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Results for “Sulfonylurea Compounds”

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At least 19 recordsLinked to original sources
PubMed1986

Effects of sulfonylurea compounds on Pneumocystis carinii.

Two sulfonylurea compounds, carbutamide and tolbutamide, were studied for efficacy against Pneumocystis carinii pneumonitis in the corticosteroid-treated rat model and compared with trimethoprim-sulfamethoxazole (TMP-SMZ). The chemical structures of these sulfonylureas are identical except that an amino group in carbutamide is replaced with a methyl group in tolbutamide. Carbutamide was totally effective in the prevention and treatment of P. carinii pneumonitis in dosages of 100 and 200 mg/kg per day. The carbutamide dosage of 50 mg/kg per day prevented the infection in 90% of animals, whereas tolbutamide in the same dosage permitted infection in 100% of animals. This study shows that carbutamide is at least as effective as TMP-SMZ in the treatment and prevention of murine P. carinii pneumonitis. The presence of an amino group in the para position on the benezene ring is a determinant for this activity.

Administration, Oral↗
PubMed1990

Divergent cardiac effects of the first and second generation hypoglycemic sulfonylurea compounds.

The effects of first and second generation hypoglycemic sulfonylureas on the incidence of ventricular ectopic beats and on the duration of transitional ventricular fibrillation in the ischemic rat heart were investigated. First generation sulfonylurea compounds (tolbutamide, carbutamide and gliclazide) in 105 preparations increased, while second generation sulfonylurea compounds (glibenclamide and glipizide) in 50 preparations decreased in a dose-dependent manner both the number of ventricular ectopic beats and the duration of transitional ventricular fibrillation during the first 30 min after ligation of the left anterior descending coronary artery. Therefore, second generation sulfonylureas should be preferred in the treatment of type 2 diabetics with ischemic heart diseases, if satisfactory metabolic control cannot be achieved by a treatment regimen and diet alone.

Animals↗
PubMed1994

Inhibition of ATP-sensitive K+ channel by a non-sulfonylurea compound KAD-1229 in a pancreatic beta-cell line, MIN 6 cell.

We studied the mechanism of action of KAD-1229, a non-sulfonylurea compound shown to stimulate insulin secretion, in a glucose responsive insulinoma cell line, MIN 6 cells. In microsomal fraction of MIN 6 cells, KAD-1229 displaced binding of [3H]glibenclamide in a concentration-dependent manner. The dissociation constant and the maximum binding capacity were 0.61 nM and 8.70 pmol/mg.protein, respectively. In inside out configuration of patch-clamp technique, KAD-1229 attenuated the opening of ATP-sensitive K+ channels. The effect of KAD-1229 was detected at 10(-8) M, and 10(-5) M KAD-1229 almost completely blocked the activity of ATP-sensitive K+ channel. When membrane potential was monitored by a perforated mode of patch clamp, KAD-1229 induced depolarization of plasma membrane, which was followed by a burst of action potentials. These action potentials were blocked by cobalt. In a fura-2-loaded single MIN 6 cell, KAD evoked an elevation of intracellular free Ca2+ concentration, [Ca2+]i. The KAD-1229-mediated elevation of [Ca2+]i was attenuated by either removal of extracellular Ca2+ or an addition of nifedipine. Finally, KAD-1229 augmented insulin secretion in MIN 6 cells in a concentration-dependent manner. KAD-1229 also enhanced the effect of glucose and nifedipine inhibited the action of KAD-1229 on insulin secretion. These results indicate that KAD-1229 stimulates insulin secretion by stimulating Ca2+ influx and that, despite the lack of sulfonylurea structure, KAD-1229 binds to sulfonylurea receptors and inhibits the activity of ATP-sensitive K+ channel in MIN 6 cells.

Action Potentials↗
PubMed1996

Sensitivity of a renal K+ channel (ROMK2) to the inhibitory sulfonylurea compound glibenclamide is enhanced by coexpression with the ATP-binding cassette transporter cystic fibrosis transmembrane regulator.

We demonstrate here that coexpression of ROMK2, an inwardly rectifying ATP-sensitive renal K+ channel (IKATP) with cystic fibrosis transmembrane regulator (CFTR) significantly enhances the sensitivity of ROMK2 to the sulfonylurea compound glibenclamide. When expressed alone, ROMK2 is relatively insensitive to glibenclamide. The interaction between ROMK2, CFTR, and glibenclamide is modulated by altering the phosphorylation state of either ROMK2, CFTR, or an associated protein, as exogenous MgATP and the catalytic subunit of protein kinase A significantly attenuate the inhibitory effect of glibenclamide on ROMK2. Thus CFTR, which has been demonstrated to interact with both Na+ and Cl- channels in airway epithelium, modulates the function of renal ROMK2 K+ channels.

Adenosine Triphosphate↗