Evidence for Functionally Distinct Subpopulations of Steroidogenic Cells in the Domestic Turkey (Meleagris gallopavo) Adrenal Gland

A body of histological and functional evidence supports the hypothesis that there are functionally distinct subpopulations of steroidogenic cells comprising the avian adrenal gland. In the present study, we tested this hypothesis by evaluating the steroidogenic responses of density-dependent subpopulations of adrenal steroidogenic cells isolated from domestic turkeys fed either a high-normal (control) sodium diet (0.4% Na+) or a Na+-restricted diet (0.04% Na+) for 8 days, the latter to stimulate the activity or appearance of possible zona glomerulos-like cells. Subpopulations were visually yet reproducibly determined by their density-dependent separation on a continuous density gradient of Percoll (45%). The subpopulations were arbitarily ascribed as being either low-density or high-density adrenal steroidogenic cells [LDAC (ρ = 1.0585 g/ml) and HDAC (ρ = 10590-1.0720 g/ml), respectively]. LDAC and HDAC comprised 95.2 and 4.8%, respectively, of the total number of adrenal steroidogenic cells isolated. The LDAC was further subdivided into three visually distinct subpopulations. The functional differences between the LDAC subpopulations is discussed but was less dramatic than the functional distinction between the HDAC subpopulation and the pooled LDAC subpopulations. Basal aldosterone production values between control LDAC and HDAC were equivalent. In addition, there were no differences in maximal aldosterone production between control LDAC and HDAC in response to [Ile5]angiotensin II (AII), the avian equivalent, [Val5]AII, K+ (as KCl), and that supported by exogenous corticosterone. However, maximal aldosterone production in response to human ACTH-(1-39)(ACTH) of the LDAC was 32% greater than that of the HDAC. NA+ restriction enhanced basal aldosterone production of the LDAC by 84% over the control LDAC. In addition, it enhanced maximal aldosterone production of the LDAC in response to AII peptides, K+, ACTH and that supported by corticosterone by 54, 164, 83, and 74%, respectively, over that of the control LDAC. However, Na+ restriction disproportionately enhanced basal aldosterone production of the HDAC by 348% over that of the control HDAC. In addition, with Na+ restriction, maximal aldosterone production of the HDAC. In addition, with Na+ restriction, maximal aldosteron production of the HDAC in response to AII, K+, and that supported by exogenous corticosterone was consistently greater than that of the LDAC. Moreover, with Na+ restriction, maximal aldosterone production of the HDAC in response to AII peptides and K+ was increased over that of the control HDAC to a greater extent than was maximal aldosterone production in response to ACTH and that supported by corticosterone (% enhancement over control was as follows: AII peptides, 502%; K+, 668%; ACTH, 273%; corticosterone, 183%). Thus, compared to its effect on the LDAC, Na+ restriction differentially enhanced aldosterone production by the HDAC and disproportionately enhanced the maximal aldosterone response of the HDAC to AII and K+. Na+ restriction also differentially affected the LDAC subpopulations but to a lesser extent than the HDAC subpopulation. In contrast to its effect on aldosterone production, Na+ restriction had no effect on basal corticosterone production, and if anything, decreased maximal ACTH-induced corticosterone production by the subpopulations. Collectively, these results provide additional evidence for the presence of zona glomerulosa-like cells in a galliform adrenal gland that are differentially sensitive to alterations in electrolyte homeostasis.