Activation of afferent cardiac sympathetic nerve fibers of the cat by pain producing substances and by noxious heat

Nishi, Katsuhide; Sakanashi, Matao; Takenaka, Fumio

doi:10.1007/bf00582206

Cited by 75 publications

(34 citation statements)

References 18 publications

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“…Thus, Uchida & Murao (1974a) reported that the ventricular nerve endings excited by bradykinin fired in time with the cardiac cycle, and they postulated that bradykinin sensitized these mechanosensitive endings to their normal stimulus, which was provided by the rhythmical mechanical changes in the ventricular wall. Nishi, Sakanashi & Takenaka (1977) confirmed that bradykinin increased the firing of mechanosensitive endings in the ventricle; they also showed that the endings were supplied by myelinated fibres. These latter investigators, however, used very high concentrations of bradykinin, which appeared to evoke only modest responses.…”

Section: Introductionmentioning

confidence: 60%

Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat.

Baker¹,

Coleridge²,

Coleridge³

et al. 1980

The Journal of Physiology

220

107

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SUMMARY1. We have examined the effect of bradykinin on impulse traffic in sympathetic afferent fibres from the heart, great vessels and pleura, and have attempted to identify cardiac nociceptors that on the basis of their functional characteristics might have a role in the initiation of cardiac pain.2. In anaesthetized cats, we recorded afferent impulses from 'single-fibre' slips of the left 2nd-5th thoracic rami communicantes and associated chain, and selected fibres arising from endings in the heart, great vessels, pericardium and pleura. We applied bradykinin solution (0 1-1.0 jug/ml.) locally to the site of the ending; we also injected bradykinin (0 3-1 0 ,ug/kg) into the left atrium.3. Afferent endings excited by bradykinin (158 of 191 tested) were of two types. The larger group (140) were primarily mechanoreceptors with Ad or C fibres (mean conduction velocity, 7-5 + 0-6 m/sec). They were very sensitive to light touch. Those located in the heart, great vessels or overlying pleura had a cardiac rhythm of discharge and were stimulated by an increase in blood pressure or cardiac volume.4. Bradykinin increased mechanoreceptor firing from 0 7 + 0.1 to 5 0 + 0 3 (mean + S.E. of mean) impulses/sec. Some endings appeared to be stimulated directly by bradykinin, others sensitized by it so that they responded more vigorously to the pulsatile mechanical stimulation associated with the cardiac cycle.5. The smaller group of eighteen endings, of which ten were in the left ventricle, were primarily chemosensitive. Most had C fibres, a few had A6 fibres (mean conduction velocity, 2-3 + 0-7 m/sec). They were insensitive to light touch. With one exception they never fired with a cardiac rhythm, and even large increases in aortic or left ventricular pressure had little effect on impulse frequency. 6. Chemosensitive endings were stimulated by bradykinin, impulse activity increasing from 0.6 + 0-2 to 15-6 + 1-3 impulses/sec and remaining above the control level for 1-3 min. The evoked discharge, which was either continuous or occurred in irregular bursts, was not secondary to mechanical changes in the heart and great vessels.

show abstract

Section: Introductionmentioning

confidence: 60%

Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat.

Baker¹,

Coleridge²,

Coleridge³

et al. 1980

The Journal of Physiology

220

107

View full text Add to dashboard Cite

show abstract

“…Previous electrophysiological studies conducted in visceral tissues, including testis (Koda et al, 1996), heart (Nishi et al, 1977), and airways (Matsumoto et al, 1992(Matsumoto et al, , 1993Riccio et al, 1996), have shown that histamine can excite polymodal nociceptors having both A␦ unit and C-unit CVs, probably through activation of the H1 receptor. The results of our studies, however, suggest that histamine excites mainly Cunit meningeal nociceptors.…”

Section: Discussionmentioning

confidence: 98%

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Zhang¹,

Strassman²,

Burstein³

et al. 2007

J Pharmacol Exp Ther

150

125

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Intracranial headaches such as migraine are thought to result from activation of sensory trigeminal pain neurons that supply intracranial blood vessels and the meninges, also known as meningeal nociceptors. Although the mechanism underlying the triggering of such activation is not completely understood, our previous work indicates that the local activation of the inflammatory dural mast cells can provoke a persistent sensitization of meningeal nociceptors. Given the potential importance of mast cells to the pain of migraine it is important to understand which mast cell-derived mediators interact with meningeal nociceptors to promote their activation and sensitization. In the present study, we have used in vivo electrophysiological single-unit recording of meningeal nociceptors in the trigeminal ganglion of anesthetized rats to examine the effect of a number of mast cell mediators on the activity level and mechanosensitivity of meningeal nociceptors. We have found that that serotonin (5-HT), prostaglandin I 2 (PGI 2 ), and to a lesser extent histamine can promote a robust sensitization and activation of meningeal nociceptors, whereas the inflammatory eicosanoids PGD 2 and leukotriene C 4 are largely ineffective. We propose that dural mast cells could promote headache by releasing 5-HT, PGI 2 , and histamine.

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“…Myocardial ischemia and hypoxia are associated with pain (SUTTON and LUETH, 1930;BURCH and DEPASQUALE, 1962;GUZMAN et al, 1962) and are accompanied by accumulation of lactic acid (UCHIDA and MURAO, 1975), bradykinin and prostaglandins (KIMURA et al, 1973;UCHIDA and MURAO, 1974d;STASZEWSKA-BARCZAK et al, 1976;NISHI et al, 1977;BAKER et al, 1980;LOMBARDI et al'., 1981;KOLEY et al, 1985). Earlier it had been suggested by LINDGREN and OLIVECRONA (1947) as well as WHITE and BLARD (1948) that sympathetic afferents participate in transmitting impulses leading to cardiac pain in man.…”

Section: Discussionmentioning

confidence: 99%

Cardiac nociceptors and ischemia: Role of sympathetic afferents in cat.

Pal

Koley²,

Bhattacharyya³

et al. 1989

Jpn.J.Physiol

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In total, 86 units were recorded from T2 and T3 left thoracic rami of cat. These receptors were located on the circumflex coronary artery, anterior descending coronary artery, and its adjacent myocardial ragions. The conduction velocity of these fibres was in the range of "C" (0.5 to 1.8 m/s) and "A b" (5.96 to 17 m/s) fibres. Out of these 86 units, only 28 units were activated by coronary occlusion. The average resting frequency of the spontaneous unit was 0.8 + 0.06 impulses/s which increased to 35±4.8 impulses/s on mechanical probing. In order to examine whether the units sensitive to coronary occlusion were also responsive to algesic agents, some of these units were studied applying lactic acid, bradykinin, prostaglandins, and nicotine. It was observed that these Ischemia-sensitive units are also sensitive to lactic acid (10 units), bradykinin (16 units), prostaglandins (12 units), and nicotine (15 units). These Ischemia-sensitive units are presumably nociceptors and activated by algestic agents that cause cardiac ischemic pain.

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Activation of afferent cardiac sympathetic nerve fibers of the cat by pain producing substances and by noxious heat

Cited by 75 publications

References 18 publications

Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat.

Search for a cardiac nociceptor: stimulation by bradykinin of sympathetic afferent nerve endings in the heart of the cat.

Sensitization and Activation of Intracranial Meningeal Nociceptors by Mast Cell Mediators

Cardiac nociceptors and ischemia: Role of sympathetic afferents in cat.

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