Contribution of central ANG II to acute stress-induced changes in baroreflex function in young rats

Department of Zoology, Brigham Young University, Provo, Utah 84602 The aim of the present investigation was to characterize the baroreflex in weaned 23- to 25-day-old rats when maternal influences were no longer present. The relationship between mean arterial pressure (MAP) and heart rate (HR) was d...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2000-10, Vol.279 (4), p.1386-R1391
1. Verfasser: Porter, James P
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Sprache:eng
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Zusammenfassung:Department of Zoology, Brigham Young University, Provo, Utah 84602 The aim of the present investigation was to characterize the baroreflex in weaned 23- to 25-day-old rats when maternal influences were no longer present. The relationship between mean arterial pressure (MAP) and heart rate (HR) was determined during baroreceptor loading with phenylephrine and baroreceptor unloading with sodium nitroprusside in conscious rats, first in the freely moving state and subsequently during acute stress. In unstressed rats, the slope of the relationship between MAP and HR was greater during baroreceptor loading than baroreceptor unloading. Acute stress significantly attenuated the slope of the response to baroreceptor loading but increased the slope of the response to baroreceptor unloading. Pretreatment with intracerebroventricular or intravenous losartan, an AT 1 receptor antagonist, or intracerebroventricular -helical corticotropin-releasing hormone ( -hCRH), a receptor antagonist, before the stress significantly reduced the stress-induced attenuation of slope during baroreceptor loading. Hence, young postweaning rats can alter baroreflex function during acute stress in a manner that would favor increases in MAP. Even at this young age, a central action of ANG II and CRH contributes to these stress-induced adaptations. angiotensin receptors; corticotropin-releasing hormone receptors; sympathetic nervous system; parasympathetic nervous system
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.2000.279.4.R1386