Weber P C, Scherer B, Siess W, Held E, Schnermann J
Klin Wochenschr. 1979 Oct 1;57(19):1021-9. doi: 10.1007/BF01479987.
The kidney has a high capacity to produce a spectrum of different acting prostaglandins (PG). In vivo and in vitro studies have shown that renal formation of PG's, possibly in the vasculature of the cortex represents an essential step in the mechanisms regulating the secretion of renin. PG's formed in the cortex seem to participate also in the control of renal vascular resistance and glomerular filtration rate. PGE2 formed in the medulla modulates the hydroosmotic action of antidiuretic hormone and influences the kidney's capacity for urine concentration. Renal PG formation is reduced by high NaCl intake and enhanced by low NaCl intake and in hypokalemic states. These findings make renal PG's good candidates for participation in the regulation of salt and water balance and in the control of blood pressure. Due to the close connection with the renin angiotensin system, alterations in renal PG formation might be involved in the etiology of high and low renin states. Thus, an impairment in the renal cortical production of vasodilating and renin-stimulating PG's could constitute the common denominator for both the reduced renin secretion and the increased vascular resistance which have been reported to be associated in essential hypertension.
肾脏具有产生一系列不同作用的前列腺素(PG)的强大能力。体内和体外研究表明,肾脏中PG的生成,可能在皮质的血管系统中,是调节肾素分泌机制中的关键步骤。皮质中生成的PG似乎也参与肾血管阻力和肾小球滤过率的控制。髓质中生成的PGE2调节抗利尿激素的水渗透作用,并影响肾脏的尿液浓缩能力。高盐摄入会降低肾脏PG的生成,而低盐摄入和低钾血症状态则会增强其生成。这些发现使肾脏PG成为参与盐和水平衡调节以及血压控制的良好候选者。由于与肾素-血管紧张素系统密切相关,肾脏PG生成的改变可能与高肾素和低肾素状态的病因有关。因此,肾脏皮质中血管舒张和肾素刺激PG生成的受损可能是原发性高血压中肾素分泌减少和血管阻力增加相关报道的共同特征。