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血管加压素对失血性尿崩症大鼠肾交感神经活动和心率的抑制作用

Inhibition of renal sympathetic activity and heart rate by vasopressin in hemorrhaged diabetes insipidus rats.

作者信息

Peuler J D, Schmid P G, Morgan D A, Mark A L

机构信息

Veterans Administration Medical Center, Cardiovascular Center, Iowa City, Iowa.

出版信息

Am J Physiol. 1990 Mar;258(3 Pt 2):H706-12. doi: 10.1152/ajpheart.1990.258.3.H706.

Abstract

Hypotensive hemorrhage paradoxically decreases renal sympathetic nerve activity (SNA) and heart rate (HR) in normal rats. Interruption of vagal reflexes by cervical vagotomy prevents these inhibitory responses but does not unmask expected increases in either renal SNA or HR. Arginine vasopressin (AVP), which increases markedly during hemorrhage, may also exert an inhibitory action on responses of renal SNA and HR to hemorrhage. We tested the hypothesis that inhibition of renal SNA and HR by hemorrhage is absent in AVP-deficient diabetes insipidus (DI) rats and is restored by intravenous AVP replacement (1 mU.kg-1.min-1 before hemorrhage and 10 mU.kg-1.min-1 during hemorrhage). We also determined whether vagotomy unmasks significant increases in renal SNA and HR during hemorrhage in DI rats and whether AVP replacement prevents these increases. Under chloralose anesthesia, hemorrhage to 50 mmHg mean arterial pressure for 8 min did not decrease renal SNA or HR in AVP-deficient DI rats but decreased (P less than 0.05) renal SNA and HR in normal Long-Evans rats and in DI rats receiving AVP replacement. After vagotomy, hemorrhage increased (P less than 0.05) renal SNA and HR in AVP-deficient DI rats but did not alter renal SNA or HR in Long-Evans rats and AVP-treated DI rats. Thus renal SNA and HR during hemorrhage were consistently higher (P less than 0.05) in AVP-deficient DI rats compared with Long-Evans or AVP-treated DI rats both before and after vagotomy. In addition, vagotomy attenuated the inhibitory action of AVP on the response of HR but not the response of renal SNA to hemorrhage in DI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在正常大鼠中,低血压性出血反而会降低肾交感神经活动(SNA)和心率(HR)。通过颈迷走神经切断术阻断迷走反射可防止这些抑制性反应,但不会揭示肾SNA或HR预期的增加。在出血期间显著增加的精氨酸加压素(AVP)也可能对肾SNA和HR对出血的反应产生抑制作用。我们检验了以下假设:在缺乏AVP的尿崩症(DI)大鼠中,出血对肾SNA和HR的抑制作用不存在,静脉注射AVP替代物(出血前1 mU·kg-1·min-1,出血期间10 mU·kg-1·min-1)可恢复这种抑制作用。我们还确定了迷走神经切断术是否会揭示DI大鼠出血期间肾SNA和HR的显著增加,以及AVP替代物是否能防止这些增加。在氯醛糖麻醉下,将平均动脉压降至50 mmHg持续8分钟,不会降低缺乏AVP的DI大鼠的肾SNA或HR,但会降低(P<0.05)正常Long-Evans大鼠和接受AVP替代物的DI大鼠的肾SNA和HR。迷走神经切断术后,出血会增加(P<0.05)缺乏AVP的DI大鼠的肾SNA和HR,但不会改变Long-Evans大鼠和接受AVP治疗的DI大鼠的肾SNA或HR。因此,在迷走神经切断术前后,缺乏AVP的DI大鼠出血期间的肾SNA和HR始终高于(P<0.05)Long-Evans大鼠或接受AVP治疗的DI大鼠。此外,迷走神经切断术减弱了AVP对DI大鼠HR反应的抑制作用,但未减弱对肾SNA对出血反应的抑制作用。(摘要截于250字)

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