Human α- and β-CGRP and rat α-CGRP are coronary vasodilators in the rat

Holman, Jennifer J.; Craig, Roger K.; Marshall, Ian

doi:10.1016/0196-9781(86)90218-4

Cited by 93 publications

(37 citation statements)

References 14 publications

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“…Differential metabolism, (due to the presence of a methionine residue in P-CGRP), could explain a lesser bioactivity of human fi-than of a-CGRP given intravenously, and the finding that f-CGRP may be more potent than a-CGRP in vitro (Holman et al, 1986), although recent studies have not found this . However, it is difficult to reconcile the differences between the results of studies in which human a-and f-CGRP were given locally (Brown & Morice, 1987;Williams et al, 1988), unless the actual amounts of biologically active a-and ,B-CGRP delivered to the tissues were different.…”

Section: Discussionmentioning

confidence: 63%

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Gardiner

Compton

Bennett

1989

British J Pharmacology

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Section: Discussionmentioning

confidence: 63%

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Gardiner

Compton

Bennett

1989

British J Pharmacology

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“…Activation of cardiac C fiber results in the release of CGRP, which induces coronary vasodilation in several animal species including rat and pig [6,9]. Therefore, it seems likely that activation of cardiac C fiber by capsaicin may relax coronary artery by releasing CGRP.…”

Section: Discussionmentioning

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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“…CGRP is a potent coronary vasodilator (Holman et al, 1986;Franco-Cereceda & Lundberg, 1987) whereas NPY is a vasoconstrictor and enhances the response to various constrictor substances in isolated blood vessels (Edvinsson et al, 1984;Andriantsitohaina & Stoclet, 1988). The functional significance of the nerves containing these peptides in the heart is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of neuropeptide Y and calcitonin gene‐related peptide on sheep coronary artery rings under oxygenated, hypoxic and simulated myocardial ischaemic conditions

Kwan

Wadsworth

Kane

1990

British J Pharmacology

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1 The effects of calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) were examined on sheep circumflex (2-2.5 mm o.d.) coronary artery rings, with and without endothelium, under oxygenated, hypoxic and simulated ischaemic conditions. The interaction between the vasoconstrictor effects of NPY and the thromboxane mimetic, U46619, was also studied. 2 Ischaemia was simulated by modification of the composition of the physiological salt solution by increasing potassium and H +, including lactate and reducing glucose and P02 .3 Hypoxia alone and simulated ischaemia increased the maximum vasodilatation produced by CGRP. CGRP (30nM) abolished and markedly reduced the contraction that was induced by hypoxia and simulated ischaemia respectively. 4 Hypoxia increased and simulated ischaemia reduced the contractile response to NPY in endothelium intact rings. When the endothelium was removed, NPY caused a contraction under ischaemic conditions only. The hypoxic and ischaemic-induced contractions were augmented by NPY (30 nM). 5 In the rings containing endothelium, NPY enhanced the contraction caused by U46619 during hypoxia only. In endothelium-denuded preparations, NPY increased or partially restored the contraction caused by U46619. 6 These results show that the responsiveness of coronary artery rings isolated from sheep to either CGRP or NPY is modified by hypoxia or simulated myocardial ischaemia.

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Human α- and β-CGRP and rat α-CGRP are coronary vasodilators in the rat

Cited by 93 publications

References 14 publications

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Regional haemodynamic effects of human α‐ and β‐calcitonin gene‐related peptide in conscious Wistar rats

Capsaicin-induced Relaxation in Rabbit Coronary Artery.

Effects of neuropeptide Y and calcitonin gene‐related peptide on sheep coronary artery rings under oxygenated, hypoxic and simulated myocardial ischaemic conditions

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