Cardiac Mechanoreceptors

Bishop, Vernon S.; Malliani, Alberto; Thorén, Peter

doi:10.1002/cphy.cp020315

Cited by 64 publications

(35 citation statements)

References 368 publications

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“…Also in the human LAD exposure to capsaicin and potassium were associated with an increased outflow of CGRP-LI in a Ca2+-dependent manner, suggesting activation of cardiac sensory nerves. In agreement with this, capsaicin has been shown by electrophysiological techniques to activate sensory C-fibre endings in the heart ventricle (Coleridge et al, 1964;Bishop et al, 1983). The relative amount of CGRP-LI released by capsaicin in the present study (15-20% of the total tissue content) is high compared to, for example, the guinea-pig heart but is likely to be due to the high concentration (10-M) of capsaicin used here in combination with the long exposure time (20 min).…”

Section: Discussionmentioning

confidence: 54%

“…Of the co-stored peptides, CGRP and SP, the relaxation caused by sensory nerve activation in the heart is probably mediated through CGRP. The extent to which other agents, as well as ischaemia, which is known to stimulate cardiac sensory nerves (Bishop et al, 1983), cause a release of CGRP with subsequent alterations in cardiac blood flow, remains to be established. It is tempting, however, to speculate about such a local efferent function of cardiac C-fibre afferents.…”

Section: Discussionmentioning

confidence: 99%

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Calcitonin gene‐related peptide and human epicardial coronary arteries: presence, release and vasodilator effects

Franco‐Cereceda

1991

British J Pharmacology

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1 In the present study, the levels of calcitonin gene-related peptide (CGRP)-like immunoreactivity (-LI) in human cardiopulmonary tissue were determined in combination with studies on CGRP-LI release from the left anterior descending coronary artery (LAD) and functional effects of CGRP on coronary arterial tone.2 The highest levels of CGRP-LI were found in the LAD followed in declining order by the bronchus, right atrium, pulmonary artery, lung and left ventricle. 3 Exposure to capsaicin evoked a clear-cut increase in CGRP-LI outflow, suggesting release from isolated large specimen of the LAD. This release was Ca2"-dependent and was markedly attenuated by incubation with the mitochondrial Ca2+-inhibitor, ruthenium red. Exposure to potassium also released CGRP-LI in a Ca2 +-dependent fashion from the LAD. 4 In functional experiments on human epicardial coronary arteries with an inner diameter of 0.4 to 0.8 mm, human CGRP alpha and beta relaxed the potassium-precontracted arteries equipotently. Substance P (SP) also relaxed these precontracted arteries but the relaxation could be prevented by incubation with methylene blue, an inhibitor of endothelium derived relaxing factor (EDRF)-mechanisms, which did not influence the effect of CGRP. 5 Capsaicin evoked a ruthenium red-sensitive relaxation of the potassium-precontracted arteries. However, ruthenium red did not affect the relaxations induced by CGRP or SP. Furthermore, the capsaicin effect was not influenced by methylene blue. 6 It is concluded that CGRP-LI is present in human cardiopulmonary tissue and can be released upon exposure to high concentrations of capsaicin as well as potassium. CGRP causes relaxation of arteries independently of EDRF activation and closely resembles the vasodilator effects of capsaicin. This supports the view that the coronary vasodilatation observed upon sensory nerve activation is mediated by CGRP. Ruthenium red inhibits capsaicin-induced CGRP-LI release and functional effects and may thus serve as an experimental tool in evaluating the function of capsaicin-evoked stimulation of peripheral nerve terminals.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Calcitonin gene‐related peptide and human epicardial coronary arteries: presence, release and vasodilator effects

Franco‐Cereceda

1991

British J Pharmacology

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“…Thus, the heart responds to sensory nerve activation by increasing the outflow of CGRP-like immunoreactivity (LI) which allows studies on the influence of various drugs on sensory nerves and contractility. There are a variety of agents known by electrophysiological experiments to activate cardiac C-fibre afferents (see Bishop et al, 1983) and several of these, including nicotine, bradykinin and ouabain, evoke a release of CGRP-LI from the isolated heart in combination with various changes in contractile activity (Franco-Cereceda et al, 1987b).…”

Section: Introductionmentioning

confidence: 99%

Ruthenium‐red inhibits CGRP release by capsaicin and resiniferatoxin but not by ouabain, bradykinin or nicotine in guinea‐pig heart: correlation with effects on cardiac contractility

