Autonomic control mechanisms in the brush possum (Trichosorus vulpecula).

The autonomic influences on some organ systems in the possum (Trichosurus vulpecula) have been studied. The work has also included aspects of possible mechanisms for the modulation of autonomic function by endogenous prostaglandins and lipids. Noradrenaline has been identified by pharmacological methods. The chemical method used was not sensitive enough to identify noradrenaline positively in the splenic tissue and in the venous effluent of the electrically stimulated spleen. Support for noradrenaline being the neurotransmitter at sympathetic nerve endings comes from indirect evidence. Phenoxybenzamine blocks the effect of sympathetic nerve stimulation in the hind limb vascular bed. Phentolamine blocks the contracture of the nictitating membrane when the preganglionic nerve is stimulated and it also blocks part of the effect induced by sympathetic nerve stimulation of the possum gut. Propranolol blocks a component of the reflex changes in heart rate induced by a variety of methods. Less direct support for noradrenaline being the adrenergic transmitter is supplied from the findings that adrenoceptors exist in a number of isolated tissues. Application of exogenous noradrenaline produces contracture of the nictitating membrane, an increased rate and force of beating of the isolated heart, a decreased blood flow in the skeletal muscle and skin of the hind limb and a reduced amplitude and tone of the spontaneously active isolated gut. The identity of the adrenoceptors has been determined by using specific pharmacological blocking agents. The receptors in the nictitating membrane and the skin are ˜í¬±-adrenoceptors because they are blocked by phenoxybenzamine or phentolamine. The receptors in the heart are ˜í‚â§-receptors because they are blocked by propranolol. Both ˜í¬±- and ˜í‚â§-adrenoceptors exist in skeletal muscle vessels, because both ˜í¬±- and ˜í‚â§-antagonists are necessary to block the effects of intra-arterial adrenaline. The possum gut reacts to catecholamines in a qualitatively similar way to the guinea pig and rabbit guts. A mixed ˜í¬± and ˜í‚⧠block, produced by the simultaneous use of phentolamine and propranolol, is necessary to inhibit the response from adrenaline, noradrenaline and isoprenaline on the possum gut. In the hind limb vascular bed maximal decrease in blood flow is achieved by sympathetic stimulation at frequencies of 15-20 Hz. At frequencies 40-100 Hz there is'a reduced response which indicates an inhibitory mechanism acting rapidly to prevent excessive sympathetic outflow at higher frequencies. Compared with the cat and dog there is a relatively small amount of noradrenaline released when the sympathetic splenic nerves of the possum are electrically stimulated. This may be due to the modulating influence of a large plasma concentration of prostaglandin F 2a . Prostaglandin E2 which is released when the splenic nerve is stimulated may also be a component for reducing noradrenaline overflow. As well as prostaglandins in the possum plasma there is also an unstable phospholipid with vasoconstrictor properties, but its function is unknown. 14 C arachidonate studies indicate that there may be some biosynthetic relationship between arachidonic acid, prostaglandins and the unknown phospholipid. There is indirect support for the role of acetylcholine as a transmitter substance in the possum. Atropine blocks the effects of exogenous acetylcholine on the isolated heart and the isolated intestine, and also blocks a component of the reflex changes in heart rate induced by different methods. Acetylcholine appears to be the transmitter at the superior cervical ganglion. The ganglion is stimulated by close arterial injection of acetylcholine and nicotine and these effects and those of preganglionic stimulation are blocked by hexamethonium. There are no sympathetic cholinergic vasodilator fibres to the possum hind limb. However, the hind limb vascular bed dilates under the influence of intra-arterial acetylcholine and the response is blocked by atropine. It appears therefore that the muscarine receptors in the hind limb are not innervated. They are about 1/5 as sensitive to acetylcholine as comparable tissue in the cat. Possible mechanisms are discussed for the \playing dead\" reaction and for the relatively poor noradrenaline overflow when sympathetic nerves are stimulated."