation. 1999;100:483–9. [PubMed]
54. Kawada T, Yamazaki T, Akiyama T, et al. Differential acetylcholine release mechanisms in the ischemic and non-ischemic myocardium. J Mol Cell Cardiol. 2000;32:405–14. [PubMed]
55. Kawada T, Yamazaki T, Akiyama T, et al. In vivo assessment of acetylcholine-releasing function at cardiac vagal nerve terminals. Am J Physiol Heart Circ Physiol. 2001;281:H139–45. [PubMed]
56. Ustinova EE, Schultz HD. Activation of cardiac vagal afferents by oxygen-derived free radicals in rats. Circ Res. 1994;74:895–903. [PubMed]
57. Schultz HD, Ustinova EE. Cardiac vagal afferent stimulation by free radicals during ischaemia and reperfusion. Clin Exp Pharmacol Physiol. 1996;23:700–8. [PubMed]
58. Webb SW, Adgey AA, Pantridge JF. Autonomic disturbance at onset of acute myocardial infarction. Br Med J. 1972;3:89–92. [PMC free article] [PubMed]
59. Thames MD, Klopfenstein HS, Abboud FM, Mark AL, Walker JL. Preferential distribution of inhibitory cardiac receptors with vagal afferents to the inferoposterior wall of the left ventricle activated during coronary occlusion in the dog. Circ Res. 1978;43:512–9. [PubMed]
60. Robertson RM, Robertson D. The Bezold-Jarisch reflex: possible role in limiting myocardial ischemia. Clin Cardiol. 1981;4:75–9. [PubMed]
61. Longhurst JC. Cardiac receptors: their function in health and disease. Prog Cardiovasc Dis. 1984;27:201–22. [PubMed]

Articles from Current Cardiology Reviews are provided here courtesy of Bentham Science Publishers