Two different biophases for adrenaline released by electrical stimulation or tyramine from the sympathetic nerve endings of the dog saphenous vein.
To study the distribution of alpha- and beta-adrenoceptors dog saphenous vein strips were electrically stimulated (2ms, 30 V, 0.25--20 Hz). The strips either had spontaneous tone (contraction experiments) or were contracted by 0.28 microM prostaglandin F2 alpha in the presence of 7 microM phentolamine (relaxation experiments). In strips without preloading or in strips preloaded with (--)-noradrenaline alpha-adrenoceptor-mediated excitatory responses were readily evoked (contraction experiments) but not beta-adrenoceptor-mediated inhibitory responses (relaxation experiments). In strips preloaded with (--)-adrenaline both alpha-(contraction experiments) and beta-effects (relaxation experiments were readily elicited by electrical stimulation and by tyramine. Thus, strips preloaded with (--)-adrenaline were used to compare alpha- with beta-effects. In these strips the latency between the beginning of the electrical stimulation and the onset of the response was longer for beta- than for alpha-responses. The same applies to responses to exogenous (--)-adrenaline. However, the ratio "latency for beta-/latency for alpha-responses" was 3.6 +/- 0.2 (n = 8) for responses to electrical stimulation and 1.8 +/- 0.1 (n = 12) for responses to (--)-adrenaline (P less than 0.001). Cocaine (12 microM) enhanced the alpha-effect elicited by electrical stimulation 2.8 +/- 0.2 (n = 7) times but did not change the beta-effect, whereas U-0521 (50 microM) enhanced the beta-effect 3.4 +/- 0.2 (n = 8) times without changing the alpha-effect. In strips preloaded with (--)-adrenaline also tyramine caused concentration-dependent beta-responses (relaxation experiments). The concentration of phentolamine and prazosin required to inhibit contractions caused by electrical stimulation were about 5--7 times higher than those required to inhibit contractions caused by exogenous adrenaline or noradrenaline, whereas propranolol was equipotent in reducing beta-responses to adrenaline released by electrical stimulation and to exogenous adrenaline. Our results strongly support the view that alpha-adrenoceptors are in close contract with the nerve endings and beta-adrenoceptors are in close proximity of COMT in a vessel with the nerve endings evenly distributed throughout the media.
D000818:Animals; D002394:Catechol O-Methyltransferase / Q000378:metabolism; D004285:Dogs; D004558:Electric Stimulation; D004837:Epinephrine / Q000378:metabolism*; D066298:In Vitro Techniques; D009411:Nerve Endings / Q000378:metabolism*; D011941:Receptors, Adrenergic / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D012501:Saphenous Vein / Q000294:innervation; D013564:Sympathetic Nervous System / Q000378:metabolism* / Q000502:physiology; D014439:Tyramine / Q000494:pharmacology*
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D002394:Catechol O-Methyltransferase; D014439:Tyramine; D004837:Epinephrine