• Publications
  • Influence
Evidence that central dopamine receptors modulate sympathetic neuronal activity to the adrenal medulla to alter glucoregulatory mechanisms
TLDR
The data demonstrate that apomorphine interacts with central DA receptors located in the hindbrain to activate sympathetic neuronal activity to the adrenal gland which subsequently releases epinephrine to alter homeostasis of glucose. Expand
Separation of phenytoin and its metabolites by high-performance liquid chromatography.
TLDR
The method is suitable for the quantitative analysis of 14 C-DPH and its metabolites in biological samples and identification of radioactive metabolites eluting from the HPLC column was performed using HPLC, GC-MS, and chemical procedures. Expand
Metabolism and disposition of cyproheptadine and desmethylcyproheptadine in pregnant and fetal rats.
TLDR
It was found that fetally administered CPH was not demethylated and, instead, epoxidated to form cyproheptadine-10,11-epoxide (CPH-epoxy). Expand
Dopamine analog-induced hyperglycemia in rats: involvement of the adrenal medulla and the endocrine pancreas.
TLDR
The following synthetic, structural analogs of dopamine were examined for their ability to produce hyperglycemia in conscious unrestrained rats: APO, RDS-127, di-n-propyldopamine, 2-dimethylamino-6,7-dihydroxytetralin, lergotrile, pergolide, bromocriptine and d-amphetamine. Expand
Phenytoin metabolism in mice.
TLDR
The constant ratio of p-HPPH/DHD excreted in urine suggests that these metabolites have a common precursor, probably an arene oxide, and the catechol metabolite of DPH arises via two different mechanisms. Expand
Evidence that drug metabolites are involved in cyproheptadine-induced loss of pancreatic insulin.
TLDR
It was found that SKF-525A pretreatment significantly protected rats from the insulin loss induced by CPH; SKF -525A alone had no effect on pancreatic insulin. Expand
Susceptibility of fetal rat endocrine pancreas to the diabetogenic action of cyproheptadine.
TLDR
Results indicate that cyproheptadine, when given to pregnant rats using a dose which produces no apparent effects in the maternal endocrine pancreas, causes abnormalities in the function of the insulin-secreting B cells in the fetal endocrine Pancreas. Expand
Inhibition of Insulin Release from Rat Pancreatic Islets by Drugs that Are Analogues of Dopamine
TLDR
Data show that selective dopamine agonists, such as RDS-127, reduce glucose-stimulated insulin release indirectly through adrenal medullary secretions, whereas the effect of less selective agonism directly inhibit the release of insulin from the endocrine pancreas. Expand
Alterations in Rat Pancreatic B-Cell Function Induced by Prenatal Exposure to Cyproheptadine
TLDR
The results are the first to demonstrate that postnatal pancreatic B-cell function can be selectively altered by prenatal exposure to an exogenous chemical. Expand
Cyproheptadine metabolites inhibit proinsulin and insulin biosynthesis and insulin release in isolated rat pancreatic islets
TLDR
The observation that CPH metabolites have higher potency than CPH to inhibit (pro)insulin synthesis, when considered with published reports on the disposition of the drug in rats, indicate that C PH metabolites, particularly DMCPH-epoxide, are primarily responsible for the insulin depletion observed when the parent compound is given to fetal and adult animals. Expand
...
1
2
...