Adrenoreception characteristics of the neurons of the superior cervical and caudal mesenteric sympathetic ganglia of the cat]

Experiments were conducted on the supeior cervical and the caudal mesenteric sympathetic ganglia of a cat; it was shown that dophamine (DA), similarly to noradrenaline (NA) and adrenaline (A), depressed the cholinergic conduction. The activity of DA in the superior sympathetic ganglion was less than that of the NA and A 2- and 3-fold, respectively, and in the caudal mesenteric ganglia DA was 50 times more active than NA by the capacity to depress the cholinergic conduction. The effects of DA and NA in the superior cervical ganglia were eliminated by dyhydroergotamine, phentholamine and haloperidol, but not by tropaphen and chlorpormazine. In the caudal mesenteric ganglia the inhibitory effect of NA was decreased by phentholamine, dihydroergotamine and chlorpromazine, but not by haloperidol. On the contrary, haloperidol and chlorpromzine decreased the depressive effect of DA on the cholinergic conduction in the caudal mesenteric ganglion, whereas phentholamine, dihydroergotamine and deseryl proved to be ineffective. It is supposed that the manifestation of the dopaminergic mechanism of inhibition of cholinergic conduction in the caudal mesenteric sympathetic ganglion could underlie the dilatation of the mesenterial and renal vessels and its hypotensive action caused by DA.     

An anti-insulin serum, but not a glucagon antagonist, alters glycemia in fed chickens.

Attempts at altering plasma glucose and, as a consequence, food intake were performed in fed broiler chickens by single i.v. injection of des-His1(Glu9) glucagon amide (a glucagon antagonist) or a non-stimulating anti-insulin serum. Plasma glucose level was not altered by des-His1(Glu9) glucagon amide but was rapidly and largely increased (for at least 2 h) by the injection of the insulin-immune serum. Hour and cumulative food intake were unaltered up to 10 h post injection. These results strongly suggest that in fed chickens, plasma glucose is mainly, if not exclusively, controlled by plasma insulin, and that the transient and heavy hyperglycemia evoked by inhibiting insulin action does not alter food intake.