Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Staszewska-Barczak, Janina; Dusting, Gregory J.

doi:10.1111/j.1440-1681.1977.tb02408.x

Cited by 33 publications

(15 citation statements)

References 23 publications

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“…Likewise, other inflammatory mediators like endothelin (4,5) , sympathetic amines (6,7) , substance P (8)(9)(10) , NGF (11,12) as well as bradykinin (13) also possess the same nociceptor sensitizing property. These mediators act directly on neuronal receptors, triggering molecular mechanisms that ultimately facilitate the electrical activity of the neuronal membrane.…”

Section: Painmentioning

confidence: 99%

Cytokine inhibitors and pain control

Verri¹,

Cunha²,

Poole³

et al. 2007

Rev. Bras. Reumatol.

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Recebido em 17/03/07. Aprovado, após revisão, em 25/09/07. Conflits of interest: nothing to disclose. RESUMOOs autores fazem uma revisão sobre evidências que demonstram o papel de citocinas em modelos experimentais de dor, discutindo possíveis terapias com alvo em citocinas para controle da dor.Palavras-chave: hiperalgesia, dor inflamatória, citocinas, nocicepção, analgesia. ABSTRACTThe authors describe the evidences supporting the role of cytokines in experimental pain, discussing possible approaches for pain control using cytokine-targeting therapies.

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Section: Painmentioning

confidence: 99%

Cytokine inhibitors and pain control

Verri¹,

Cunha²,

Poole³

et al. 2007

Rev. Bras. Reumatol.

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“…The responses to higher doses of kallikrein (0t1-1P0 U) and to the maximal dose of each of the two kinins (1 gg) were significantly reduced by treatment of the heart surface with the antagonist peptide (Fig. 4) (Uchida & Murao, 1974;Baker et al 1980) and such stimulation elicits a reflex activation of the cardiovascular system (Staszewska-Barezak et al 1976;Staszewska-Barczak & Dusting, 1977;Weaver et al 1983). The present study has shown that tissue kallikrein, like bradykinin, is capable of inducing reflex increases in blood pressure and heart rate when applied to the ventricular surface of the dog heart.…”

Section: Effects Of Epicardial Treatment By Aprotininmentioning

confidence: 99%

Participation of the kallikrein‐kinin‐receptor system in reflexes arising from neural afferents in the dog epicardium.

Staszewska-Woolley

Woolley

1989

The Journal of Physiology

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SUMMARY1. Reflexogenic effects of bradykinin, lysyl-bradykinin and endogenously formed kinins on neural afferents of the left ventricular epicardium were studied in anaesthetized, open-chest dogs.2. Epicardial application of either bradykinin (001-10 tg), lysyl-bradykinin (001-1O jug) or tissue kallikrein (0003-1 U) consistently resulted in dose-related increases in blood pressure and heart rate. The pressor and heart rate responses to epicardial kallikrein were slower in onset and longer lasting than those evoked by bradykinin or lysyl-bradykinin. The effects of kallikrein, but not those of exogenous kinins, were subject to tachyphylaxis. The application of higher doses of kallikrein (0 1 or 1 U) also resulted in long-lasting desensitization of the epicardium to the effects of bradykinin.3. Treatment of the epicardium with a proteinase inhibitor, aprotinin, prevented the reflexogenic effects of kallikrein but not those of bradykinin or lysyl-bradykinin. Treatment with aprotinin also counteracted post-kallikrein desensitization of sensory receptors of the ventricular epicardium to the reflexogenic effect of bradykinin.4. Superfusion of the epicardium with a selective B2 receptor antagonist, D-Arg[Hyp3,Thi5 8,D-Phe7]-bradykinin, was equally effective in antagonizing the reflexogenic effects of kallikrein, bradykinin and lysyl-bradykinin.5. We conclude that the response to epicardial application of kallikrein indicates an ample presence of endogenous substrate for local formation of bradykinin and/or related kinins. These then initiate reflex activation of the cardiovascular system by interacting with specific B2 receptors associated with sympathetic afferent neurones in the dog epicardium. We suggest that the kallikrein-kinin-receptor system has a role in the reflex functioA of the cardiac sympathetic afferents in both physiological and pathological conditions.

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“…Cardiac receptors with both A and C afferent fibres are excited by local application of bradykinin to the surface of the left ventricle (1, 9,20), and this leads to sympathetically-mediated reflex increases in arterial pressure and heart rate (17,19). Pericardial receptors connected to sympathetic afferent fibres are also excited by bradykinin (1), as well as by mechanical stimulation (11,21), but their reflex actions are not known.…”

Section: Introductionmentioning

confidence: 98%

Reflex effects evoked from the parietal pericardium in the dog: Comparison with responses from the visceral pericardium

1983

Self Cite

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Experiments were performed on anaesthetized, open-chest dogs to determine the reflex effects on systemic blood pressure and heart rate produced by stimulation of the parietal pericardium with bradykinin and nicotine, and to compare these effects with those evoked by application of these substances to the visceral pericardium (epicardium) of the left ventricle. Bradykinin (0.01-6.0 micrograms) elicited reflex increases in blood pressure and heart rate when applied either to the parietal pericardium or to the ventricular epicardium; the responses evoked from both sites were dose-dependent from the threshold of 0.01 micrograms to a maximum at 1.0 micrograms of bradykinin. The reflex effects of bradykinin were not affected by either vagotomy or phrenic nerve section, but were suppressed by bilateral sectioning of the upper thoracic (T1-T4) white rami communicantes and stellectomy. In contrast to bradykinin, nicotine (20-100 micrograms) failed to produce any change in blood pressure and heart rate when applied to the parietal pericardium and evoked depressor responses when applied to the epicardium of the left ventricle; these depressor effects of nicotine were abolished by vagotomy. The results indicate that sympathetic, but not vagal, afferent endings innervating the parietal pericardium are susceptible to chemical stimulation. Bradykinin is a powerful algesic agent and is formed and released locally during inflammation. We suggest, therefore, that the pericardial sympathetic pressor reflex is nociceptive in nature and can be activated when kinin formation occurs during pericardial inflammation.

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Sympathetic Cardiovascular Reflex Initiated by Bradykinin‐induced Stimulation of Cardiac Pain Receptors in the Dog

Cited by 33 publications

References 23 publications

Cytokine inhibitors and pain control

Cytokine inhibitors and pain control

Participation of the kallikrein‐kinin‐receptor system in reflexes arising from neural afferents in the dog epicardium.

Reflex effects evoked from the parietal pericardium in the dog: Comparison with responses from the visceral pericardium

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