Lichardus B, Veress A T, Field L J, Sonnenberg H
Department of Physiology, University of Toronto, Canada.
Physiol Res. 1994;43(3):145-50.
Transgenic mice overexpressing a transthyretin promoter-ANF structural fusion gene have a life-long reduction in arterial blood pressure compared to nontransgenic littermates. The present study was designed to test the hypothesis that the high plasma level of ANF in the transgenic mice inhibits the renin-angiotensin and/or vasopressin systems, thereby causing the hypotension. Mice were anaesthetized with Inactin and arterial pressure and heart rate were monitored before and during Saralasin infusion and vasopressin V1 receptor blockade. Effectiveness of the blockade was determined by injection of angiotensin and vasopressin before and during Saralasin and V1 receptor antagonist administration. Saralasin was associated with hypotension in both transgenic and nontransgenic mice. The decrease in blood pressure was proportionally greater in the transgenic animals. Vasopressin receptor blockade had little effect on blood pressure in either group. Heart rates were not different between the groups during any maneuver. We conclude that the chronic hypotensive effect of ANF overproduction does not involve the inhibition of either renin-angiotensin or vasopressin systems. The data, however, suggest that the renin-angiotensin system may be stimulated in the ANF-transgenic mice.
与非转基因同窝小鼠相比，过度表达转甲状腺素蛋白启动子 - 心钠素结构融合基因的转基因小鼠动脉血压终生降低。本研究旨在验证以下假设：转基因小鼠中的心钠素高血浆水平抑制肾素 - 血管紧张素和/或血管升压素系统，从而导致低血压。用安泰酮麻醉小鼠，并在输注沙拉新和阻断血管升压素V1受体之前及期间监测动脉血压和心率。通过在输注沙拉新和给予V1受体拮抗剂之前及期间注射血管紧张素和血管升压素，来确定阻断的有效性。沙拉新在转基因和非转基因小鼠中均与低血压相关。转基因动物的血压下降幅度相对更大。血管升压素受体阻断对两组小鼠的血压影响很小。在任何操作过程中，两组小鼠的心率均无差异。我们得出结论，心钠素过量产生的慢性降压作用并不涉及对肾素 - 血管紧张素或血管升压素系统的抑制。然而，数据表明肾素 - 血管紧张素系统在ANF转基因小鼠中可能受到刺激。
