Henrotte J G, Santarromana M, Franck G, Guicheney P, Boulu R, Bourdon R
Centre National de la Recherche Scientifique, Faculty of Pharmacy, INSERM U7, Hôpital Necker, Paris, France.
J Hypertens. 1992 Jun;10(6):553-9. doi: 10.1097/00004872-199206000-00008.
Higher cardiac zinc levels have been observed previously in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto (WKY) rats. However, this difference was established in adult males only and needed to be confirmed on a larger number of animals of both sexes. We also explored the respective roles of genetic and environmental factors in the genesis of this zinc anomaly as well as the causal relations with hypertension.
Cardiac zinc levels were determined in adult male and female SHR and WKY rats originating from various colonies and submitted to various experimental conditions (anaesthesia, stress). These determinations were also performed in 3-week prehypertensive SHR and in adult Wistar rats submitted or not to deoxycorticosterone acetate-salt-induced hypertension.
Zinc levels were measured by flame atomic absorption spectrophotometry.
In adults, cardiac zinc content was significantly higher in SHR than in WKY rats irrespective of sex and experimental conditions. In young prehypertensive rats, the difference between SHR and WKY cardiac zinc levels was also very significant. Experimental hypertension induced in Wistar rats did not entail any significant rise in cardiac zinc levels.
These findings indicated that the higher cardiac zinc of SHR is not secondary to blood pressure elevation. High erythrocyte zinc, previously described in SHR, together with the present data suggest the occurrence of a primary genetic defect leading to high intracellular zinc in SHR. The possible role of this zinc anomaly in the development of hypertension and/or cardiac hyperplasia is discussed.
先前观察到，与Wistar-Kyoto（WKY）大鼠相比，自发性高血压大鼠（SHR）心脏锌水平更高。然而，这种差异仅在成年雄性大鼠中得到证实，需要在更多的雌雄两性动物中进行确认。我们还探讨了遗传和环境因素在这种锌异常发生中的各自作用，以及与高血压的因果关系。
测定来自不同种群并处于不同实验条件（麻醉、应激）下的成年雄性和雌性SHR及WKY大鼠的心脏锌水平。这些测定也在3周龄的高血压前期SHR以及接受或未接受醋酸脱氧皮质酮盐诱导高血压的成年Wistar大鼠中进行。
采用火焰原子吸收分光光度法测量锌水平。
在成年大鼠中，无论性别和实验条件如何，SHR的心脏锌含量均显著高于WKY大鼠。在年轻的高血压前期大鼠中，SHR和WKY大鼠心脏锌水平的差异也非常显著。Wistar大鼠诱导的实验性高血压并未导致心脏锌水平显著升高。
这些发现表明，SHR心脏锌含量较高并非继发于血压升高。先前在SHR中描述的高红细胞锌，以及目前的数据表明，存在一种原发性遗传缺陷，导致SHR细胞内锌含量升高。本文讨论了这种锌异常在高血压和/或心脏增生发展中的可能作用。
