Regulation of tissue noradrenaline in the rat myocardial infarction model of chronic heart failure

Robert Zelis, Barry Clemson, Robert Baily, Dwight Davis

Research output: Contribution to journalArticle

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Abstract

Objective: The aim was to evaluate mechanisms regulating tissue noradrenaline in congestive heart failure. Methods: Tissue noradrenaline was measured in the conscious post myocardial infarction rat model of congestive heart failure and in sham operated rats (1) under control conditions, (2) 6 h after inhibition of tyrosine hydroxylase by the intraperitoneal administration of α-methyl-paratyrosine (AMPT) (100 mg·kg-1 every 2 h), (3) 6 h after AMPT with desipramine pretreatment (0.3 mg·kg-), and (4) following exhaustive exercise after AMPT. Tissue noradrenaline was extracted with perchloric acid and measured by high performance liquid chromatography with electrochemical detection. Results: In control animals without drug, tissue noradrenaline concentration was lower in the following tissues in the rats with myocardial infarction compared with the sham operated group: left and right ventricles, spleen, soleus and white gastrocnemius muscles, kidney cortex, and tail artery. After AMPT, tissue noradrenaline concentration in the sham operated group was significantly lower than control; in the myocardial infarction group the fall in noradrenaline was only significant in the kidney, and group differences were no longer present. In the sham operated animals, coadministration of desipramine with AMPT attenuated the fall in tissue noradrenaline caused by AMPT in the heart and spleen. With exercise to exhaustion, cardiac noradrenaline was lower in rats with myocardial infarction than in sham operated rats, but higher in the soleus muscle. Conclusions: These data suggest that tissue noradrenaline depletion in congestive heart failure is not isolated to the heart, and it occurs despite activation of mechanisms that might be operating to conserve neuronal noradrenaline. One mechanism may be reduced organ blood flow to retard diffusion of noradrenaline into the circulation. If this increases interstitial noradrenaline concentration, it would facilitate prejunctional α2 receptor restraint on noradrenaline release. Metabolic coronary vasdilatation during exercise reverses this process, and makes the heart most susceptible to noradrenaline depletion in congestive heart failure.Cardiovascular Research 1992;26:933-938.

Original languageEnglish (US)
Pages (from-to)933-938
Number of pages6
JournalCardiovascular Research
Volume26
Issue number10
DOIs
StatePublished - Jan 1 1992

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Norepinephrine
Heart Failure
Myocardial Infarction
Desipramine
Heart Ventricles
Skeletal Muscle
Spleen
Kidney Cortex
Tyrosine 3-Monooxygenase
Tail
Arteries
High Pressure Liquid Chromatography
Kidney

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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abstract = "Objective: The aim was to evaluate mechanisms regulating tissue noradrenaline in congestive heart failure. Methods: Tissue noradrenaline was measured in the conscious post myocardial infarction rat model of congestive heart failure and in sham operated rats (1) under control conditions, (2) 6 h after inhibition of tyrosine hydroxylase by the intraperitoneal administration of α-methyl-paratyrosine (AMPT) (100 mg·kg-1 every 2 h), (3) 6 h after AMPT with desipramine pretreatment (0.3 mg·kg-), and (4) following exhaustive exercise after AMPT. Tissue noradrenaline was extracted with perchloric acid and measured by high performance liquid chromatography with electrochemical detection. Results: In control animals without drug, tissue noradrenaline concentration was lower in the following tissues in the rats with myocardial infarction compared with the sham operated group: left and right ventricles, spleen, soleus and white gastrocnemius muscles, kidney cortex, and tail artery. After AMPT, tissue noradrenaline concentration in the sham operated group was significantly lower than control; in the myocardial infarction group the fall in noradrenaline was only significant in the kidney, and group differences were no longer present. In the sham operated animals, coadministration of desipramine with AMPT attenuated the fall in tissue noradrenaline caused by AMPT in the heart and spleen. With exercise to exhaustion, cardiac noradrenaline was lower in rats with myocardial infarction than in sham operated rats, but higher in the soleus muscle. Conclusions: These data suggest that tissue noradrenaline depletion in congestive heart failure is not isolated to the heart, and it occurs despite activation of mechanisms that might be operating to conserve neuronal noradrenaline. One mechanism may be reduced organ blood flow to retard diffusion of noradrenaline into the circulation. If this increases interstitial noradrenaline concentration, it would facilitate prejunctional α2 receptor restraint on noradrenaline release. Metabolic coronary vasdilatation during exercise reverses this process, and makes the heart most susceptible to noradrenaline depletion in congestive heart failure.Cardiovascular Research 1992;26:933-938.",
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Regulation of tissue noradrenaline in the rat myocardial infarction model of chronic heart failure. / Zelis, Robert; Clemson, Barry; Baily, Robert; Davis, Dwight.

In: Cardiovascular Research, Vol. 26, No. 10, 01.01.1992, p. 933-938.

Research output: Contribution to journalArticle

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AB - Objective: The aim was to evaluate mechanisms regulating tissue noradrenaline in congestive heart failure. Methods: Tissue noradrenaline was measured in the conscious post myocardial infarction rat model of congestive heart failure and in sham operated rats (1) under control conditions, (2) 6 h after inhibition of tyrosine hydroxylase by the intraperitoneal administration of α-methyl-paratyrosine (AMPT) (100 mg·kg-1 every 2 h), (3) 6 h after AMPT with desipramine pretreatment (0.3 mg·kg-), and (4) following exhaustive exercise after AMPT. Tissue noradrenaline was extracted with perchloric acid and measured by high performance liquid chromatography with electrochemical detection. Results: In control animals without drug, tissue noradrenaline concentration was lower in the following tissues in the rats with myocardial infarction compared with the sham operated group: left and right ventricles, spleen, soleus and white gastrocnemius muscles, kidney cortex, and tail artery. After AMPT, tissue noradrenaline concentration in the sham operated group was significantly lower than control; in the myocardial infarction group the fall in noradrenaline was only significant in the kidney, and group differences were no longer present. In the sham operated animals, coadministration of desipramine with AMPT attenuated the fall in tissue noradrenaline caused by AMPT in the heart and spleen. With exercise to exhaustion, cardiac noradrenaline was lower in rats with myocardial infarction than in sham operated rats, but higher in the soleus muscle. Conclusions: These data suggest that tissue noradrenaline depletion in congestive heart failure is not isolated to the heart, and it occurs despite activation of mechanisms that might be operating to conserve neuronal noradrenaline. One mechanism may be reduced organ blood flow to retard diffusion of noradrenaline into the circulation. If this increases interstitial noradrenaline concentration, it would facilitate prejunctional α2 receptor restraint on noradrenaline release. Metabolic coronary vasdilatation during exercise reverses this process, and makes the heart most susceptible to noradrenaline depletion in congestive heart failure.Cardiovascular Research 1992;26:933-938.

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