Bilaterally adrenalectomized female SPF Wistar rats were given tap water containing various concentrations of sodium chloride to drink ad lib. After a survival period of 14 days the animals were killed by perfusion-fixation. Their brains were removed, fixed in picric acid formalin solution and embedded in Paraplast. Serial sections of median eminence and hypophysial posterior lobe were cut and stained with crotonaldehyde-fuchsine. In the stained sections the amount of CRF-granules visible in the external zone of the median eminence, and the amount of "classical" neurosecretory material (NSM) occuring in the internal zone of the median eminence and in the posterior lobe of the hypophysis were estimated. After administration of drinking solutions to which 0%-1% sodium chloride were added, the amount of CRF-gr anules increased with increasing NaCL uptake, whereas the amount of "classical" NSM was not changed. Application of tap water containing 2% NaCl led to a marked decrease in the amount of "classical" NSM but did only slightly impair the amount of CRF-granules. From the findings it is concluded that 1. following bilateral adrenalectomy administration of sodium chloride inhibits the secretion of CRF-granules; 2. CRF-granules and "classical" NSM, although histochemical identical, have different functional significances; 3. the mechanisms regulating the secretion of CRF-granules are different from those controlling the release of "classical" NSM.

The investigations were performed on 3 groups of untreated, spontaneously hypertensive Wistar rats of the Okamoto line. All the rats in Group I developed arterial hypertension within 16 weeks of birth and 33 percent of them developed cataracts within 22 weeks. Reserpine application suppressed hypertension and cataract development in all the animals in Group II. After unilateral adrenalectomy and contralateral adrenal enucleation (Group III), hypertension and cataracts developed in both treated and untreated animals; in the former, however, blood pressure was about 10 percent higher and cataracts developed about 6 weeks earlier than in the untreated rats. These findings support the hypothesis that arterial hypertension may be involved in cataract development.