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Temperate and boreal mammals undergo seasonal changes in pelage that facilitate thermoregulation in winter and summer. We investigated photoperiodic influences on pelage characteristics of male Siberian and Syrian hamsters. Fur density (mg fur/cm2 skin) was measured by weighing the shavings of fur patches removed from the dorsal and ventral surfaces of hamsters maintained in long days (LDs) or transferred to short days (SDs). Patches were reshaved 3 wk later to assess fur regrowth (mg regrown fur/cm2 skin). Fur density was greater in SD than in LD Siberian hamsters after 11 wk of differential phototreatment. The onset of increased fur density in SDs was accompanied by a transient increase in fur regrowth (11-14 wk on the dorsal surface and 7-10 and 11-14 wk on the ventral surface), suggestive of a seasonal molting process. Fur density, body mass, and pelage color of Siberian hamsters returned to values characteristic of LD males after a similar duration of prolonged (>27 wk) SD treatment and appear to be regulated by a similar or common interval-timing mechanism. In Syrian hamsters, dorsal fur density, fur regrowth, and hair lengths were greater in SD than in LD males. Castration increased and testosterone (T) treatment decreased dorsal and ventral fur regrowth in LD and SD hamsters, but the effects of T manipulations on fur density were limited to a decrease in dorsal fur density after T treatment. Decreased circulating T in SDs likely contributes to the seasonal molt of male hamsters by increasing the rate of fur growth during the transition to the winter pelage.

The effects of neuropeptide Y (NPY) and norepinephrine (NE) on the secretion of human tracheal gland (HTG) cells in culture were examined using the bronchial inhibitor (BrI) as a secretory marker. NPY by itself provoked no change in secretion, neither in intracellular Ca2+ nor in adenosine 3',5'-cyclic monophosphate (cAMP) levels. NE induced transient intracellular Ca2+ mobilization and an increase of intracellular cAMP and also, as previously described, a short-time concentration-dependent decrease of BrI secreted by HTG cells. When applied together on HTG cells, NPY and NE induced an increase of intracellular cAMP, a discrete sustained increase of basal intracellular Ca2+, and a long-lasting inhibition of secretion. Our data suggest that NPY acts for human tracheal gland cells as a NE neuromodulator rather than as a neurotransmitter. Thus culture of HTG cells appears to be an interesting pharmacological support for studying inhibition of bronchial secretion and could be applied in the study of pathologies where hypersecretion is observed, such as cystic fibrosis.

Proglumide, a glutaramic acid derivative, inhibits the acid secretory effects of gastrin and is said to be a specific gastrin receptor blocking agent. In the current study we have shown that proglumide inhibits the binding of gastrin to its receptor in rat oxyntic gland mucosa and tested whether this receptor is also responsible for the trophic effect of gastrin. In the first study 400 mg/kg proglumide injected with 250 micrograms/kg pentagastrin every 8 h for 48 h totally prevented the trophic effects of pentagastrin in rat oxyntic gland mucosa. Parameters measured included DNA synthesis and DNA, RNA, and protein content. In a second study the lowest maximally effective dose of proglumide was determined to be 100 mg/kg. The trophic effect of pentagastrin was inhibited in duodenal mucosa, colonic mucosa, and pancreas as well as oxyntic gland mucosa. These data demonstrate that proglumide blocks the trophic action of exogenous gastrin and suggest that the trophic effect of gastrin is mediated by the gastrin receptor.

Parenchymal cells of exocrine glands have been reported to develop numerous large vacuoles when intensely stimulated either pharmacologically, electrically, or physiologically. We have found that tracheal submucosal glands of the cat form similar vacuoles in response to alpha-adrenergic stimulation. Light and electron microscope examination of tracheal submucosal glands stimulated in vitro with methoxamine (10(-4) M) reveals that only serous cells of the gland acini develop vacuoles. Ductal cells and mucous acinar cells do not form vacuoles. Furthermore, several lines of evidence indicate that within serous cells vacuoles arise from secretory granules, which apparently swell as they accumulate fluid during intense stimulation. The following paper describes some of the factors and characteristics of stimulus-induced vacuolation.

Several factors affecting the stimulus-induced vacuolation in cat tracheal submucosal glands described in a companion paper [Am. J. Physiol. 241 (Cell Physiol. 10): C18-C24, 1981] were examined. Stimulation with predominantly alpha-adrenergic, beta-adrenergic, and cholinergic agonists at various concentrations and in the presence of appropriate blockers showed that alpha-adrenergic or cholinergic stimulation is more effective in inducing vacuolation than beta-adrenergic stimulation. In addition, Ca- or HCO3- deficient incubation medium or low incubation temperature either blocked or significantly decreased the vacuolation response. Stimulation in the presence of the Na-K-ATPase inhibitor ouabain prevented vacuolation. The known roles of these factors in fluid transport are consistent with the possibility that stimulus-induced vacuolation possibly arises in response to disturbances in cytoplasmic fluid, which are induced in the secretory cell when the fluid component of secretion is intensely stimulated. A model is presented that possibly relates the observed responses to intracellular event and suggests the possibility of ion pumps in the apical membrane.

This review describes the various types of sebaceous glands, their locations, and where possible their different functions. All sebaceous glands are similar in structure and secrete sebum by a holocrine process. However, the nature of this secretion and the regulation of the secretory process seem to differ among the various types of glands. Methods for measuring sebum secretion and assessing sebaceous gland activity are also described. The area of major interest during the last 20 years has undoubtedly been the mechanisms that control sebaceous gland function. Most studies have focused on the endocrine control and in particular on the role of androgens and pituitary hormones, although evidence suggests that nonendocrine factors may also be important. However, many questions remain and during the next few years attention will certainly be given to the role of retinoids and their mode of action in the treatment of acne.

In this study we report on isoproterenol-induced changes in short-circuit current (SCC) that are located in the glands of the frog skin. Following complete inhibition of the SCC with amiloride (10(-4) M), the addition of isoproterenol (9.0 X 10(-7) M) to the serosal side of the skin elicits a significant increase in SCC from 0.6 +/- 0.1 to 3.9 +/- 0.5 microA/cm2 (p less than 0.001). The conductance is doubled, and both effects are blocked completely with the beta-blocking agent propranolol. In the split-skin preparation, in which no glands are present, there is no current response to isoproterenol following amiloride. This indicates that the amiloride-insensitive isoproterenol-stimulated SCC resides in the glands. In the intact skin, removal of sodium (choline replacement) from the serosal (but not the mucosal) medium abolishes this current change. The postisoproterenol current change in amiloride-inhibited skins is also dependent on the presence of chloride in the serosal bath. Preincubation of the amiloride-inhibited skin with ouabain (10(-4) M) for 10 min prior to the addition of isoproterenol reduces the isoproterenol response by 50%. These results indicate that there is a sodium- and chloride-dependent ouabain-sensitive secretory mechanism in the skin glands of the frog that is responsible for the development of the isoproterenol-stimulated SCC observed in the presence of amiloride.