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在最后区损伤的大鼠出血期间,心动过缓增强,但肾交感神经抑制未增强。

Enhanced bradycardia but not renal sympathoinhibition during hemorrhage in rats with area postrema lesions.

作者信息

Edwards G L, Johnson A K, Peuler J D

机构信息

Department of Physiology and Pharmacology, University of Georgia, Athens 30602.

出版信息

Am J Physiol. 1994 Aug;267(2 Pt 2):H569-73. doi: 10.1152/ajpheart.1994.267.2.H569.

DOI:10.1152/ajpheart.1994.267.2.H569
PMID:8067412
Abstract

Hypotensive hemorrhage inhibits renal sympathetic nerve activity (SNA) and heart rate (HR) in rats. The area postrema (AP) is reported to modulate autonomic responses to arginine vasopressin (AVP) and may be a site where circulating AVP influences SNA and HR during hypotensive hemorrhage. We found a similar renal sympathoinhibition in AP-lesioned (APX) and sham-lesioned (Sham) rats during hypotensive hemorrhage and a greater bradycardia in APX compared with Sham rats. Further inhibition of renal SNA with AVP infusion was not observed in APX rats, although the bradycardic action of AVP infusion was comparable to that in Sham rats. Thus the AP attenuates bradycardia but not renal sympathoinhibition during hypotensive hemorrhage in normal rats. Nonetheless, an intact AP permits further reduction in renal SNA during infusion of AVP. If AVP contributes to hypotensive hemorrhage-induced renal sympathoinhibition, its action may occur at sites other than the AP or at the AP where such action is counterbalanced by sympathoexcitatory factor(s) also activated during hypotensive hemorrhage. Finally, enhanced bradycardia during hypotensive hemorrhage in APX rats suggests it may not be the site of action for AVP-induced bradycardia in intact rats.

摘要

低血压性出血会抑制大鼠的肾交感神经活动(SNA)和心率(HR)。据报道,最后区(AP)可调节对精氨酸加压素(AVP)的自主反应,并且可能是循环中的AVP在低血压性出血期间影响SNA和HR的部位。我们发现在低血压性出血期间,AP损伤(APX)大鼠和假手术(Sham)大鼠存在类似的肾交感神经抑制,并且与Sham大鼠相比,APX大鼠的心动过缓更明显。尽管AVP输注的心动过缓作用与Sham大鼠相当,但在APX大鼠中未观察到AVP输注对肾SNA的进一步抑制作用。因此,在正常大鼠低血压性出血期间,AP可减轻心动过缓,但不能减轻肾交感神经抑制。尽管如此,完整的AP在AVP输注期间可使肾SNA进一步降低。如果AVP促成低血压性出血诱导的肾交感神经抑制,其作用可能发生在AP以外的部位,或者发生在AP部位,但在低血压性出血期间也被激活的交感兴奋因子抵消了这种作用。最后,APX大鼠在低血压性出血期间心动过缓加剧,这表明它可能不是AVP诱导完整大鼠心动过缓的作用部位。

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