Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: Role of nitric oxide and CGRP?

P. Ferdinándy, T. Csont, C. Csonka, Marianna Török, M. Dux, J. Németh, László I. Horváth, L. Dux, Z. Szilvássy, G. Jancsó

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Abstract

Among several mediators, nitric oxide (NO) and calcitonin gene-related peptide (CGRP) were suggested to be involved in the mechanism of preconditioning. We examined the possible role of the cardiac capsaicin-sensitive sensory innervation in pacing-induced preconditioning, as well as in the cardiac NO and CGRP content. Wistar rats were treated subcutaneously with capsaicin or its solvent in the sequence of 10, 30, and 50 mg/kg increasing single daily doses for 3 days to deplete neurotransmitters of the sensory innervation. Isolated hearts from both groups were then subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats per minute for 5 min with 5 min interpacing periods, or time-matched non-preconditioning perfusion, followed by a 10-min coronary occlusion. NO content of left ventricular tissue samples was assayed by electron-spin resonance, and CGRP release was determined by radioimmunoassay. CGRP immunohistochemistry was also performed. In the non-preconditioned, solvent-treated group, coronary occlusion decreased cardiac output (CO) from 68.1 to 32.1 mL/min, increased left ventricular end-diastolic pressure (LVEDP) from 0.58 to 1.90 kPa, and resulted in 200 mU/min/g LDH release. Preconditioning significantly increased ischaemic CO to 42.9 mL/min (P <0.05), decreased ischaemic LVEDP to 1.26 kPa (P <0.05) and decreased LDH release to 47 mU/min/g (P <0.05) in the solvent-treated group. Preconditioning did not confer protection in the capsaicin-pretreated group (ischaemic CO: 35.6 mL/min; LVEDP: 1.76 kPa; LDH 156 mU/min/g). Capsaicin-treatment markedly decreased cardiac NO content, CGRP release, and CGRP-immunoreactivity. Conclusions: (i) The presence of an intact local sensory innervation is a prerequisite to elicit pacing-induced preconditioning in the rat heart. (ii) A significant portion of cardiac basal NO content may be of neural origin. (iii) Release of NO and CGRP from capsaicin-sensitive nerves may be involved in the mechanism of pacing-induced preconditioning.

Original languageEnglish
Pages (from-to)356-363
Number of pages8
JournalNaunyn-Schmiedeberg's Archives of Pharmacology
Volume356
Issue number3
DOIs
Publication statusPublished - 1997

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Calcitonin Gene-Related Peptide
Capsaicin
Nitric Oxide
Cardiac Output
Coronary Occlusion
Blood Pressure
Electron Spin Resonance Spectroscopy
Radioimmunoassay
Neurotransmitter Agents
Wistar Rats
Perfusion
Immunohistochemistry

Keywords

  • Calcitonin gene-related peptide
  • Capsaicin
  • Electron-spin resonance
  • Immunohistochemistry
  • Nitric oxide
  • Preconditioning
  • Rapid pacing
  • Rat heart

ASJC Scopus subject areas

  • Pharmacology

Cite this

@article{9a3efd1286f9456c9965377c901785b4,
title = "Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts: Role of nitric oxide and CGRP?",
abstract = "Among several mediators, nitric oxide (NO) and calcitonin gene-related peptide (CGRP) were suggested to be involved in the mechanism of preconditioning. We examined the possible role of the cardiac capsaicin-sensitive sensory innervation in pacing-induced preconditioning, as well as in the cardiac NO and CGRP content. Wistar rats were treated subcutaneously with capsaicin or its solvent in the sequence of 10, 30, and 50 mg/kg increasing single daily doses for 3 days to deplete neurotransmitters of the sensory innervation. Isolated hearts from both groups were then subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats per minute for 5 min with 5 min interpacing periods, or time-matched non-preconditioning perfusion, followed by a 10-min coronary occlusion. NO content of left ventricular tissue samples was assayed by electron-spin resonance, and CGRP release was determined by radioimmunoassay. CGRP immunohistochemistry was also performed. In the non-preconditioned, solvent-treated group, coronary occlusion decreased cardiac output (CO) from 68.1 to 32.1 mL/min, increased left ventricular end-diastolic pressure (LVEDP) from 0.58 to 1.90 kPa, and resulted in 200 mU/min/g LDH release. Preconditioning significantly increased ischaemic CO to 42.9 mL/min (P <0.05), decreased ischaemic LVEDP to 1.26 kPa (P <0.05) and decreased LDH release to 47 mU/min/g (P <0.05) in the solvent-treated group. Preconditioning did not confer protection in the capsaicin-pretreated group (ischaemic CO: 35.6 mL/min; LVEDP: 1.76 kPa; LDH 156 mU/min/g). Capsaicin-treatment markedly decreased cardiac NO content, CGRP release, and CGRP-immunoreactivity. Conclusions: (i) The presence of an intact local sensory innervation is a prerequisite to elicit pacing-induced preconditioning in the rat heart. (ii) A significant portion of cardiac basal NO content may be of neural origin. (iii) Release of NO and CGRP from capsaicin-sensitive nerves may be involved in the mechanism of pacing-induced preconditioning.",
keywords = "Calcitonin gene-related peptide, Capsaicin, Electron-spin resonance, Immunohistochemistry, Nitric oxide, Preconditioning, Rapid pacing, Rat heart",
author = "P. Ferdin{\'a}ndy and T. Csont and C. Csonka and Marianna T{\"o}r{\"o}k and M. Dux and J. N{\'e}meth and Horv{\'a}th, {L{\'a}szl{\'o} I.} and L. Dux and Z. Szilv{\'a}ssy and G. Jancs{\'o}",
year = "1997",
doi = "10.1007/PL00005062",
language = "English",
volume = "356",
pages = "356--363",
journal = "Naunyn-Schmiedeberg's Archives of Pharmacology",
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TY - JOUR

T1 - Capsaicin-sensitive local sensory innervation is involved in pacing-induced preconditioning in rat hearts

T2 - Role of nitric oxide and CGRP?

