肾恶性和自发性高血压大鼠肾小球冷冻切片中的心房钠尿肽受体。

M Marin-Grez, C Grigelat, P Heinz-Erian, J M Heim, H G Klein
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摘要

在“恶性”高血压大鼠(2K-1C)和自发性高血压大鼠(PHR)的肾小球冷冻切片中检测anp受体的亲和力(KD)和容量(Bmax)。血浆ANP浓度在2K-1C组(P < 0.05)和PHR组(P < 0.02)均高于对照组(P < 0.05), rANP99-126和ANP103-123的KD和Bmax无显著差异。ANP介导的2K-1C大鼠cGAMP释放也未受影响。ANP-C肾小球受体(即与ANP103-123结合的示踪剂的移位)在“恶性”高血压和PHR大鼠的任何一个肾脏中都没有下调,并且具有不变的肽结合亲和力。rANP99-126的Bmax与rANP103-123的Bmax (ANP-A受体结合)的差异表明,剪切肾中ANP-A受体适度上调,而对侧肾中2K-1C的下调(2K-1C,右vs左,P < 0.05)。由于[ANP]pl以及ANP的Bmax和KD在两种高血压模型中相似,[ANP]pl/ANP受体系统的变化不能完全解释“恶性”高血压大鼠明显的尿钠现象。
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Atrial-natriuretic-peptide receptors in glomerular cryosections of renal malignant and spontaneously hypertensive rats.

ANP-receptors affinities (KD) and capacities (Bmax) were assayed in cryosections of glomeruli from 'malignant' hypertensive rats (2K-1C) and spontaneously hypertensive rats (PHR). Plasma ANP concentration was twofold higher in 2K-1C (P < 0.05) and PHR (P < 0.02) than in the respective controls, KD and Bmax for rANP99-126 and ANP103-123 did not differ. ANP mediated cGAMP release in 2K-1C rats was also unaffected. ANP-C glomerular receptors (i.e. displacement of tracer binding with ANP103-123) were not down-regulated and had unchanged peptide binding affinity in either kidney of rats with 'malignant' hypertension and in PHR. The difference between Bmax for rANP99-126 and Bmax for rANP103-123 (ANP-A receptor binding) indicates moderate up-regulation of ANP-A receptors in the clipped, and down-regulation in the contralateral kidney of 2K-1C (2K-1C, right vs. left, P < 0.05). Since [ANP]pl, and also Bmax and KD for ANP were similar in both hypertension models investigated, changes of the [ANP]pl/ANP-receptor system can not completely explain the marked natriuresis of rats with 'malignant' hypertension.

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