Article date: December 1991
By: A.M. Evans, K.L. Green, in Volume 104, Issue 4, pages 787-792
The ability of the selective dopamine receptor agonists, fenoldopam and SKF38393 (D1) and quinpirole and LY163502 (D2), to mimic the effect of dopamine on cockroach salivary gland acinar cells has been investigated.
Intracellular recordings of the membrane potential established that all the agonists mimicked dopamine (i.e. they induced a hyperpolarization which was occasionally followed by a depolarization), whether applied by addition to the superfusate or locally by pressure ejection.
The rank order of potency of the agonists to induce a hyperpolarization was (equipotent molar ratio relative to dopamine in parentheses): dopamine (1) ≫ fenoldopam (1000) > SKF38393 (3500) > LY163502 (13750) > quinpirole (35000).
The agonists also elicited secretion from the salivary gland when superfused onto the preparation. SKF38393 and quinpirole did not induce the same maximum rate of secretion as dopamine. The rank order of potency of the agonists was (minimum effective concentration in parentheses): dopamine (0.03 μm) > fenoldopam (4.8 μm) > SKF38393 (40.8 μm) > quinpirole (132 μm).
Both the hyperpolarizing and secretory responses to all the agonists were antagonized by the selective D1 antagonist, (+)‐SCH23390, but not the selective D2 antagonist, (±)‐sulpiride.
These results support the idea that the same receptors mediate both the hyperpolarizing and secretory responses, and that they are similar to the mammalian D1 receptor.
The ability of the selective dopamine receptor agonists, fenoldopam and SKF38393 (D1) and quinpirole and LY163502 (D2), to mimic the effect of dopamine on cockroach salivary gland acinar cells has been investigated.
Intracellular recordings of the membrane potential established that all the agonists mimicked dopamine (i.e. they induced a hyperpolarization which was occasionally followed by a depolarization), whether applied by addition to the superfusate or locally by pressure ejection.
The rank order of potency of the agonists to induce a hyperpolarization was (equipotent molar ratio relative to dopamine in parentheses): dopamine (1) ≫ fenoldopam (1000) > SKF38393 (3500) > LY163502 (13750) > quinpirole (35000).
The agonists also elicited secretion from the salivary gland when superfused onto the preparation. SKF38393 and quinpirole did not induce the same maximum rate of secretion as dopamine. The rank order of potency of the agonists was (minimum effective concentration in parentheses): dopamine (0.03 μm) > fenoldopam (4.8 μm) > SKF38393 (40.8 μm) > quinpirole (132 μm).
Both the hyperpolarizing and secretory responses to all the agonists were antagonized by the selective D1 antagonist, (+)‐SCH23390, but not the selective D2 antagonist, (±)‐sulpiride.
These results support the idea that the same receptors mediate both the hyperpolarizing and secretory responses, and that they are similar to the mammalian D1 receptor.
DOI: 10.1111/j.1476-5381.1991.tb12507.x
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