Increased Spontaneous Activity And Reduced Inotropic Response To Catecholamines In Ventricular Myocytes From Footshock-stressed Rats.

dc.creatorPenna, Larissa B
dc.creatorBassani, Rosana A
dc.date2010-Jan
dc.date2015-11-27T13:17:41Z
dc.date2015-11-27T13:17:41Z
dc.date.accessioned2018-03-29T01:10:34Z
dc.date.available2018-03-29T01:10:34Z
dc.identifierStress (amsterdam, Netherlands). v. 13, n. 1, p. 73-82, 2010-Jan.
dc.identifier1607-8888
dc.identifier10.3109/10253890902951778
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/19697264
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/198770
dc.identifier19697264
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1299003
dc.descriptionExposure to stressors has been shown to change atrial responsiveness to catecholamines, but it is not clear yet how it affects the ventricular myocardium, which plays a major role in the catecholamine-stimulated increase in cardiac output. Adult male rats were submitted to restraint (RST) or footshock (FS) sessions for 3 days. Reactivity to agonists of the beta-adrenergic pathway was analyzed in left ventricular myocytes isolated from stressed and control rats (CTR). Whereas no significant changes were detected after RST, enhancement of catecholamine-induced spontaneous activity, accompanied by decrease in inotropic maximal response, was observed in myocytes from FS rats. Changes were reversed by beta(1)-, but not by alpha(1)-or beta(2)-adrenoceptor (AR) blockade. Similar alterations were seen in response to forskolin. However, responsiveness to 3-isobutyl-1-methylxanthine and CaCl(2) was comparable in control and FS groups. A significant negative correlation was observed between the maximally stimulated spontaneous activity rate and contraction amplitude. Results indicate that: (a) enhanced automatism during adrenergic stimulation of myocytes from FS rats is mediated by beta(1)-ARs and seems to involve post-receptor mechanisms, probably decreased cAMP degradation; (b) the exaggerated spontaneous activity, which may contribute to generation of catecholaminergic arrhythmias, might limit the development of the inotropic response.
dc.description13
dc.description73-82
dc.languageeng
dc.relationStress (amsterdam, Netherlands)
dc.relationStress
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subject1-methyl-3-isobutylxanthine
dc.subjectAdrenergic Agents
dc.subjectAnimals
dc.subjectCalcium
dc.subjectDose-response Relationship, Drug
dc.subjectElectroshock
dc.subjectIsoproterenol
dc.subjectMale
dc.subjectMuscle Contraction
dc.subjectMyocardium
dc.subjectMyocytes, Cardiac
dc.subjectNorepinephrine
dc.subjectPhosphodiesterase Inhibitors
dc.subjectPrazosin
dc.subjectRandom Allocation
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReceptors, Adrenergic, Alpha-1
dc.subjectReceptors, Adrenergic, Beta-1
dc.subjectReceptors, Adrenergic, Beta-2
dc.subjectRegression Analysis
dc.subjectStress, Physiological
dc.titleIncreased Spontaneous Activity And Reduced Inotropic Response To Catecholamines In Ventricular Myocytes From Footshock-stressed Rats.
dc.typeArtículos de revistas


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