Franco‐Cereceda

Lou

Lundberg

1991

British J Pharmacology

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1 The possible influence of ruthenium-red (RR) on contractility and outflow of calcitonin gene-related peptide (CGRP)-like and neuropeptide Y (NPY)-like immunoreactivity (LI) from the heart of the guineapig induced by capsaicin, resiniferatoxin, nicotine, ouabain or bradykinin was studied in vitro. 2 In the isolated right atrium, exposure to capsaicin evoked an increase in contractile rate and tension simultaneously with an enhanced outflow of CGRP-LI, indicating release from the atria. Repeated administration of capsaicin induced tachyphylaxis. Incubation with RR markedly attenuated the capsaicinevoked release of CGRP-LI while no clear-cut effects were seen on contractile tension or rate. 3 In the isolated whole heart, perfusion with capsaicin induced an increased outflow of CGRP-LI and stimulated heart rate, while a negative inotropic effect was observed. A second administration of capsaicin to the same preparations failed to influence the CGRP-LI outflow and in these experiments the positive chronotropic effect was absent while the negative inotropic action remained unchanged. Capsaicinperfusion in the presence of RR failed to induce any increased outflow of CGRP-LI from the hearts or changes in contractile activity. However, after 1 h of rinsing with Tyrode solution repeated capsaicin perfusion in the absence of RR caused a clear-cut (60% of control) release of CGRP-LI and contractile responses were restored.4 Perfusion with resiniferatoxin evoked a RR-sensitive, clear-cut increased CGRP-LI output without any effects on contractile force or heart rate. Repeated administration of resiniferatoxin induced tachyphylaxis with respect to outflow. Capsaicin perfusion after resiniferatoxin did not influence cardiac rate, force or CGRP-LI outflow suggesting development of cross-tachyphylaxis. 5 Perfusion with RR did not influence the outflow of CGRP-LI or contractility changes evoked by perfusion with nicotine, ouabain or bradykinin. In addition, the release of NPY-LI by nicotine remained unchanged in the presence of RR. Furthermore, the positive chronotropic effect of human CGRP alpha remained intact in the presence of RR. 6 It is concluded that RR selectively inhibits capsaicin-and resiniferatoxin-induced excitation of cardiac sensory nerves as revealed by inhibition of both CGRP-LI release and the cardiostimulatory action of capsaicin. RR also seems to protect the cardiac capsaicin-sensitive fibres from the development of tachyphylaxis to capsaicin. Finally, RR prevents the capsaicin-evoked negative inotropic effect which is not related to activation of sensory nerves.

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“…Veratrum alkaloids stimulate receptors that are activated by other chemicals (chemoreceptors) and receptors that are activated by changes in ventricular volume (mechanoreceptors) (Baker, Coleridge & Coleridge, 1979;Bishop, Malliani & Thoren, 1983). Attenuation of the baroreflex in our experiments could therefore have resulted from chemoreceptor stimulation, mechanoreceptor stimulation, or both.…”

Section: Mechanism Of Veratrine's Effect On the Baroreflexmentioning

confidence: 89%

Intracoronary veratrine attenuates carotid baroreceptor reflex regulation of blood pressure in conscious dogs.

Denison

Stephenson

Hull

et al. 1992

The Journal of Physiology

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SUMMARY1. The effect of activation of left ventricular cardiac receptors on carotid baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance was determined in conscious dogs. Previous studies in conscious subjects assessed only the effect on baroreflex control of heart rate.2. Dogs with denervated aortic baroreceptors were equipped with aortic flow probes, cardiac pacing electrodes, and catheters in the aorta, vena cava, and left circumflex coronary artery. Both carotid sinus regions were prepared for reversible vascular isolation.3. Left ventricular receptors were stimulated by an infusion of veratrine (0-1-1P0 gug kg-' min-') into the left circumflex coronary artery. 4. Veratrine infusion decreased control blood pressure only 10+2 mmHg, but it decreased the range of baroreflex control of blood pressure by 50% and decreased maximum baroreflex gain by 42 %. Both the cardiac output and total peripheral resistance components of the baroreflex were attenuated.5. Baroreflex control of blood pressure was unaffected by intravenous veratrine or by intracoronary infusion of vehicle.6. Intracoronary veratrine had no effect after autonomic ganglionic blockade. 7. When cardiac output was kept nearly constant (by ,-adrenergic and cholinergic receptor blockade or by fl-blockade and cardiac pacing), intracoronary veratrine still attenuated baroreflex control of blood pressure and total peripheral resistance. Veratrine impaired the ability of the baroreflex to utilize cz-adrenergic mechanisms to control total peripheral resistance.8. We conclude that activation of ventricular receptors attenuates baroreflex regulation of blood pressure in conscious dogs through an attenuation of baroreflex control of both cardiac output and total peripheral resistance.

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Cardiac Mechanoreceptors

Cited by 64 publications

References 368 publications

Calcitonin gene‐related peptide and human epicardial coronary arteries: presence, release and vasodilator effects

Calcitonin gene‐related peptide and human epicardial coronary arteries: presence, release and vasodilator effects

Ruthenium‐red inhibits CGRP release by capsaicin and resiniferatoxin but not by ouabain, bradykinin or nicotine in guinea‐pig heart: correlation with effects on cardiac contractility

Intracoronary veratrine attenuates carotid baroreceptor reflex regulation of blood pressure in conscious dogs.

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