Abstract
Sodium nitroprusside (SNP) has been reported to be a potent stimulator of cGMP formation in different tissues, including pancreatic islets. The present study aimed at comparing the effects of sodium nitroprusside and dibutyryl cGMP on 86Rb outflow, 45Ca outflow, short-term 45Ca uptake, cytosolic Ca 2+ concentration and insulin release from rat pancreatic islet cells. The data indicate that cGMP potentiates whilst SNP inhibits the glucose-induced insulin release. This inhibitory effect appears to be mediated by the activation of ATP-sensitive K + channels leading to a decrease in Ca 2+ influx and subsequent reduction in cytosolic free Ca 2+ concentration. Whathever the exact mechanism(s) underlying the capacity of sodium nitroprusside to enhance the K + permeability of the B-cell membrane, the drug appears to be an unadequate pharmacological tool to characterize the involvement of cGMP in the insulin secretory process. The experimental results also suggest that cGMP potentiates glucose-induced insulin release without affecting ionic movements.
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Schedule a callMore From: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
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