The goal of the present investigation was to determine in the squirrel monkey the source and pattern of inhibin, a hormone known to effect reproductive steroid levels via pituitary and ovarian mechanisms. Since this seasonally polyestrous species is known to have elevated serum levels of reproductive steroids compared to other primates, the levels of ovarian alpha subunit mRNA expression and serum total alpha inhibin, estradiol, progesterone, and luteinizing hormone were measured and compared to human levels. Expression of the alpha subunit was robust in monkey luteal tissue compared to expression in human luteal tissue. Squirrel monkey serum inhibin peaked 4 days after the luteinizing hormone surge and correlated with progesterone changes. These luteal serum levels of inhibin were greater than 12 times higher than the human levels yet bio-LH activities were less than in the human during the luteal phase. Inhibin concentrations during the nonbreeding season were generally half the levels measured in the breeding season and undetectable in ovariectomized animals. However, exogenous FSH stimulation induced a marked rise in inhibin, which correlated with an estradiol rise. In conclusion, abundant alpha inhibin subunit expression in the luteal ovary of the squirrel monkey and loss of serum delectability in ovariectomized animals indicates that the principle source of inhibin in the squirrel monkey is the ovary. Elevated serum inhibin levels during the luteal phase concurrent with ovulatory-size follicular development is unique among species studied thus far. Possible simultaneous inhibin production from both follicular and luteal tissue may be responsible for the exceptionally high inhibin levels.

The goal of the present investigation was to determine in the squirrel monkey the source and pattern of inhibin, a hormone known to effect reproductive steroid levels via pituitary and ovarian mechanisms. Since this seasonally polyestrous species is known to have elevated serum levels of reproductive steroids compared to other primates, the levels of ovarian alpha subunit mRNA expression and serum total alpha inhibin, estradiol, progesterone, and luteinizing hormone were measured and compared to human levels. Expression of the alpha subunit was robust in monkey luteal tissue compared to expression in human luteal tissue. Squirrel monkey serum inhibin peaked 4 days after the luteinizing hormone surge and correlated with progesterone changes. These luteal serum levels of inhibin were greater than 12 times higher than the human levels yet bio‐LH activities were less than in the human during the luteal phase. Inhibin concentrations during the non‐breeding season were generally half the levels measured in the breeding season and undetectable in ovariectomized animals. However, exogenous FSH stimulation induced a marked rise in inhibin, which correlated with an estradiol rise. In conclusion, abundant alpha inhibin subunit expression in the luteal ovary of the squirrel monkey and loss of serum delectability in ovariectomized animals indicates that the principle source of inhibin in the squirrel monkey is the ovary. Elevated serum inhibin levels during the luteal phase concurrent with ovulatory‐size follicular development is unique among species studied thus far. Possible simultaneous inhibin production from both follicular and luteal tissue may be responsible for the exceptionally high inhibin levels. Am. J. Primatol. 47:165–179, 1999. © 1999 Wiley‐Liss, Inc.

Introduction:The esophageal submucosal glands (SMG) in humans and several other mammalian species secrete bicarbonate and mucins into the esophageal lumen. These secretions contribute to esophageal defense against refluxed gastric acid. We recently demonstrated HCO3 Ϫ secretion in the SMG-bearing pig esophagus and showed that it could be stimulated approximately two-folds by carbachol. Bicarbonate secretion was blocked by removal of HCO3 Ϫ from the serosal bath and by treatment with DIDS, a nonselective anion transport inhibitor. We have also identified by immunohistochemistry the presence of carbonic anhydrase (CA) II, and of Na + -(HCO3 Ϫ )n and Cl Ϫ /HCO3 Ϫ transporters in the glandular cells. To investigate further the cellular mechanisms of HCO3 Ϫ secretion in SMG, we studied its dependence on Cl Ϫ and the role of CA. Methods: Pig esophagi were stripped of their muscularis propria, keeping the mucosa and submucosal glands intact. The esophagi were cannulated, mounted, and bathed in a chamber, which allowed independent perfusion of the esophageal lumen. Bicarbonate secretion was measured by using a recirculated unbuffered saline solution into the lumen and pH stat technique. Results: Mean basal bicarbonate secretion was 0.11 Ϯ 0.01 µEq/cm 2 /hour (n = 5). Removal of serosal Cl Ϫ abolished HCO3 Ϫ secretion within ~ 60 minutes (0.018 Ϯ 0.01 µEq/cm 2 /hour). Subsequent addition of carbachol in the absence of Cl Ϫ did not stimulate HCO3 Ϫ secretion. The membrane permeable CA inhibitor methazolamide (0.2 mM) added serosally completely inhibited basal and carbachol stimulated HCO3 Ϫ secretion. The impermeant CA inhibitor benzolamide (0.01 mM) partially inhibited HCO3 Ϫ secretion from 0.07 Ϯ 0.005 to 0.05 Ϯ 0.01 µEq/cm 2 /hour, which was not further stimulated by carbachol. Conclusions: HCO3 Ϫ secretion is mediated by carbonic anhydrase dependent mechanism(s). Intracellular and extracellular CA are involved in this process. Transport mechanisms responsible for HCO3 Ϫ secretion are dependent on the presence of Cl Ϫ .