Biogenic Amine‐Stimulated Cyclic Adenosine‐3′,5′‐Monophosphate Formation in the Rat Carotid Body

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Abstract
The s.c. injection of isoprenaline, salbutamol, histamine and adrenaline [epinephrine] to rats, which were subsequently killed by microwave irradiation, resulted in a rapid increase in the cAMP content of the carotid body. On the other hand, noradrenaline [norepinephrine], dopamine, adenosine and 5-hydroxytryptamine, at doses at least 100 times greater than that of isoprenaline, did not significantly alter the cyclic nucleotide content in vivo. The response to isoprenaline was dose related, with an ED50 of 15 .mu.g .cntdot. kg-1, and reached a peak level 1-1.5 min after injection. Incubation of intact carotid bodies with isoprenaline (10-5 M) in vitro also resulted in a 10-fold increase in cAMP content. The in vivo response to isoprenaline could be blocked stereo-selectively by propranolol and ICI 118.551 [erythro-DL-1-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol], a .beta.2-selective antagonist, blocks the isoprenaline-elicited increase in cAMP completely at a dose of 30 .mu.g .cntdot. kg-1; whereas betaxolol, a .beta.1-selective antagonist, was ineffective, even at a dose of 300 .mu.g .cntdot. kg-1. Hypoxia (5% O2 in 95% N2) did not result in a significant increase in the cAMP content, nor did it significantly alter the isoprenaline-stimulated increase in the cAMP content of the rat carotid body. Some catecholamines may stimulate cAMP formation by interacting with a .beta.2-adrenoceptor in the rat carotid body.