Hypertension, Vol 14, 191-202, Copyright © 1989 by American Heart Association
MA Adams, A Bobik and PI Korner
We compared blood pressure, hindquarter vascular resistance properties,
left ventricular weight, and norepinephrine kinetics, in spontaneously
hypertensive rats (SHR) and weight-matched normotensive Wistar-Kyoto (WKY)
rats at 4, 9, 14, 20, 30, and 50 weeks of age. At 4 weeks, systolic and
mean blood pressure measurements were the same in both strains, but the
vascular resistance of the fully dilated hindquarter bed was significantly
higher in SHR than in WKY rats, with a much larger difference during
maximum constriction. Plots of resistance at maximum dilatation and at
maximum constriction against body weight suggest that a component of the
increase in vascular muscle mass in SHR occurred in the neonatal period
preceding hypertension followed by a later component related to the rise in
blood pressure. By contrast, left ventricular hypertrophy was minimal at 4
weeks and most of its development paralleled the rise in blood pressure.
Sympathetic activity, assessed by norepinephrine fractional rate constant,
was higher in SHR than in WKY rats in the left ventricle and kidney through
most of the period between 4 and 50 weeks, but was similar in both strains
in the muscle bed. This pattern of sympathetic activity will accentuate
hypertension once cardiac and vascular hypertrophy are fully established.
In all regions, norepinephrine tissue concentration was higher in young SHR
and could potentiate the trophic effects of growth factors in early
vascular hypertrophy. We suggest that the initial (primary) component of
vascular hypertrophy precedes the rise in blood pressure and may be
critical in the pathogenesis of hypertension. Possible reasons for the
short delay in the rise in blood pressure in young SHR, once the vascular
"amplifier" has been established, include high vascularity, immaturity of
smooth muscle, and delay in the development of left ventricular
hypertrophy.
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