Pharmacologic analysis of positive chronotropic and inotropic responses to octopamine.

Chiba, Shigetoshi

doi:10.1620/tjem.118.247

Cited by 4 publications

(1 citation statement)

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“…The stimulatory effects of noradrenaline and adrenaline on progesterone production and the ability of the ß-adrenergic antagonist propranolol to inhibit this response is consistent with previous results (Condon & Black, 1976;Jordan et al, 1978;Harwood et al, 1980;Ratner et ai, 1980;Norjavaara et al, 1982). In other mammalian tissues octopamine has been reported to interact with a-and ß-adrenergic receptors (Fujiwara, Keisuke, Hideo, Takashi & Yoshiko, 1968), exclusively with areceptors (Kelly & Burks, 1974;Kleinrok, 1979) or exclusively with ß-adrenergic receptors (Chiba, 1976). The ability of propranolol but not phentolamine to inhibit the steroidogenic response to octopamine, synephrine and deoxyadrenaline suggests that their action is mediated by ß-adrenergic receptors.…”

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confidence: 88%

A role for alternative pathway catecholamines in the regulation of steroidogenesis in cow luteal cells

Battista¹,

Condon²

1986

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Summary. Incubation of bovine luteal cells with the alternative pathway catecholamines octopamine, synephrine and deoxyadrenaline at concentrations of 10 \ m=-\ 6 to 10\m=-\3 m enhanced the production of progesterone (P < 0\m=.\05).Tryamine did not alter basal progesterone production (P > 0\m=.\05). Addition of noradrenaline and adrenaline at concentrations of 10 \ m=-\ 4 to 10\m=-\7 m significantly elevated the production of progesterone (P < 0\m=.\05). The steroidogenic response to noradrenaline and adrenaline was greater than that for octopamine, synephrine and deoxyadrenaline (P < 0\m=.\05).Response to both primary (10\m=-\6 m) and alternative (10\m=-\4 m) pathway catecholamines was inhibited by propranolol (10\m=-\5m, P < 0\m=.\05) but not phentolamine (10\m=-\5m, P > 0\m=.\05). These results demonstrate that octopamine, synephrine and deoxyadrenaline can affect steroidogenesis by bovine luteal cells, and their action is mediated by \g=b\-adrenergicreceptors.

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