RENAL MICROPUNCTURE STUDY OF NORMOTENSIVE AND MILAN HYPERTENSIVE RATS BEFORE AND AFTER DEVELOPMENT OF HYPERTENSION
RENAL MICROPUNCTURE STUDY OF NORMOTENSIVE AND MILAN HYPERTENSIVE RATS BEFORE AND AFTER DEVELOPMENT OF HYPERTENSION
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DOI：
10.1038/ki.1978.68
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发表时间：
1978-01-01
影响因子：
19.6
通讯作者：
BIANCHI, G
中科院分区：
文献类型：
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作者：
BAER, PG;BIANCHI, G
早期对肾移植和钠代谢的研究表明，米兰品系遗传性高血压大鼠（MHS）的高血压原因是肾功能改变。为了确定活性因子，使用显微穿刺研究了3个不同年龄的正常（NR）和MHS大鼠的肾功能的几个指标：A）26至30天，在高血压发展之前（pre-MHS）; B）35至40天;和C）75至90天，在高血压发展之后。在A组中，前MHS大鼠的单个肾单位滤过率[SNFR]和近端肾小管液体向远端肾单位的输送较NR明显降低。C组MHS大鼠的上述值明显高于NR组。仅在C组中，MHS大鼠的肾小球显著少于NR大鼠。在A组中，MHS大鼠的GFR [肾小球滤过率]低于NR大鼠。在C组中，不再有任何显著差异。在MAP [平均血压]相等的情况下，除A组SNFR在MHS中显著较低外，所有组的SNFR均相等。MHS大鼠的GP [肾小球毛细血管压]显著高于NR大鼠（A组，+5.2 mmHg; C组，+6.7 mmHg）。在预MHS大鼠中，麻醉显著增加了两个品系之间的血压差（P < 0.001）。在成年MHS大鼠中未观察到这种效应。这可能会增加MHS前和NR之间的GP差异。MHS大鼠的传入有效滤过压（EFPA）值也较高（A组为+2.9 mmHg，C组为+6.8 mmHg），但麻醉的影响可能再次解释了MHS前和NR之间的差异。在成年MHS和NR大鼠中，全身动脉压的绝对差异中只有22%传递到肾小球毛细血管，而在年轻大鼠中传递了33%的差异。这些值表明肾小球导水率降低。MHS大鼠发生高血压的主要原因可能是SNFR降低。
Earlier studies of renal transplantation and of sodium metabolism indicated that the cause of high blood pressure in the Milan strain of genetically hypertensive rats (MHS) was altered renal function. To pinpoint the active factors, micropuncture was used to study several indices of renal function in normal (NR) and MHS rats at 3 different ages: A) 26 to 30 days, before development of hypertension (pre-MHS); B) 35 to 40 days; and C) 75 to 90 days, after the development of hypertension. In group A, the pre-MHS rats had significantly lower values for single nephron filtration rate [SNFR] and late proximal tubular fluid delivery to the distal nephron than did the NR. In group C, the values in the MHS rats were significantly higher than those of the NR. In group C only, the MHS rats had significantly fewer glomeruli than did the NR rats. In group A, the GFR [glomerular filtration rate] of the MHS rats was lower than that of the NR rats. In group C, there was no longer any significant difference. At equal MAP [mean blood pressure], SNFR was equal in all the groups, except group A, where SNFR was significantly lower in MHS. GP [glomerular capillary pressure] was significantly higher in MHS rats than in NR rats (group A, +5.2 mm Hg; group C, +6.7 mm Hg). In the pre-MHS rats, anesthesia significantly increased (P < 0.001) the blood pressure difference between the 2 strains. This effect was not seen in the adult MHS rats. This may increase the differences in GP between pre-MHS and NR. Afferent effective filtration pressure (EFPA) values were also higher in MHS rats (+2.9 mm Hg in group A, +6.8 mm Hg in group C), but once again the effects of anesthesia probably account for the differences in magnitude seen between pre-MHS and NR. Only 22% of the absolute differences in systemic arterial pressure in the adult MHS and NR rats was transmitted to the glomerular capillary, while 33% of the difference was transmitted in the younger rats. These values suggest a reduced glomerular hydraulic conductivity. The primary cause of development of hypertension in the MHS rats may be a decrease in SNFR.