Abstract
Chronic cold stress of rats (4 °C; 1–3 weeks) induced a marked increase in gene expression (adrenal medulla; superior cervical ganglia), tissue content (mesenteric arterial bed) and nerve stimulation-induced overflow of NPY-immunoreactivity (NPYir) from the perfused mesenteric arterial bed. In contrast increased NPY neurotransmission was offset by an apparent decrease in the evoked overflow of norepinephrine (NE) due to a presumed deactivation of NE by nitric oxide (NO), despite increased sympathetic nerve activity. The net effect of these offsetting system was no change in basal or the evoked increase in perfusion pressure (sympathetic tone). It is concluded that differences in NPY and NE transmission act as an important compensatory mechanism preventing dramatic changes in arterial pressure when sympathetic nerve activity is high during cold stress.
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