AU - Ferdinándy, P.

AU - Csont, T.

AU - Csonka, C.

AU - Török, Marianna

AU - Dux, M.

AU - Németh, J.

AU - Horváth, László I.

AU - Dux, L.

AU - Szilvássy, Z.

AU - Jancsó, G.

PY - 1997

Y1 - 1997

N2 - Among several mediators, nitric oxide (NO) and calcitonin gene-related peptide (CGRP) were suggested to be involved in the mechanism of preconditioning. We examined the possible role of the cardiac capsaicin-sensitive sensory innervation in pacing-induced preconditioning, as well as in the cardiac NO and CGRP content. Wistar rats were treated subcutaneously with capsaicin or its solvent in the sequence of 10, 30, and 50 mg/kg increasing single daily doses for 3 days to deplete neurotransmitters of the sensory innervation. Isolated hearts from both groups were then subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats per minute for 5 min with 5 min interpacing periods, or time-matched non-preconditioning perfusion, followed by a 10-min coronary occlusion. NO content of left ventricular tissue samples was assayed by electron-spin resonance, and CGRP release was determined by radioimmunoassay. CGRP immunohistochemistry was also performed. In the non-preconditioned, solvent-treated group, coronary occlusion decreased cardiac output (CO) from 68.1 to 32.1 mL/min, increased left ventricular end-diastolic pressure (LVEDP) from 0.58 to 1.90 kPa, and resulted in 200 mU/min/g LDH release. Preconditioning significantly increased ischaemic CO to 42.9 mL/min (P <0.05), decreased ischaemic LVEDP to 1.26 kPa (P <0.05) and decreased LDH release to 47 mU/min/g (P <0.05) in the solvent-treated group. Preconditioning did not confer protection in the capsaicin-pretreated group (ischaemic CO: 35.6 mL/min; LVEDP: 1.76 kPa; LDH 156 mU/min/g). Capsaicin-treatment markedly decreased cardiac NO content, CGRP release, and CGRP-immunoreactivity. Conclusions: (i) The presence of an intact local sensory innervation is a prerequisite to elicit pacing-induced preconditioning in the rat heart. (ii) A significant portion of cardiac basal NO content may be of neural origin. (iii) Release of NO and CGRP from capsaicin-sensitive nerves may be involved in the mechanism of pacing-induced preconditioning.

AB - Among several mediators, nitric oxide (NO) and calcitonin gene-related peptide (CGRP) were suggested to be involved in the mechanism of preconditioning. We examined the possible role of the cardiac capsaicin-sensitive sensory innervation in pacing-induced preconditioning, as well as in the cardiac NO and CGRP content. Wistar rats were treated subcutaneously with capsaicin or its solvent in the sequence of 10, 30, and 50 mg/kg increasing single daily doses for 3 days to deplete neurotransmitters of the sensory innervation. Isolated hearts from both groups were then subjected to either preconditioning induced by three consecutive periods of pacing at 600 beats per minute for 5 min with 5 min interpacing periods, or time-matched non-preconditioning perfusion, followed by a 10-min coronary occlusion. NO content of left ventricular tissue samples was assayed by electron-spin resonance, and CGRP release was determined by radioimmunoassay. CGRP immunohistochemistry was also performed. In the non-preconditioned, solvent-treated group, coronary occlusion decreased cardiac output (CO) from 68.1 to 32.1 mL/min, increased left ventricular end-diastolic pressure (LVEDP) from 0.58 to 1.90 kPa, and resulted in 200 mU/min/g LDH release. Preconditioning significantly increased ischaemic CO to 42.9 mL/min (P <0.05), decreased ischaemic LVEDP to 1.26 kPa (P <0.05) and decreased LDH release to 47 mU/min/g (P <0.05) in the solvent-treated group. Preconditioning did not confer protection in the capsaicin-pretreated group (ischaemic CO: 35.6 mL/min; LVEDP: 1.76 kPa; LDH 156 mU/min/g). Capsaicin-treatment markedly decreased cardiac NO content, CGRP release, and CGRP-immunoreactivity. Conclusions: (i) The presence of an intact local sensory innervation is a prerequisite to elicit pacing-induced preconditioning in the rat heart. (ii) A significant portion of cardiac basal NO content may be of neural origin. (iii) Release of NO and CGRP from capsaicin-sensitive nerves may be involved in the mechanism of pacing-induced preconditioning.

KW - Calcitonin gene-related peptide

KW - Capsaicin

KW - Electron-spin resonance

KW - Immunohistochemistry

KW - Nitric oxide

KW - Preconditioning

KW - Rapid pacing

KW - Rat heart

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U2 - 10.1007/PL00005062

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JO - Naunyn-Schmiedeberg's Archives of Pharmacology

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