Open Access
Influence of sino-aortic baroreceptor denervation on catecholamines, catecholamine-synthesizing enzymes and choline acetyltransferase activity in the brainstem nuclei of the rat.
Author(s) -
Kazuo Nakamura,
Keiji Nakamura
Publication year - 1981
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.31.95
Subject(s) - baroreceptor , catecholamine , denervation , choline acetyltransferase , brainstem , medicine , endocrinology , chemistry , acetylcholine , blood pressure , heart rate
At one week after sino-aortic baroreceptor denervation in the rat, aortic blood pressure and plasma contents of epinephrine and dopamine beta-hydroxylase (DBH) activity were elevated during resting and conscious states. Stress-induced elevation of blood pressure and plasma epinephrine were markedly pronounced. These changes disappeared at four weeks after denervation. Sino-aortic deafferentation decreased choline acetyltransferase (ChAc) activity in the nucleus tractus solitarii (NTS) and locus coeruleus (LC) and increased DBH activity, norepinephrine levels, phenylethanolamine N-methyltransferase (PNMT) activity and epinephrine levels in the LC, accompanied with a reduction of DBH activity and norepinephrine contents in the nucleus hypothalamicus posterior. These alterations were confirmed one week after denervation but did not persist for a period of four weeks. At four weeks after denervation, ChAc activity was significantly decreased in the nucleus dorsalis nerve of the vagi but not in ;the nucleus ambiguus. During the transient hypertensive phase, sino-aortic deafferentation did not alter DBH and PNMT activities in the NTS, A2 cell and A1 cell areas, and both catecholamine levels in the NTS. In conclusion, sino-aortic denervation transiently decreased ChAc activity in the NTS and LC, and enhanced synthesis and accumulation of norepinephrine and epinephrine in the LC accompanied with a decrease in norepinephrine contents and DBH activity in the nucleus hypothalamicus posterior, causally resulting in short-lasting labile hypertension and activation of the adrenal medulla.