Adrenergic control of swimbladder blood flow was analysed in blood-perfused preparations of the European eel as well as in situ by recording the changes in swimbladder blood flow and blood pressure following an injection of catecholamine into the dorsal artery. In blood-perfused swimbladder preparations, injection of the alpha-adrenergic agonist phenylephrine into the perfusion loop caused a marked dose-dependent increase in perfusion pressure at constant flow, while injection of the beta-agonist isoproterenol slightly decreased perfusion pressure. The beta-effect was not as pronounced as the alpha-adrenergic vasoconstriction and was observed only during the first application of catecholamine in each preparation. In situ injection of adrenaline (final concentration 10(-8)-10(-9) mol kg-1 body mass) into the dorsal aorta caused a dose-dependent transient increase in dorsal aortic blood pressure and in cardiac output which, after 5-10 min, returned to resting levels. Swimbladder perfusion also increased initially after an injection of adrenaline, but after about 1-2 min suddenly decreased and then slowly recovered to preinjection levels. Following the injection of adrenaline into the dorsal aorta, blood pressure changes in vessels at the swimbladder pole of the rete mirabile revealed a similar biphasic pattern with an initial increase, a subsequent decrease and a slow return to preinjection levels, while pressure in the arterial influx vessel of the rete resembled dorsal aortic pressure. After injection of the beta-blocker propranolol, adrenaline evoked a smaller initial increase in blood flow, but the subsequent reduction in flow was even more pronounced. Injection, in addition, of the alpha-adrenergic blocker phentolamine abolished the sharp adrenaline-induced decrease in swimbladder perfusion. It is concluded that alpha- and beta-adrenergically controlled resistance vessels are located close to the rete mirabile, probably at the arterial entrance into the rete. These vessels control perfusion of the rete mirabile and of the swimbladder and are thus involved in the control of gas deposition into the swimbladder.

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