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首页> 外文期刊>American Journal of Physiology >B-type natriuretic peptide 8-32, which is produced from mature BNP 1-32 by the metalloprotease meprin A, has reduced bioactivity.
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B-type natriuretic peptide 8-32, which is produced from mature BNP 1-32 by the metalloprotease meprin A, has reduced bioactivity.

机译：B型利钠肽肽8-32是由金属蛋白酶meprin A从成熟的BNP 1-32中产生的，具有降低的生物活性。

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摘要

32-amino acid B-type natriuretic peptide (BNP 1-32) plays an important role in cardiovascular homeostasis. Recently, it was reported that BNP 1-32 is cleaved by the metalloprotease meprin A to BNP 8-32, the bioactivity of which is undefined. We hypothesized that BNP 8-32 has reduced vasodilating and natriuretic bioactivity compared with BNP 1-32 in vivo. Human BNP 8-32 and BNP 1-32 were compared in a crossover study in eight anesthetized normal canines. After a preinfusion clearance, BNP 1-32 was infused at 30 ng.kg(-1) x min(-1) for 45 min followed by a 60-min washout and a second preinfusion clearance. Then, equimolar BNP 8-32 was infused. In half of the studies, the peptide sequence was reversed. Changes with peptides from the respective preinfusion clearance to infusion clearance were compared with paired tests. Mean arterial pressure was reduced by both BNP 8-32 and BNP 1-32 (-8 +/- 3 vs. -6 +/- 2 mmHg, P = 0.48). Changes in right atrial pressure, pulmonary capillary wedge pressure, heart rate, cardiac output, and glomerular filtration rate were similar. However, urinary sodium excretion increased less with BNP 8-32 than with BNP 1-32 (+171 +/- 24 vs. +433 +/- 43 muEq/min; P = 0.008), as did urinary potassium excretion, urine flow, and renal blood flow. While BNP 8-32 has similar vasodilating actions as BNP 1-32, its diuretic and natriuretic actions are reduced, suggesting a role for meprin A in the regulation of BNP 1-32 bioactivity in the kidney. Meprin A inhibition may be a potential strategy to increase the bioactivity of endogenous and exogenous BNP 1-32 in cardiovascular diseases.
机译：32个氨基酸的B型利钠尿肽（BNP 1-32）在心血管稳态中起重要作用。近来，有报道称金属蛋白酶甲氧戊酸蛋白酶A将BNP 1-32裂解为BNP 8-32，其生物活性尚不确定。我们假设与体内BNP 1-32相比，BNP 8-32降低了血管舒张和利钠生物活性。在一项交叉研究中比较了八种麻醉的正常犬的人BNP 8-32和BNP 1-32。输注前清除后，以30 ng.kg（-1）x min（-1）注入BNP 1-32 45分钟，然后冲洗60分钟并进行第二次输注前清除。然后，注入等摩尔的BNP 8-32。在一半的研究中，肽序列被颠倒了。将肽从相应的输注前清除率到输注清除率的变化与配对测试进行了比较。 BNP 8-32和BNP 1-32均降低了平均动脉压（-8 +/- 3 vs. -6 +/- 2 mmHg，P = 0.48）。右心房压力，肺毛细血管楔压，心率，心输出量和肾小球滤过率的变化相似。然而，BNP 8-32的尿钠排泄增加少于BNP 1-32（+171 +/- 24 vs. +433 +/- 43 muEq / min; P = 0.008），尿钾排泄，尿流增加和肾血流量。尽管BNP 8-32具有与BNP 1-32相似的血管舒张作用，但其利尿和利钠作用却有所降低，这表明美普林A在调节肾脏中BNP 1-32生物活性方面发挥了作用。 Meprin A抑制可能是增加内源性和外源性BNP 1-32在心血管疾病中的生物活性的潜在策略。

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