Stimulation of cardiac sympathetic nerve activity by central angiotensinergic mechanisms in conscious sheep

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dc.contributor.authorWatson, AMD
dc.contributor.authorMogulkoc, R
dc.contributor.authorMcAllen, RM
dc.contributor.authorMay, CN
dc.date.accessioned2020-03-26T16:55:29Z
dc.date.available2020-03-26T16:55:29Z
dc.date.issued2004
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractCentral actions of angiotensin play an important role in cardiovascular control and have been implicated in the pathogenesis of hypertension and heart failure. One feature of centrally or peripherally administered angiotensin is that the bradycardia in response to an acute pressor effect is blunted. It is unknown whether after central angiotensin this is due partly to increased cardiac sympathetic nerve activity (CSNA). We recorded CSNA and arterial pressure in conscious sheep, at least 3 days after electrode implantation. The effects of intracerebroventricular infusions of ANG II ( 3 nmol/h for 30 min) and artificial cerebrospinal fluid (CSF) ( 1 ml/h) were determined. The response to intracerebroventricular hypertonic saline (0.6 M NaCl in CSF at 1 ml/h) was examined as there is evidence that hypertonic saline acts via angiotensinergic pathways. Intracerebroventricular angiotensin increased CSNA by 23 +/- 7% (P < 0.001) and mean arterial pressure (MAP) by 7.6 +/- 1.2 mmHg (P < 0.001) but did not significantly change heart rate (n = 5). During intracerebroventricular ANG II the reflex relation between CSNA and diastolic blood pressure was significantly shifted to the right (P < 0.01). Intracerebroventricular hypertonic saline increased CSNA (+9.4 +/- 6.6%, P < 0.05) and MAP but did not alter heart rate. The responses to angiotensin and hypertonic saline were prevented by intracerebroventricular losartan (1 mg/h). In conclusion, in conscious sheep angiotensin acts within the brain to increase CSNA, despite increased MAP. The increase in CSNA may account partly for the lack of bradycardia in response to the increased arterial pressure. The responses to angiotensin and hypertonic saline were losartan sensitive, indicating they were mediated by angiotensin AT-1 receptors.en_US
dc.identifier.doi10.1152/ajpregu.00708.2003en_US
dc.identifier.endpageR1056en_US
dc.identifier.issn0363-6119en_US
dc.identifier.issn1522-1490en_US
dc.identifier.issue6en_US
dc.identifier.pmid14751846en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpageR1051en_US
dc.identifier.urihttps://dx.doi.org/10.1152/ajpregu.00708.2003
dc.identifier.urihttps://hdl.handle.net/20.500.12395/19208
dc.identifier.volume286en_US
dc.identifier.wosWOS:000221443600010en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherAMER PHYSIOLOGICAL SOCen_US
dc.relation.ispartofAMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectangiotensin IIen_US
dc.subjectbaroreflexen_US
dc.subjecthypertonic salineen_US
dc.subjectintracerebroventricularen_US
dc.subjectlosartanen_US
dc.titleStimulation of cardiac sympathetic nerve activity by central angiotensinergic mechanisms in conscious sheepen_US
dc.typeArticleen_US

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