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Increased Intracellular Ca2+ Is Not Coinherited With an Inferred Major Gene Locus for Hypertension (ht) in the Spontaneously Hypertensive Rat

Hypertension is characterized by a complex mode of inheritance, consisting of the accumulation and interaction of major and minor genes. The existence of a single major gene locus (ht) has been demonstrated in the backcross analysis of spontaneously hypertensive rats (SHR) and normotensive Donryu ra...

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Published in:American journal of hypertension 1997-03, Vol.10 (3), p.282-288
Main Authors: Ohno, Yoichi, Matsuo, Koichi, Suzuki, Hiromichi, Tanase, Hisao, Takano, Toshiya, Saruta, Takao
Format: Article
Language:English
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Summary:Hypertension is characterized by a complex mode of inheritance, consisting of the accumulation and interaction of major and minor genes. The existence of a single major gene locus (ht) has been demonstrated in the backcross analysis of spontaneously hypertensive rats (SHR) and normotensive Donryu rats. Intracellular Ca2+ concentration ([Ca2+]i) determines the tonus of vascular smooth muscle. It has been hypothesized that abnormal Ca2+ transport is an inheritable trait with profound influence on the development of hypertension. Backcross analysis between SHR and Donryu rats was performed to demonstrate ht and to dissect polygenic hypertensive traits through ht and abnormal intracellular Ca2+ metabolism. Among the parental strains, systolic blood pressure and thrombin-stimulated [Ca2+]i in platelets were significantly greater in SHR than in Donryu and F1 rats. The backcrossed rats were distributed into two clusters on a scattergram of blood pressure versus [Ca2+]i, demonstrating the existence of ht. The blood pressure level was correlated with thrombin-stimulated [Ca2+]i in each cluster. Increased [Ca2+]i in platelets was not coinherited with ht and was considered to be a minor inheritable hypertensive trait discriminated from ht. Therefore, [Ca2+]i in platelets is an inadequate marker for searching ht. © 1997 American Journal of Hypertension, Ltd. Am J Hypertens 1997;10:282–288
ISSN:0895-7061
1941-7225
1879-1905
DOI:10.1016/S0895-7061(96)00383-4