Noradrenaline Release in Rats During Prolonged Cold‐stress and Repeated Swim‐stress

Abstract

Plasma noradrenaline concentration in rats was measured during prolonged cold‐stress and repeated swim‐stress. Cold exposure for 6 h caused a rise in plasma noradrenaline which reached a peak at 4 h. Administration of desmethylimipramine and normetanephrine to block neuronal and extraneuronal uptake of noradrenaline raised plasma noradrenaline concentration without changing the pattern of the response to cold exposure. Repeated cold exposure on subsequent days produced no change in the pattern of plasma noradrenaline concentration. Five successive 1‐min swims at 30‐min intervals caused a rise in plasma noradrenaline concentration which was maximal after the third swim. It is suggested that prolonged and repeated activation of sympathetic nerve terminals leads to a decline in noradrenaline release.

Changes in Sympathetic Nerve Terminals in the Heart of Cold‐Exposed Rats

“…The present results show that the changes in plasma noradrenaline concentration seen during cold exposure (Benedict et al, 1979) are accompanied by neurochemical changes in the sympathetic nerve terminals of the heart. These include changes in vesicular noradrenaline content, uptake, storage capacity, and DBH activity.…”

“…In rats exposed to 4°C for a period of 6 h there is first a progressive increase in plasma noradrenaline, which reaches a peak after 4 h and then declines toward control level. A similar pattern is seen when animals are exposed to repeated bouts of 1 min of swim stress interspersed with 30 min of rest; the rise in plasma noradrenaline increases during the first three successive swim sessions, and declines during the next two (Benedict et al, 1979). In a recent study a similar transient in-crease in noradrenaline release was reported during restraint stress (Konarska et al, 1989).…”

“…The concentration of noradrenaline circulating in plasma is widely used as an index of release of this neurotransmitter from sympathetic nerve terminals (Benedict et al, 1978). Using this measure, it has been shown that both physiological stress, such as cold or swimming (rats: Benedict et al, 1979), and psychological stress, such as the Stroop colour work conflict test (human subjects: Freyschuss et al, 1990) increase the release of noradrenaline in the periphery. This increase is not sustained, however.…”

An investigation of the role of adrenergic innervation in the regulation of the extraneuronal uptake of [3H]‐isoprenaline into rat vasa deferentia and atria

“…It has been found previously (Leduc, 1961a,b;Benedict et al, 1979) that chronic cold exposure results in a rapid (24 h) increase in noradrenaline excretion. Noradrenaline excretion then declines slowly, although it remains elevated after one month.…”

Autonomic neuropathy in transgenic mice caused by immunotoxin targeting of the peripheral nervous system

“…Particularly, some regulatory mechanism to ensure the steady-state levels of catecholamines might be activated in response to cell damages. In general, exposure of animals to stress causes activation of the sympathetic nervous system eliciting the synthesis and release of catecholamines (Kvetnȃnský and Mikulaj, 1970;Benedict et al, 1979) , which is accompanied by activation of catecholamine-synthesizing enzymes and an increase in the number of storage vesicles (Masserano et al, 1981;Fillenz et al, 1993). It is well known that a response in TH is one of the important processes that regulate catecholamine production; TH activity is modulated by post-translational modification of the protein via phosphorylation and transcriptional activation of the gene (reviewed by Kumer and Vrana, 1996).…”