In vitro effects of capsaicin: antiarrhythmic and antiischemic activity

DʼAlonzo, Albert J.; Grover, Gary J.; Darbenzio, Raymond B.; Heß, Thomas; Sleph, Paul G.; Dzwonczyk, Steven; Zhu, Jia L.; Sewter, Joseph C.

doi:10.1016/0014-2999(94)00653-o

Cited by 45 publications

(24 citation statements)

References 25 publications

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“…Our previous studies have shown that, in the isolated rat heart, the protection by ischaemic preconditioning is abolished by CGRP 8-37 , a CGRP receptor antagonist . Pretreatment with capsaicin, which evokes CGRP release from sensory nerves, can mimic the protection of ischaemic preconditioning (D'Alonzo et al 1995;Li et al 1996;Peng et al 1996). More recently, it has been reported that, in the rat pretreated with capsaicin to destroy sensory innervation, the protection of pacing-induced preconditioning is abolished (Ferdinandy et al 1997a).…”

Section: Discussionmentioning

confidence: 99%

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Tang

Dai

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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Early cardioprotection can be achieved by a brief ischaemia of noncardiac tissues. Our study examined whether a brief ischaemia of the small intestine induces both early and delayed cardioprotection in the rabbit and assessed the possible mechanism involved in the activation of capsaicin-sensitive sensory nerves. The plasma concentration of creatine kinase (CK) and infarct size (necrotic zone/left ventricular zone) after 30 min coronary artery occlusion and 180 min reperfusion were determined in rabbits. Infarct size was 35.5+/-6.8% in the control non-preconditioned group. Preconditioning induced by a brief period of 10-min small intestine ischaemia significantly reduced infarct size (6.5+/-1.9%, P<0.01 vs. the control non-preconditioned group) and decreased CK release (3092+/-236 and 1094+/-117 U/l for myocardial ischaemia-reperfusion and preconditioning plus myocardial ischemia-reperfusion, respectively, P<0.01), and the protection was partly abolished by pretreatment with capsaicin (50 mg/kg, s.c.) 4 days before the experiments. A brief period of anterior mesenteric artery occlusion caused an increase in the plasma level of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI), an effect which was abolished by pretreatment with capsaicin. Similar protection was shown in the animals subjected to a brief period of anterior mesenteric artery occlusion 24 h before coronary artery occlusion, and this delayed protection was also abolished partly by pretreatment with capsaicin. Capsaicin treatment (50 mg/kg, s.c.) alone also protected the ischaemic myocardium. The results suggest that brief ischaemia of the small intestine induces both early and delayed protection against reperfusion-induced myocardial injury, and the effects are, at least partly, related to the activation of capsaicin-sensitive sensory nerves.

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Section: Discussionmentioning

confidence: 99%

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Tang

Dai

et al. 1999

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Based on these comparative observations, it could be proposed that capsaicin, through its various effects on the I Na , may have antiarrhythmic properties, although further and pointed experiments are necessary to confirm this hypothesis. In support of this is the fact that D'Alonzo et al (13) have already described that capsaicin (10 -30 M) has antiarrhythmic and antiischemic properties on isolated perfused rat and guinea pig heart, although these authors did not observe any change in Vmax or amplitude of the action potential in their experimental model.…”

Section: Discussionsupporting

confidence: 50%

Voltage-Activated Sodium Current Is Inhibited by Capsaicin in Rat Atrial Myocytes

Milesi

Rebolledo

Alvis

et al. 2001

Biochemical and Biophysical Research Communications

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“…In coronary artery, capsaicin has been reported to increase coronary flow and decrease ischemic ventricular tachycardia which may be related to the decrease in Ca 2+ influx [2]. The authors suggest a protective role of capsaicin on the ischemic cardiac damage through maintaining adequate coronary flow.…”

mentioning

confidence: 86%

“…Capsaicin relaxes bronchial smooth muscle through activation of Ca 2+ -activated K + channels [5,24], or constricts cerebral arteries by increasing Ca 2+ influx [4]. The inhibitory effect of capsaicin on Ca 2+ and K + current in cultured aortic smooth muscle cells has also been reported [15].In coronary artery, capsaicin has been reported to increase coronary flow and decrease ischemic ventricular tachycardia which may be related to the decrease in Ca 2+ influx [2]. The authors suggest a protective role of capsaicin on the ischemic cardiac damage through maintaining adequate coronary flow.…”

mentioning

confidence: 99%

Capsaicin-induced Relaxation in Rabbit Coronary Artery.

