Seymour A A, Marsh E A, Mazack E K, Stabilito I I, Blaine E H
Hypertension. 1985 May-Jun;7(3 Pt 2):I35-42. doi: 10.1161/01.hyp.7.3_pt_2.i35.
Synthetic atrial natriuretic factor (Arg-Arg-Ser-Ser-Cys-Phe-Gly-Gly-Arg-Ile-Asp-Arg-Ile-Gly-Ala-Gln-Ser-Gly -Leu- Gly-Cys-Asn-Ser-Phe-Arg-Tyr-COOH [disulfide bond between cysteines]) was infused intravenously into conscious normotensive and deoxycorticosterone, one-kidney, one-clip, and two-kidney, one-clip hypertensive rats. Mean arterial pressure, urine volume, and electrolyte excretion rates were measured during a 20-minute infusion of a single dose (ranging from 0-1520 pmol/min) into each animal; 95 to 380 pmol/minute of synthetic atrial natriuretic factor maximally reduced mean arterial pressure by -20 +/- 4, -29 +/- 2, and -39 +/- 7 mm Hg in normotensive, one-kidney, one-clip, and two-kidney, one-clip hypertensive rats, respectively. In deoxycorticosterone rats, a dose of 760 pmol/minute was required to produce the largest depressor response (-58 +/- 12 mm Hg). Sodium excretion increased to 8.8 +/- 2.5 muEq/minute at 760 pmol/minute in normotensive rats, to 6.5 +/- 1.1 muEq/minute at 50 pmol/minute in deoxycorticosterone rats, and to 5.8 +/- 1.5 muEq/minute at 95 pmol/minute in one-kidney, one-clip animals. The natriuretic effect was consistently greater at all doses of synthetic atrial natriuretic factor in the two-kidney, one-clip hypertensive model, in which the maximum response was 15.3 +/- 4.7 muEq/minute at 190 pmol/minute. The changes in urine volume and excretion rates of potassium and chloride tended to parallel the increases in sodium excretion in each model. Interestingly, the maximally effective hypotensive dose of synthetic atrial natriuretic factor was different from the maximally effective natriuretic dose in all four groups.(ABSTRACT TRUNCATED AT 250 WORDS)
将合成心房利钠因子(精氨酸 - 精氨酸 - 丝氨酸 - 丝氨酸 - 半胱氨酸 - 苯丙氨酸 - 甘氨酸 - 甘氨酸 - 精氨酸 - 异亮氨酸 - 天冬氨酸 - 精氨酸 - 异亮氨酸 - 甘氨酸 - 丙氨酸 - 谷氨酰胺 - 丝氨酸 - 甘氨酸 - 亮氨酸 - 甘氨酸 - 半胱氨酸 - 天冬酰胺 - 丝氨酸 - 苯丙氨酸 - 精氨酸 - 酪氨酸 - 羧基 [半胱氨酸之间存在二硫键])静脉注射到清醒的正常血压大鼠以及脱氧皮质酮、单肾单夹和双肾单夹高血压大鼠体内。在向每只动物静脉注射单剂量(范围为0 - 1520皮摩尔/分钟)持续20分钟的过程中,测量平均动脉压、尿量和电解质排泄率;在正常血压、单肾单夹和双肾单夹高血压大鼠中,95至380皮摩尔/分钟的合成心房利钠因子分别使平均动脉压最大降低 - 20±4、 - 29±2和 - 39±7毫米汞柱。在脱氧皮质酮大鼠中,需要760皮摩尔/分钟的剂量才能产生最大降压反应( - 58±12毫米汞柱)。在正常血压大鼠中,760皮摩尔/分钟时钠排泄增加到8.8±2.5微当量/分钟,在脱氧皮质酮大鼠中,50皮摩尔/分钟时增加到6.5±1.1微当量/分钟,在单肾单夹动物中,95皮摩尔/分钟时增加到5.8±1.5微当量/分钟。在双肾单夹高血压模型中,在所有合成心房利钠因子剂量下,利钠作用始终更大,在190皮摩尔/分钟时最大反应为15.3±4.7微当量/分钟。在每个模型中,尿量以及钾和氯排泄率的变化往往与钠排泄的增加平行。有趣的是,在所有四组中,合成心房利钠因子的最大有效降压剂量与最大有效利钠剂量不同。(摘要截短于250字)