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血管加压素与大鼠恶性脱氧皮质酮高血压

Vasopressin and malignant deoxycorticosterone hypertension in rats.

作者信息

Möhring J, Möhring B, Petri M, Haack D

出版信息

Clin Sci Mol Med Suppl. 1976 Dec;3:45s-48s. doi: 10.1042/cs051045s.

Abstract
  1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.
摘要
  1. 研究了精氨酸加压素在大鼠恶性脱氧皮质酮(DOC)高血压发病机制中的作用。2. 在患有恶性DOC高血压的大鼠中,容量耗竭和血清渗透压升高后,血浆精氨酸加压素浓度增加了十倍以上。3. 注射精氨酸加压素特异性抗体血清可使患有恶性DOC高血压的大鼠血压显著下降,而注射血管紧张素II抗血清则不影响血压。4. 在表现为良性病程的DOC高血压大鼠中,与正常血压对照大鼠相比,精氨酸加压素的血浆浓度增加了两倍;注射精氨酸加压素抗血清可导致血压显著但小幅下降。5. 得出结论,在恶性DOC高血压的发病机制中,精氨酸加压素可能发挥肾素-血管紧张素系统在恶性肾性高血压发病机制中所起的作用。

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