Zukowska-Grójec Z, Wocial B, Chodakowska J, Januszewicz W
Acta Physiol Pol. 1980 Nov-Dec;31(6):613-22.
The influence of stress on the metabolism of adrenaline (A) and noradrenaline (NA) in the prosencephalon (PC) and rhombencephalon (RC) of SHR and normotensive Wistar rats (WR) was studied. After intraperitoneal injection of 3H-tyrosine, radioactivity of 3H-adrenaline (3H-A), 3H-noradrenaline (3H-NA), total 3H-3-methoxy-4-hydroxyphenylglycol (3H-MHPG), total 3H-3,4-dihydroxyphenylglycol (3H-DHPG) and 3H-vanillylmandelic acid (3H-VMA) was measured in PC and RC of SHR and WR, non-stressed or subjected to running stress. Stress induced a significant decrease of 3H-A level in PC and RC of 8-week-old SHR while no stress-related changes in 3H-NA level were found in either part of the brain of SHR. In RC, 3H-A level was lower in older than in younger non-stressed SHR and decreased further after stress. In all SHR, stress enhanced formation of total 3H-MHPG and/or 3H-DHPG in PC, while increased 3H-VMA level was found only in PC of 24-week-old and in RC of 8-week-old stressed SHR. The results suggest that the decrease of the level of 3H-A in the brain of SHR is involved in their reaction to stress and may depend on increased metabolism mainly to glycols but also to VMA. The lower 3H-NA and 3H-A levels in the prosencephalon of non-stressed young and older SHR, concomitant with unaltered or elevated formation of their metabolites, may suggest higher release of the transmitters involved in the pathogenesis of spontaneous hypertension.
研究了应激对自发性高血压大鼠(SHR)和正常血压Wistar大鼠(WR)前脑(PC)和后脑(RC)中肾上腺素(A)和去甲肾上腺素(NA)代谢的影响。腹腔注射3H-酪氨酸后,在未应激或经受跑步应激的SHR和WR的PC和RC中测量了3H-肾上腺素(3H-A)、3H-去甲肾上腺素(3H-NA)、总3H-3-甲氧基-4-羟基苯乙二醇(3H-MHPG)、总3H-3,4-二羟基苯乙二醇(3H-DHPG)和3H-香草扁桃酸(3H-VMA)的放射性。应激导致8周龄SHR的PC和RC中3H-A水平显著降低,而在SHR大脑的任何部位均未发现3H-NA水平与应激相关的变化。在RC中,未应激的老年SHR的3H-A水平低于年轻SHR,应激后进一步降低。在所有SHR中,应激增强了PC中总3H-MHPG和/或3H-DHPG的形成,而仅在24周龄应激SHR的PC和8周龄应激SHR的RC中发现3H-VMA水平升高。结果表明,SHR大脑中3H-A水平的降低参与了它们对应激的反应,可能主要取决于糖二醇和VMA代谢的增加。未应激的年轻和老年SHR前脑中较低的3H-NA和3H-A水平,与其代谢产物形成未改变或升高相伴,可能提示参与自发性高血压发病机制的递质释放增加。