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急性输注血管加压素对正常血压和去氧皮质酮盐高血压大鼠血压及血浆血管紧张素II的影响。

Effect of acute vasopressin infusion on blood pressure and plasma angiotensin II in normotensive and DOCA-salt hypertensive rats.

作者信息

Morton J J, Garcia del Rio C, Hughes M J

出版信息

Clin Sci (Lond). 1982 Feb;62(2):143-9. doi: 10.1042/cs0620143.

Abstract
  1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min(-1) kg(-1) for 1 hr into normal, sham-operated and DOCA-salt hypertensive rats. Complete vasopressin/blood pressure dose-response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA-salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 +/- SD 3.7 fmol/ml) than either the normal (3.9 +/- 2.3, P less than 0.01) or the sham-operated rats (4.5 +/- 2.4, P less than 0.01). 3. The DOCA-salt hypertensive rats did not have my detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min(-1) kg(1), when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22-23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA- salt hypertensive rats (10.5 +/- 2.3, 14.5 +/- 4.5 and 8.0 +/- 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA-salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA-salt hypertension may contribute to the suppression of renin and angiotensin II in this state.
摘要
  1. 向正常大鼠、假手术大鼠和去氧皮质酮盐性高血压大鼠静脉输注精氨酸加压素,剂量分别为0.5、2、6、18或54 ng·min⁻¹·kg⁻¹,持续1小时。根据每次输注结束时测得的循环血浆加压素浓度,构建完整的加压素/血压剂量反应曲线。2. 去氧皮质酮盐性高血压大鼠的基础血浆加压素浓度(11.1±标准差3.7 fmol/ml)高于正常大鼠(3.9±2.3,P<0.01)和假手术大鼠(4.5±2.4,P<0.01)。3. 与两个正常血压组相比,去氧皮质酮盐性高血压大鼠的升压敏感性未发现明显增强。4. 正常大鼠和假手术大鼠在加压素输注剂量达到2 ng·min⁻¹·kg⁻¹(此时血浆浓度在30至40 fmol/ml之间)之前,血压无显著升高。5. 在正常大鼠和假手术大鼠中输注低于升压剂量的加压素,使血浆浓度达到22 - 23 fmol/ml,可将血浆血管紧张素II完全抑制至与去氧皮质酮盐性高血压大鼠基础值相似的水平(分别为10.5±2.3、14.5±4.5和8.0±1.6 fmol/ml)。6. 这些发现表明,加压素参与去氧皮质酮盐性高血压的机制尚不清楚;加压素浓度的短期变化似乎对正常血压调节不重要;正常大鼠中加压素的微小生理变化可能对肾素分泌调节很重要;去氧皮质酮盐性高血压中所见的加压素浓度升高可能导致该状态下肾素和血管紧张素II的抑制。

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