[Animal models for hypertensive diseases (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Kihara.
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Studies of cardiac hypertrophy in spontaneously hypertensive rats have indicated that left ventricular hypertrophy occurred even in the prehypertensive stage. These findings suggested that other factors besides blood pressure levels, and including possibly a genetic predisposition to myocardial hypertrophy, could play a role in structural cardiovascular alterations in spontaneously hypertensive rats. More recent studies have confirmed these anatomic results; left ventricular hypertrophy was vectorcardiographically detected even in the prehypertensive stage in voth young stroke-prone rats and stroke-resistant spontaneously hypertensive rats. Further, a close relation was found between degree of left ventricular hypertrophy and vascular hypertrophy or hyperplasia; this suggests that early detection of left ventricular hypertrophy may be a useful indicator of the incipient stage of structural vascular changes in genetic hypertension.
Salmonella, but not Escherichia coli, was attracted to citrate, a distinction that is understandable in view of the inability of E. coli to transport tricarboxylic acids. The Salmonella response to citrate and to two previously described attractants, aspartate and malate, was mutually noncompetitive. Citrate taxis different from citrate uptake in that it did not require Na+, was constitutive, and was not repressible by glucose.
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