Yeon

Kwon

Lee

et al. 2001

The Journal of Veterinary Medical Science

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ABSTRACT. In the present study mechanism of inhibitory effects of capsaicin on the contractility of rabbit coronary artery were studied by measurement of isometric tension and intracellular Ca 2+ concentration. Capsaicin (1 µM to 30 µM) relaxed the coronary artery pre-contracted with prostaglandin (PG) F 2α (1 µM) in a concentration-dependent manner. The PGF 2α -induced increase in intracellular Ca 2+ concentration was also inhibited. The effects of capsaicin were readily reversed by washing capsaicin from the bath. Capsaicin-induced relaxation was not attenuated by pretreatment with capsazepine (1 µM), a blocker of vanilloid receptor or ruthenium red (1 µM), a blocker of non-selective cation channel. Previous exposure to a high concentration of capsaicin (100 µM) or repeated application of capsaicin did not eliminate the relaxation response to subsequent application of capsaicin. Increasing the external K + concentration to 80 mM significantly attenuated the capsaicin-induced relaxation with simultaneous change in intracellular Ca 2+ concentration. Pretreatment with iberiotoxin (100 nM), a blocker of Ca 2+ -activated K + channel, only partially inhibited the capsaicin-induced relaxation. However, application of 4-aminopyridine (4-AP, 1 mM), a blocker of delayed rectifier K + current significantly inhibited the capsaicin-induced relaxation with concomitant attenuation of the effect on intracellular Ca 2+ concentration. These results indicate that capsaicin may have a direct relaxing effect on the smooth muscle contractility, and relaxation may be due to activation of the 4-AP-sensitive, delayed rectifier K + channels in the rabbit coronary artery. Capsaicin is a pungent constituent of red peppers and known to activate sensory nerve fibers via vanilloid receptor [20,[22][23]. Acute administration of capsaicin releases neuropeptide from sensory nerve endings, such as substance P, calcitonin gene related peptide (CGRP) and neurokinin A [7,17]. These neuropeptides seem to play a role in the regulation of vascular and airway smooth muscle tone [8,16,21]. In addition to this neuropeptide-mediated effect, capsaicin has a diverse effect on smooth muscle contractility and ion channel activity, depending on the species and preparations. Capsaicin relaxes bronchial smooth muscle through activation of Ca 2+ -activated K + channels [5,24], or constricts cerebral arteries by increasing Ca 2+ influx [4]. The inhibitory effect of capsaicin on Ca 2+ and K + current in cultured aortic smooth muscle cells has also been reported [15].In coronary artery, capsaicin has been reported to increase coronary flow and decrease ischemic ventricular tachycardia which may be related to the decrease in Ca 2+ influx [2]. The authors suggest a protective role of capsaicin on the ischemic cardiac damage through maintaining adequate coronary flow. However, it is uncertain whether capsaicin relaxes coronary artery through the release of neuropeptide such as CGRP, or through the direct inhibition of coronary smooth muscle [3,8,15]. Thus, the primary...

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In vitro effects of capsaicin: antiarrhythmic and antiischemic activity

Cited by 45 publications

References 25 publications

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Involvement of capsaicin-sensitive sensory nerves in early and delayed cardioprotection induced by a brief ischaemia of the small intestine

Voltage-Activated Sodium Current Is Inhibited by Capsaicin in Rat Atrial Myocytes

Capsaicin-induced Relaxation in Rabbit Coronary Artery.

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