Gontijo J R, Kopp U C
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Hypertension. 1994 Jun;23(6 Pt 2):1063-7. doi: 10.1161/01.hyp.23.6.1063.
In anesthetized rats we examined whether calcitonin gene-related peptide activated renal pelvic sensory receptors and, if so, whether activation of renal pelvic calcitonin gene-related peptide receptors contributes to the inhibitory renorenal reflex response to renal mechanoreceptor stimulation. Calcitonin gene-related peptide (0.0026, 0.026, 0.26, and 2.6 mumol/L) administered into the renal pelvis increased ipsilateral afferent renal nerve activity in a concentration-dependent fashion (32 +/- 14%, 69 +/- 19%, 93 +/- 26%, and 253 +/- 48% [all P < .01], respectively). The increases in ipsilateral afferent renal nerve activity elicited by calcitonin gene-related peptide were associated with increases in contralateral urinary sodium excretion. The calcitonin gene-related peptide receptor antagonist human CGRP (h-CGRP) (8-37) (0.01, 0.1, 1.0, and 10 mumol/L) decreased the ipsilateral afferent renal nerve activity response to renal pelvic administration of calcitonin gene-related peptide (0.26 mumol/L) in a concentration-dependent fashion (29 +/- 4%, 33 +/- 12%, 76 +/- 9% [P < .01], and 86 +/- 13% [P < .01], respectively). In the presence of renal pelvic perfusion with vehicle, an increase in ureteral pressure of 5, 10, and 20 mm Hg increased ipsilateral afferent renal nerve activity by 13 +/- 7%, 41 +/- 7% (P < .01), and 95 +/- 15% (P < .01) and contralateral urinary sodium excretion by 8 +/- 1%, 24 +/- 4%, and 42 +/- 7% (all P < .05). The ipsilateral afferent renal nerve activity and contralateral natriuretic responses to graded increases in ureteral pressure (5 to 20 mm Hg) were unaltered by renal pelvic perfusion with h-CGRP (8-37) at 1.0 and 10 mumol/L.(ABSTRACT TRUNCATED AT 250 WORDS)
在麻醉大鼠中，我们研究了降钙素基因相关肽是否激活肾盂感觉受体，如果是，肾盂降钙素基因相关肽受体的激活是否有助于对肾机械感受器刺激的肾-肾抑制反射反应。向肾盂内注射降钙素基因相关肽（0.0026、0.026、0.26和2.6 μmol/L）以浓度依赖性方式增加同侧肾传入神经活动（分别为32±14%、69±19%、93±26%和253±48%[均P<.01]）。降钙素基因相关肽引起的同侧肾传入神经活动增加与对侧尿钠排泄增加相关。降钙素基因相关肽受体拮抗剂人降钙素基因相关肽（h-CGRP）（8-37）（0.01、0.1、1.0和10 μmol/L）以浓度依赖性方式降低对肾盂注射降钙素基因相关肽（0.26 μmol/L）的同侧肾传入神经活动反应（分别为29±4%、33±12%、76±9%[P<.01]和86±13%[P<.01]）。在肾盂用溶媒灌注的情况下，输尿管压力增加5、10和20 mmHg使同侧肾传入神经活动增加13±7%、41±7%（P<.01）和95±15%（P<.01），使对侧尿钠排泄增加8±1%、24±4%和42±7%（均P<.05）。用1.0和10 μmol/L的h-CGRP（8-37）进行肾盂灌注未改变对输尿管压力分级增加（5至20 mmHg）的同侧肾传入神经活动和对侧利钠反应。（摘要截短于250字）
