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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Handa M, Kondo K, Suzuki H, Saruta T

Clin Sci (Lond). 1983 Jul;65(1):37-42. doi: 10.1042/cs0650037.

Oral administration of dexamethasone (about 2.5 X 10(-7) mol/day) caused hypertension in rats. The blood pressure rose from 108 +/- 6 (mean +/- SD) to 156 +/- 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. In this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein-kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

给大鼠口服地塞米松（约2.5×10⁻⁷摩尔/天）可导致高血压。血压在第7天从108±6（平均值±标准差）升至156±17毫米汞柱。尿量和尿钠排泄增加。血浆肾素活性和血浆醛固酮不变。然而，在整个实验过程中，前列腺素E2（UPGE2V）和激肽释放酶（Ukall.V）的尿排泄量显著降低。2. 同时给予卡托普利可部分预防血压升高。在这组大鼠中，血浆肾素活性升高，UPGE2V和Ukall.V的降低得到部分预防。3. 根据这些结果，提示除肾素 - 血管紧张素系统参与外，激肽释放酶 - 激肽系统和前列腺素系统的抑制是导致地塞米松高血压作用的因素之一。

Handa M, Kondo K, Suzuki H, Saruta T

Clin Sci (Lond). 1983 Jul;65(1):37-42. doi: 10.1042/cs0650037.

Oral administration of dexamethasone (about 2.5 X 10(-7) mol/day) caused hypertension in rats. The blood pressure rose from 108 +/- 6 (mean +/- SD) to 156 +/- 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E2 (UPGE2V) and kallikrein (Ukall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. In this group of rats, the plasma renin activity was elevated and the reductions in UPGE2V and Ukall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein-kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.

给大鼠口服地塞米松（约2.5×10⁻⁷摩尔/天）可导致高血压。血压在第7天从108±6（平均值±标准差）升至156±17毫米汞柱。尿量和尿钠排泄增加。血浆肾素活性和血浆醛固酮不变。然而，在整个实验过程中，前列腺素E2（UPGE2V）和激肽释放酶（Ukall.V）的尿排泄量显著降低。2. 同时给予卡托普利可部分预防血压升高。在这组大鼠中，血浆肾素活性升高，UPGE2V和Ukall.V的降低得到部分预防。3. 根据这些结果，提示除肾素 - 血管紧张素系统参与外，激肽释放酶 - 激肽系统和前列腺素系统的抑制是导致地塞米松高血压作用的因素之一。