Studies on the neurogenic short-term control of adrenomedullary hormone synthesis

Abstract

The adrenomedullary hormone release induced by physostigmine 0.5 to I mg/kg i.p. in rats was markedly potentiated by the a-adrenergic blocking agent phentolamine. This drug combination caused a considerable elevation of adrenal dopamine, a decrease in adrenal fl-hydroxylated catecholamines and an increase in plasma cate&olamine levels. The monoexponential disappearance of dopamine aflcer treatment with a-methyttyrosine was accelerated by physostigmine plus phentolamine, which thus seem to increase the rate of dopamine synthesis considerably, presumably by activating tyrosine hydroxylase.Spinal transection at C7 caused a decrease in adrenal dopamine, an increase in fi-hydroxylated catecholamines and a decrease in plasma cate&olamine levels. Moreover, the actions of physostigmine and phentolamine described above were completely prevented. These effects are thus presumably mediated via supraspinal centers. Chlorisondamine and atropine prevented the adrenomedullary hormone release induced by physostigmine plus phentolamine but did not, or only partially, prevent the increase in adrenal dopamine.It is concluded that physostigmine plus phentolamine, like insulin, appear to stimulate a neurogenic mechanism leading to an activation of adrenomedullary tyrosine hydroxylase. This mechanism appears to operate in-* The main results of this paper were reported at the III. International Catecholamine Symposium, Strasbourg 1973 (see Carlsson et aL, 1973), journaI of Neural Transmission 35/3 t4 182 A. Carlsson and M. Lindqvist:dependently of adrenomedullary hormone release and may stimulate catechotamine synthesis even at elevated adrenal catecholamine levels, suggesting that end-product inhibition of tyrosine hydroxylase is not of major importance. The neurogenic control of adrenomedullary synthesis does not seem to involve nicotinic or muscarinic receptors in the adrenal medulla; possibly a non-cholinergic mechanism operates at this level.

Reduced Adrenal Amine Synthesis in Spontaneously Hypertensive Rats After Long‐term Treatment With Propranolol

“…The most obvious explanation for lowered catecholamine synthetic activity of adrenal medullary or sympathetic ganglion cells would be reduced impulse frequency in the sympathetic system (see e.g. SHORT COMMUNICATIONS 319 Carlsson & Lindqvist, 1974). Such an interpretation of the data is supported by the finding of Lewis & Haeusler (1975) of reduced splanchnic discharge in the conscious rabbit after intravenous propranolol administration.…”

“…SHORT COMMUNICATIONS 319 Carlsson & Lindqvist, 1974). Such an interpretation of the data is supported by the finding of Lewis & Haeusler (1975) of reduced splanchnic discharge in the conscious rabbit after intravenous propranolol administration.…”

Influence of Neonatal Hypothyroidism on Adrenal Tyrosine Hydroxylase Activation in the Young Rat

“…It seems now well established that adrenal tyrosine hydroxylase activation produces a transient increase in the dopamine content of the gland (Carlsson & Lindqvist 1974;Almgren et al 1979;Snider & Kuchel 1983). Previous results from our laboratory (Gripois et al 1987) show that hypothyroidism largely impairs the dopamine increase in the adrenals of the young rat following insulin treatment, confirming the present results.…”

Role of catecholamines and vasopressin in cardiovascular responses to bilateral dorsolateral transection of the medulla oblongata in the rat.

“…The residual moderate increase in plasma catecholamines found in CHLOtreated rats was mostly in E levels and could be attributed to only partial blockade of adrenal medullary dicharge, which is known to be relatively resistant to ganglionic blockade. 24 Although insufficient to induce significant tachycardia, the residual release of adrenomedullary catecholamines in ganglion-blocked rats restored heart rates to preganglion blockade levels and could have contributed, in part, to the pressor response evoked by DMK-cut. In addition to the enhanced sympathomedullary discharge, DMK-cut may interrupt neural connections from the dorsal vagal nucleus and therefore diminish parasympathetic outflow.…”