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Neuropeptide Y (NPY) induced inhibition of preganglionic nerve stimulation evoked release of adrenalin and noradrenaline in the pithed rat

 

作者: P. DAHLÖF,   K. PERSSON,   J. M. LUNDBERG,   C. DAHLÖF,  

 

期刊: Acta Physiologica Scandinavica  (WILEY Available online 1988)
卷期: Volume 132, issue 1  

页码: 51-57

 

ISSN:0001-6772

 

年代: 1988

 

DOI:10.1111/j.1748-1716.1988.tb08297.x

 

出版商: Blackwell Publishing Ltd

 

关键词: adrenalin;neuropeptide Y;noradrenaline;pithed rat;sympathetic neurotransmission

 

数据来源: WILEY

 

摘要:

NPY, a peptide with 36 amino acid residues, is co‐stored together with noradrenaline (NA) in cardiac and sympathetic perivascular nerves as well as with adrenalin (A) in adrenal chromaffin cells. NPY is released together with NA from sympathetic nerves and with A from the adrenal glands and appears to be involved in the control of sympathetic neurotransmission.The aim of the present study was to analyse the effect of NPY on the preganglionic nerve stimulation (PNS) evoked increases in plasma A and NA concentrations in pithed rats. In the first part of the study (I) only one PSN period (2 Hz for 45 s) was performed in each rat and the control group was compared to the NPY treated group. In the second part of the study (II) two PNS periods (1 Hz for 45 s) were performed in each rat, which either received saline or NPY before the second PNS. Thus, interindividual changes between the responses to the first and second PNS in control and NPY rats could be compared.In both study I and II, systemic infusion of NPY (2 μg kg‐1min1i.v.) significantly reduced the PNS‐induced increase in plasma A by 26% and 42%, respectively (P<0.05). However, the increase in plasma NA elicited by PNS was significantly reduced only in study II by 23% (P<0.05). Infusion of NPY did not affect basal heart rate in either of the studies, but significantly increased basal blood pressure by about 10 mmHg. The blood pressure responses to PNS were significantly greater in NPY treated rats.It is concluded that PNS‐evoked release of A and NA is under inhibitory control of NPY. The inhibition of NA release from the sympathetic nerve terminals is most probably due to a prejunctional site of action, whereas the reduced secretion of A could be due to a local effect of NPY in the adrenal medulla,. The negative influence of NPY on A and NA release appears to be compensated for by the additional facilitatory action of NPY on the postjunctioned responses to these catech

 

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