Share L, Crofton J T
Fed Proc. 1984 Jan;43(1):103-6.
There is evidence for an increased secretion of vasopressin in most models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension, one- and two-kidney renal hypertension, partial nephrectomy-salt hypertension, the spontaneously hypertensive rat (SHR), the Dahl salt-sensitive rat on a high-salt diet, and human essential hypertension. In most forms of hypertension, there is also an increased pressor responsiveness to vasopressin as well as to other pressor agents. Blockade of vasopressin with either a competitive antagonist or a specific antiserum lowered blood pressure substantially in DOC-salt hypertension, two-kidney, one-clip hypertension, the stroke-prone SHR with well-established hypertension, and the Dahl S rat treated with captopril. In rats with diabetes insipidus, one- and two-kidney renal hypertension, but not DOC-salt hypertension, can be produced. There is evidence that vasopressin can contribute to some models of hypertension as either a pressor or an antidiuretic agent.
有证据表明,在大多数高血压模型中,抗利尿激素的分泌会增加,例如脱氧皮质酮(DOC)-盐性高血压、单肾和双肾肾性高血压、部分肾切除-盐性高血压、自发性高血压大鼠(SHR)、高盐饮食的Dahl盐敏感大鼠以及人类原发性高血压。在大多数高血压类型中,对抗利尿激素以及其他升压剂的升压反应性也会增强。使用竞争性拮抗剂或特异性抗血清阻断抗利尿激素,可使DOC-盐性高血压、双肾单夹高血压、已患严重高血压的易中风SHR以及用卡托普利治疗的Dahl S大鼠的血压大幅降低。在患有尿崩症的大鼠中,可以产生单肾和双肾肾性高血压,但不能产生DOC-盐性高血压。有证据表明,抗利尿激素作为一种升压剂或抗利尿剂,可导致某些高血压模型的形成。