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心房利钠肽的细胞生物学

Cell biology of atrial natriuretic peptide.

作者信息

Huot C, Tremblay J, Hamet P

机构信息

Clinical Research Institute of Montreal, Canada.

出版信息

Blood Vessels. 1991;28(1-3):84-92. doi: 10.1159/000158847.

DOI:10.1159/000158847
PMID:1848128
Abstract

Atrial natriuretic peptide (ANP) exhibits a wide spectrum of cardiovascular, endocrine, metabolic and renal actions. cGMP is the major mediator of ANP at the cellular level and only tissues possessing particulate guanylate cyclase appear to present ANP-induced actions. Three types of ANP receptors have recently been cloned. Two of them (A and B receptors) are homologous and contain guanylate cyclase catalytic domains. The C receptor could possibly regulate the metabolic fate of ANP. Data obtained by the radiation inactivation method suggest the presence of an inter- or intramolecular inhibitory component of nearly 90 kilodaltons that represses the catalytic activity of guanylate cyclase within its membrane environment. The mechanism of guanylate cyclase stimulation by ANP could involve this inhibitory component. Preliminary data suggest that the hyperresponsiveness of the particulate guanylate cyclase/cGMP system in hypertension occurs through modulation of the inhibitory component.

摘要

心房利钠肽(ANP)具有广泛的心血管、内分泌、代谢和肾脏作用。环磷酸鸟苷(cGMP)是ANP在细胞水平的主要介质,只有具有颗粒型鸟苷酸环化酶的组织似乎才会出现ANP诱导的作用。最近克隆出了三种类型的ANP受体。其中两种(A和B受体)是同源的,含有鸟苷酸环化酶催化结构域。C受体可能调节ANP的代谢命运。通过辐射失活法获得的数据表明,存在一种近90千道尔顿的分子间或分子内抑制成分,该成分在膜环境中抑制鸟苷酸环化酶的催化活性。ANP刺激鸟苷酸环化酶的机制可能涉及这种抑制成分。初步数据表明,高血压中颗粒型鸟苷酸环化酶/cGMP系统的高反应性是通过抑制成分的调节而发生的。

相似文献

1
Cell biology of atrial natriuretic peptide.心房利钠肽的细胞生物学
Blood Vessels. 1991;28(1-3):84-92. doi: 10.1159/000158847.
2
Increased cyclic guanosine monophosphate production and overexpression of atrial natriuretic peptide A-receptor mRNA in spontaneously hypertensive rats.自发性高血压大鼠中环磷酸鸟苷生成增加及心钠素A受体mRNA过表达
J Clin Invest. 1993 Nov;92(5):2499-508. doi: 10.1172/JCI116858.
3
The protein kinase domain of the ANP receptor is required for signaling.
Science. 1989 Sep 22;245(4924):1392-4. doi: 10.1126/science.2571188.
4
Differential activation by atrial and brain natriuretic peptides of two different receptor guanylate cyclases.心房钠尿肽和脑钠尿肽对两种不同受体鸟苷酸环化酶的差异激活作用。
Nature. 1989 Sep 7;341(6237):68-72. doi: 10.1038/341068a0.
5
Characterization of the functional domains of the natriuretic peptide receptor/guanylate cyclase by radiation inactivation.利用辐射失活法对利钠肽受体/鸟苷酸环化酶功能结构域的表征
J Biol Chem. 1991 May 5;266(13):8171-5.
6
Inhibition of atrial natriuretic peptide-induced cyclic GMP accumulation in the bovine endothelial cells with anti-atrial natriuretic peptide receptor antiserum.用抗心钠素受体抗血清抑制牛内皮细胞中心钠素诱导的环鸟苷酸积累。
J Biol Chem. 1989 Jan 5;264(1):641-5.
7
Vascular natriuretic peptide receptor-linked particulate guanylate cyclases are modulated by nitric oxide-cyclic GMP signalling.血管钠尿肽受体相关颗粒型鸟苷酸环化酶受一氧化氮-环鸟苷酸信号通路调节。
Br J Pharmacol. 2003 Aug;139(7):1289-96. doi: 10.1038/sj.bjp.0705365.
8
Atrial natriuretic factor receptor heterogeneity and stimulation of particulate guanylate cyclase and cyclic GMP accumulation.心房利钠因子受体的异质性以及对颗粒型鸟苷酸环化酶和环鸟苷酸积累的刺激作用。
Endocrinol Metab Clin North Am. 1987 Mar;16(1):79-105.
9
Stimulation of atrial natriuretic peptide receptor/guanylyl cyclase- A signaling pathway antagonizes the activation of protein kinase C-alpha in murine Leydig cells.刺激心房利钠肽受体/鸟苷酸环化酶-A信号通路可拮抗小鼠睾丸间质细胞中蛋白激酶C-α的激活。
Biochim Biophys Acta. 1997 Apr 24;1356(2):221-8. doi: 10.1016/s0167-4889(96)00168-1.
10
cGMP-mediated inhibition of TNF-alpha production by the atrial natriuretic peptide in murine macrophages.环磷酸鸟苷(cGMP)介导的心房利钠肽对小鼠巨噬细胞肿瘤坏死因子-α(TNF-α)产生的抑制作用
J Immunol. 2000 Jul 1;165(1):175-81. doi: 10.4049/jimmunol.165.1.175.

引用本文的文献

1
Increased cyclic guanosine monophosphate production and overexpression of atrial natriuretic peptide A-receptor mRNA in spontaneously hypertensive rats.自发性高血压大鼠中环磷酸鸟苷生成增加及心钠素A受体mRNA过表达
J Clin Invest. 1993 Nov;92(5):2499-508. doi: 10.1172/JCI116858.
2
Volume status influences atrial peptide-induced water conductivity changes in leopard frog mesenteric capillaries.容量状态影响豹蛙肠系膜毛细血管中心房肽诱导的水传导率变化。
J Physiol. 1992 Feb;447:33-47. doi: 10.1113/jphysiol.1992.sp018989.