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Hypertension, Vol 10, 328-338, Copyright © 1987 by American Heart Association
RM Lee, CR Triggle, DW Cheung and MD Coughlin
Neonatal sympathectomy of spontaneously hypertensive rats (SHR) and control
Wistar-Kyoto rats (WKY) was performed by a combined treatment with
antiserum to nerve growth factor and guanethidine during the first 4 weeks
after birth. The development of hypertension was completely prevented in
the treated SHR: at 28 to 30 weeks of age, systolic blood pressure of
treated SHR was 139 +/- 2 mm Hg as compared with 195 +/- 8 mm Hg in
untreated SHR. The extent of sympathectomy was verified by
histofluorescence. Fluorescence histochemistry for catecholamine-
containing nerves showed a complete absence of adrenergic nerves in the
mesenteric arteries of treated rats. A supersensitivity to norepinephrine
was exhibited by mesenteric arteries, anococcygeus muscle, and tail
arteries from the treated SHR and WKY. In the mesenteric vascular bed,
maximal response to norepinephrine was significantly reduced by
sympathectomy. Sympathectomy also abolished the responses (e.g., generation
of excitatory junctional potentials) of tail arteries to electrical
stimulation of perivascular nerves. Morphometric measurements of three
categories of mesenteric arteries showed that sympathectomy had no effect
on the hypertrophic change of smooth muscle cells in the conducting
vessels, but it prevented the hyperplastic changes of the muscle cells from
reactive, muscular arteries and small resistance vessels. These results
suggest that one of the primary roles of the overactive sympathetic nervous
system in the development of hypertension in SHR is manifested through its
trophic effect on the arteries of SHR. This trophic effect appears to cause
a hyperplastic change in the smooth muscle cells in the reactive and
resistance vessels, thereby contributing to the development of hypertension
in older SHR.
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Structural and functional consequence of neonatal sympathectomy on the blood vessels of spontaneously hypertensive rats
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