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An interrelationship between atrial natriuretic peptide (ANP) and the renin-angiotensin system has been established. Both of these hormonal systems are modulated by sodium balance. The role of the beta-adrenoceptor in the regulation of release of ANP is not clear. We therefore undertook a study to examine changes in atrial-specific granule number and plasma ANP level following beta-adrenoceptor blockade in rats on low and high sodium intakes. A low-sodium diet, as compared with a high-sodium diet, elevated right and left atrial-specific granule number (right atria 54.6 +/- 8.7 vs. 42.3 +/- 5.7; left atria 47.7 +/- 7.7 vs. 30.6 +/- 3.4 granules/unit area) and plasma renin activity (28 +/- 3.7 vs. 5.4 +/- 0.8 ng AI/ml/hr). Plasma ANP levels were lower in the low-sodium animals (98 +/- 34 vs. 345 +/- 38 pg/ml). When treated with the nonspecific beta-adrenoceptor blocker propranolol, the elevated plasma renin activity and atrial-specific granule number in rats on a low sodium intake were significantly less. Neither of these parameters changed in rats on a high sodium intake. Conversely, propranolol treatment resulted in lower plasma ANP levels in rats with high sodium intake. The already-suppressed plasma ANP level in rats on a low-sodium diet was unaltered with beta-adrenoceptor blockade. The results suggest that dietary sodium intake is an important determinant of the response of atrial-specific granule number and plasma ANP levels following beta-adrenoceptor blockade with propranolol.

Since previous studies have shown that an active pineal gland exerts an inhibitory effect on circulating levels of thyroxin in the Syrian hamster, a study was conducted to determine whether the histology and ultrastructure of the thyroid gland supported the conclusions drawn from the hormone data. The ultrastructure of thyroid glands of blinded male Syrian hamsters was compared to that of intact controls kept under a 14L/10D photoperiod, to that of blinded hamsters also pinealectomized, and to that of blinded hamsters receiving 80 micrograms/ml of melatonin in the drinking water. Serum thyroxin (T4) and serum thyrotropin (TSH) concentrations were determined by radioimmunoassay. After 10 weeks serum thyroxin concentrations were less than 50% of controls and concentrations were significantly reduced. EM examination revealed that blinded hamsters had an increased number of follicular cells with flattened epithelium and nondilated endoplasmic reticulum compared to intact controls. In blinded hamsters that were pinealectomized or treated with melatonin in the drinking water, the ultrastructure of the thyroid was not different from controls and serum thyroxin concentrations were restored to near normal. These ultrastructural data support the conclusion that the pineal gland is required to obtain inhibition of the pituitary-thyroid axis in blinded hamsters and that melatonin has a counter-inhibitory effect when administered via the drinking water.

This study was aimed at developing a model in the rhesus monkey for the human gynecologic disorder termed the polycystic ovary syndrome (PCOS). The effects of chronic constant androgen exposure upon quantitative ovarian morphology and ovulatory function were examined. Twenty-five normally cycling females, aged 4-12 yr and weighing 3.3-8.2 kg, were enrolled in the study in random fashion. Seventeen animals were implanted subcutaneously (s.c.) with 10 or 25 mg testosterone-filled silastic tubing so as to maintain steady serum levels of testosterone averaging 80 ng/dl (low-dose group, n = 8) and 115 ng/dl (high-dose group, n = 9) for 13-16 months. Eight animals served as controls (sham implants); in these, mean serum testosterone levels averaged 24 ng/dl. No effect of androgen treatment was observed on ovulatory function as gauged by periodic luteal phase progesterone determinations and the presence of a fresh corpus luteum at laparoscopy. Menstrual cycle frequency (number of cycles over number of months of observation) was, however, slightly but significantly (P less than 0.05) reduced in the high-dose (88.9%) vs. the control (96.7%) and low-dose (95.0%) groups. Quantitative morphology, performed by light microscopy on a single ovary obtained from 16 of the 25 animals and read in a blinded fashion, revealed no differences in ovarian weight, capsular width and numbers, size, or proportion of healthy and atretic follicles among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of the streptozotocin rat model for diabetes has been questioned by the appearance of extrapancreatic cytotoxicity, notably renal and hepatic. In this study the model was made specific to diabetic, drug-induced, and starvation effects on parameters of testicular histology. Formulation of orthogonal contrast expressions permitted the statistical separation of these influences. Tubules from moderately diabetic animals showed frequent thinning, and premature desquamation of pachytene spermatocytes and early spermatids from the germinal epithelium. Results showed that only diabetes significantly decreased seminiferous tubule diameter and increased testicular blood vessel numbers. In addition, significant alteration from the control pattern of tubule stage distribution was noted, particularly at stages IX-XI. Due to the inclusion of a drug-treated but nondiabetic group, streptozotocin itself was shown to have no significant effect on these parameters.

The ultrastructure of the fetal rat anterior pituitary gland is described at term (day 22) and during experimentally prolonged gestation (days 23, 24, 25). The latter was achieved by daily subcutaneous injections of five mg progesterone to gravid females from the twentieth through the twenty-fourth day. Using morphological criteria for classifying pituitary cells (Moriarty, '73), six different types were observed: thyrotrophs, gonadotrophs, corticotrophs, mammotrophs, somatotrophs and non-granulated cells. During prolonged gestation (days 24 and 25 only), cells designated as cor-ticotrophs revealed changes suggesting increased activity, i.e., proliferation and dilation of the endoplasmic reticulum, dilated Golgi membranes and a reduction of secretory granules. In addition, meconium staining, which is indicative of fetal distress, was also observed on days 24 and 25. The ultrastructural changes noted suggest an increase in corticotroph activity due to fetal hypoglycemia and hypoxia which are known to occur as a result of placental insufficiency during prolonged gestation (Roux et al., '64; Vorherr, '75; Thliveris, '76).

The ultrastructure of the fetal rat adrenal gland is described at full-term (day 22) and during artificially prolonged gestation (days 23, 24, 25). The latter was achieved by daily subcutaneous injections of seven mg progesterone to gravid females from the twentieth through the twenty-fourth day. Cortical and medullary cells contained well developed organelles at all stages. Nonetheless, zonation of the gland was not yet distinct. Whereas the zona glomerulosa and zona fasciculata were fairly well delineated, the zona reticularis and medulla were as yet poorly defined. The latter regions were intermingled, and thus collectively referred to as the “zona reticulo-medullaris.” During prolonged gestation (days 24 and 25 only), many cells of the zona fasciculata and zona reticulo-medullaris contained dilated smooth endoplasmic reticulum and numerous enlarged mitochondria. Enlarged mitochondria were observed also in medullary cells concurrent with a paucity of catecholamine storage granules. Moreover, meconium staining, which is indicative of fetal stress, was also observed on days 24 and 25. The ultrastructural changes observed were interpreted to be an expression of response by the fetal adrenal gland to fetal stress produced by as yet undetermined factors arising during prolonged gestation.