The effects of insulin and cortisol on saturated phosphatidylcholine synthesis are examined in fetal type II cell cultures and in mixed cell cultures containing type II cells and fibroblasts. In 19-day fetal rat lung type II cell cultures, 100 nM cortisol and 2 nM insulin have no significant effect. Fibroblast-pneumonocyte factor results in enhanced saturated phosphatidylcholine synthesis by fetal type II cells. The significant stimulatory effect of cortisol in mixed-cell cultures is abolished in the presence of insulin or of monoclonal antibodies to fibroblast-pneumonocyte factor. Incubation of type II cells with conditioned media from fibroblasts exposed to cortisol results in increased saturated phosphatidylcholine synthesis. This process is not stimulated when type II cells are incubated with conditioned media from fibroblasts exposed to insulin and cortisol (or to insulin alone). These observations demonstrate that insulin inhibits cortisol induction of lung maturation and suggest that this antagonism results from an inhibitory effect of insulin on the elaboration of fibroblast-pneumonocyte factor by fetal lung fibroblasts.
The non‐selective NOS inhibitor L‐NAME has been shown to reduce cholinergic‐mediated sweating in humans. We tested the hypothesis that the effect of NOS inhibition on sweat gland out is mediated through the ability of NO to activate KCa1.1 channels. We generated stimulus response curves using: lactated‐Ringers, 50 mM TEA, 20 mM L‐NAME and a cocktail of 50 mM TEA plus 20 mM L‐NAME (n=10). Local sweat rate (SR) was measured by passing dry gas through a small sweat capsule mounted on the skin. The skin was stimulated at a constant current intensity of 2.5 mA for 30 s at frequencies of 0.2, 1, 2, 4, 6, 8, 12, 16, 32, and 64 Hz using two small stainless‐steel stimulating electrodes. We plotted the area under the SR‐time curve versus stimulus frequency. All data were expressed as the area under the local SR‐time curve (AUC) and normalize to the peak AUC response during Saline control trials (% AUC peak). During Ringers perfusion, peak local sweat output averaged 99.6 ± 5.7 AUC % peak which was significantly (p<0.0001) reduced by application of 50 mM TEA to 61.7 ± 22.7 AUC %peak. Addition of 20 mM L‐NAME to the 50 mM TEA solution produced an additional 20% reduction in peak SR to 42.5 ± 21.1 %AUC peak (p <0.05). These data support the hypothesis that sudomotor control of sweat gland activity is modulated by the presence of TEA sensitive K+ channels and the activity of an intrinsic NOS enzyme in the epithelial cells of the human sweat glands. Further, the ability of L‐NAME to produce an additional reduction in peak SR following 50 mM TEA indicates that the influence of NOS on local SR is not likely mediated via a modulation of TEA sensitive K+ channels.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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