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PubMed1991

Impaired prednisolone sensitivities of the endocrine system and peripheral-blood lymphocytes are closely related to clinical incidence in renal transplantation.

Endocrine- and immune-responses to prednisolone and their relation to clinical incidence were assessed in 19 renal transplant recipients. All of the patients were treated with prednisolone and cyclosporin. Response of the hypothalamic-pituitary-adrenal (HPA) system to prednisolone was evaluated by measuring serum cortisol concentration. Cortisol concentration before transplantation was 126.7 +/- 38.6 ng mL-1, while it decreased to 4.1 +/- 2.5 ng mL-1 within the period characterized by a cumulative dose of prednisolone from 300 to 700 mg. A statistically significant high incidence (P less than 0.01) of acute rejections was observed in low HPA responders; (mean cortisol concentration during prednisolone treatment exceeded 3.0 ng mL-1), 6 of 12 with a low HPA response to prednisolone showed signs of rejection, while none of the 7 with a high HPA response showed signs of rejection. The concentrations of prednisolone suppressing the in-vitro response of pretransplant lymphocytes to concanavalin A by 50% (ID50) were determined. Lymphocytes from 8 patients were extremely insensitive (ID50 greater than 500 ng mL-1), and 5 of the 8 showed signs of rejection. Lymphocytes from the other 11 patients showed high sensitivity (ID50 less than 500 ng mL-1), and only one of those showed signs of rejection. Thus, a significantly high incidence of rejection was observed in low lymphocyte-responders to prednisolone (P less than 0.05). The results suggest that an insensitive endocrine response to prednisolone correlates with an impaired lymphocyte response to the steroid, and that both of the indices are related to occurrence of rejection. Evaluation of these pharmacodynamic parameters in combination may serve as a guideline for successful immunosuppressive therapy in renal transplantation.

Adult↗
PubMed1983

Pancreatic polypeptide: a unique model for vagal control of endocrine systems.

Pancreatic polypeptide (PP) is a hormone synthesized only in the duodenal pancreas where the PP cell is the dominating endocrine cell type. The secretion of PP is regulated by food-intake and by plasma glucose--in both cases through vagal cholinergic mechanisms. In vitro cholinergic stimulation is 4-10 times as potent as any other stimulatory mechanism, e.g. beta-adrenergic stimulation. Although other agents such as gastrointestinal hormones and neuropeptides are potent stimulators of PP secretion in vivo, their action is totally eliminated by blockade of the muscarinic receptor and in several cases also abolished by vagotomy. Furthermore, these peptides have no or only a weak effect in vitro. The stimulation of PP secretion by hypoglycemia and inhibition by hyperglycemia is mediated also through an efferent vagal mechanism. Under extreme hypoglycemia the stimulation of PP release becomes partially atropine resistant, although still totally dependent on the vagus; conceivably the release of other transmitters, like e.g. VIP, is activated under these circumstances. In the basal state, PP secretion is under oscillating cholinergic tone. Thus, the secretion of PP is unique in the way that the cholinergic, vagal stimulation is not only the most powerful stimulatory mechanism, but also the key through which other mechanisms act. PP secretion can be used, e.g. as a sensitive indicator of autonomic disorders in patients with diabetes.

Acetylcholine↗