Limas C, Limas C J, Ragan D, Freis E D
Lab Invest. 1976 Jun;34(6):606-10.
Renomedullary interstitial cells (RIC) are known to synthesize and release prostaglandins which may play a significant role in the development or severity of hypertension. The medulla of the spontaneously hypertensive rat contains RIC which are morphologically very similar to those previously described in the normotensive rat. The granularity of the RIC, however, was increased in the spontaneously hypertensive rat compared to normotensive Wistars (9.6 +/- 2.34 versus 5.3 +/- 2.05 granules per cell, respectively, p less than 0.001) or treated spontaneously hypertensive rats (7.2 +/- 1.65 granules per cell, p less than 0.001). Granule counts also increased in the presence of mild and moderate degrees of renal arteriolar sclerosis, but decreased in long standing hypertension with more severe and extensive lesions involving both arteries and arterioles. These results are consistent with the hypothesis that the RIC respond to an elevation of blood pressure in the spontaneously hypertensive rats by increased release of antihypertensive substances. In addition, the decrease in granularity of the RIC in the presence of extensive renal arteriolar and arterial damage suggests reduced ability to compensate for the elevated blood pressure and thus may contribute to the acceleration of hypertension.
肾髓质间质细胞（RIC）已知可合成并释放前列腺素，这些前列腺素可能在高血压的发生或严重程度中起重要作用。自发性高血压大鼠的髓质含有RIC，其形态与先前在正常血压大鼠中描述的非常相似。然而，与正常血压的Wistar大鼠相比，自发性高血压大鼠的RIC颗粒度增加（分别为每个细胞9.6±2.34个颗粒与5.3±2.05个颗粒，p<0.001），或与经治疗的自发性高血压大鼠相比（每个细胞7.2±1.65个颗粒，p<0.001）。在轻度和中度肾小动脉硬化存在时颗粒计数也增加，但在长期高血压且伴有更严重和广泛的累及动脉和小动脉的病变时颗粒计数减少。这些结果与以下假设一致，即自发性高血压大鼠中的RIC通过增加释放抗高血压物质来应对血压升高。此外，在广泛的肾小动脉和动脉损伤存在时RIC颗粒度的降低表明其补偿血压升高的能力降低，因此可能导致高血压的加速发展。
