An atrial peptide is a potent renal vasodilator substance.
An atrial peptide is a potent renal vasodilator substance.
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心房肽是一种有效的肾血管扩张物质。
作者：
T. Oshima;M. Currie;D. Geller;P. Needleman
大鼠心房提取物的肾动脉内给药在麻醉大鼠中激发浓度依赖性肾血管舒张（不依赖于前列腺素或多巴胺释放）。心房浸提液不会改变骨骼肌组织（后肢）血管阻力或全身动脉血压。通过凝胶过滤获得的心房提取物的高分子量肽级分仅在蛋白水解活化后（体外）或在静脉内（即，全身性体内活化）给药。心房提取物的低分子量肽级分作为肾血管扩张剂在动脉内有活性，已被进一步纯化以产生两种主要肽。21个氨基酸的肽，命名为心房肽I，以前被证明是利钠的，并放松肠道，但不是血管平滑肌条。这种肽对肾阻力的动脉内作用很小或没有作用。由23个氨基酸组成的肽（心房肽I的苯丙氨酸-精氨酸C末端延伸），命名为心房肽II，在肠和血管条上具有利钠和痉挛作用（体外），并且在体内是一种有效的肾血管扩张剂。因此，心脏心房提取物中存在的肾血管舒张活性似乎来源于选择性产生23个氨基酸的肽，心房肽素II的蛋白水解过程。随着苯丙氨酸-精氨酸C-末端的丢失而进一步裂解，如心房肽素I所发生的，显著抑制肾血管舒张。
Renal intra-arterial administration of rat atrial extracts elicits a concentration dependent renal vasodilation (independent of prostaglandin or dopamine release) in anesthetized rats. The atrial extracts do not alter skeletal musculature (hindlimb) vascular resistance or systemic arterial blood pressure. The high molecular weight peptide fraction of atrial extracts obtained by gel filtration, reduces renal resistance intra-arterially only after proteolytic activation (in vitro) or following intravenous (i.e., systemic in vivo activation) administration. The low molecular weight peptide fraction of the atrial extract which is active intra-arterially as a renal vasodilator has been further purified to yield two major peptides. The 21 amino acid peptide, designated atriopeptin I, was previously demonstrated to be natriuretic and to relax intestinal but not vascular smooth muscle strips. This peptide exerted little or no intra-arterial effect on renal resistance. The 23 amino acid peptide (the phenylalanine-arginine C terminal extension of atriopeptin I), designated atriopeptin II, was natriuretic and spasmolytic (in vitro) on both intestinal and vascular strips and was a potent renal vasodilator in vivo. Thus, the renal vasodilator activity present in cardiac atrial extracts appears to derive from a proteolytic process which selectively generates the 23 amino acid peptide, atriopeptin II. Further cleavage with the loss of phenylalanine-arginine C-terminal, as occurs with atriopeptin I, markedly suppresses the renal vasodilation.