Stimulation of cyclic GMP accumulation by sodium nitroprusside is potentiated via a Gs mechanism in intact pinealocytes
| Autor: | Beatrix H. White, David C. Klein |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Nitroprusside
medicine.medical_specialty Cholera Toxin Gs alpha subunit Adrenergic receptor Vasoactive intestinal peptide Stimulation medicine.disease_cause Biochemistry Pineal Gland Pinealocyte Cellular and Molecular Neuroscience chemistry.chemical_compound GTP-Binding Proteins Internal medicine medicine Animals Cyclic GMP Cells Cultured Forskolin Cholera toxin Colforsin Adrenergic beta-Agonists Rats Receptors Adrenergic Endocrinology chemistry Sodium nitroprusside Adrenergic alpha-Agonists medicine.drug |
| Zdroj: | Journal of neurochemistry. 64(2) |
| ISSN: | 0022-3042 |
| Popis: | Cyclic GMP accumulation in pinealocytes is elevated > 100-fold by norepinephrine (NE) through a mechanism involving conjoint activation of alpha 1- and beta 1-adrenergic receptors. Little or no stimulation occurs if either alpha 1- or beta 1-adrenergic receptors alone are activated. It appears that alpha 1-adrenergic effects are mediated by Ca2+ acting in part through nitric oxide (NO), and beta 1-adrenergic effects are mediated by Gs. In the study presented here we investigated effects of adrenergic agonists or related postreceptor-active agents on stimulation of pineal cyclic GMP accumulation by the NO generator sodium nitroprusside (NP). The cyclic GMP response to NP (1 mM) was potentiated by NE and isoproterenol (ISO) but not by phenylephrine, indicating that activation of beta 1-adrenergic receptors potentiates the effects of NP. Similarly, vasoactive intestinal peptide (VIP), cholera toxin (CTX), and forskolin, all of which are known to mimic the effects of ISO in this system, also potentiated the effects of NP. In contrast, neither dibutyryl cyclic AMP nor agents that elevate intracellular Ca2+ levels caused marked potentiation of the effects of NP on pineal cyclic GMP. Depletion (90%) of Gs alpha by 21-h treatment with CTX reduced beta-adrenergic potentiation of NP. These findings indicate that beta-adrenergic agonists and VIP potentiate the effects of NP through a mechanism involving Gs. The molecular basis of this action may be an increase in guanylyl cyclase responsiveness to NO. |
| Databáze: | OpenAIRE |
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