Co-Authors:
Bayorh, M.A., Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States
Zukowska-Grojec, Z., Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States
Ezra, D., Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States
Feuerstein, G.Z., Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, USUHS, Bethesda, MD, United States
Kopin, I.J., Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD, United States, Autonomic Research Unit, Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, United States
Abstract:
In rats between the ages of 4 and 12 or 14 weeks, repeated daily subcutaneous administration of arachidonate (AA) at a dose of 50 or 200 mg/kg significantly retarded the development of hypertension in spontaneously hypertensive rats (SHR) but did not alter the normal age-related increase in blood pressures (BP) of normotensive (WKY) rats. Heart rates (HR) and plasma levels of norepinephrine (NE), but not epinephrine, were lower in AA-treated SHR than in saline-treated animals. AA-treated SHR and WKY gained less weight than the saline-treated controls. In pithed AAtreated SHR, stimulation of the sympathetic outflow (50 V, for 1 minute at 0.3 or 3.0 Hz) and intravenous administration of NE (0.3 or 3.0 g/kg) evoked smaller pressor responses than in salinetreated controls, but the stimulation-evoked increases in plasma catecholamines were unchanged by AA treatment. These results indicated that, in SHR, chronic AA treatment reduces BP by mechanisms that do not directly affect NE release from sympathetic nerves. There appears to be both reduced central nervous system activation of the sympathetic outflow and diminshed responses to peripheral sympathetic stimulation and exogeneous NE which may be secondary to the reduced vascular hypertrophy that usually accompanies the development of high BP in SHR.
תפריט נגישות
ניגודיות עדינה
מונוכרום
הדגשת קישורים
חסימת אנימציה
פונט קריא
סגור
איפוס הגדרות נגישות
להורדת מודול נגישות חינם
