Effect of neonatal sympathectomy on the development of angiotensin
ii - induced hypertension.
Csiky, Botond, and Geza Simon.
Department of Medicine, VA Medical Center and University of
Minnesota, Minneapolis, MN 55417
APStracts 3:0366H, 1996.
In the early stage of ANG II-induced hypertension, we tested whether
sympathectomy prevented the autopotentiation of vasoconstrictor
responses by ANG II, and in the chronic, established phase of
hypertension, whether the antihypertensive effect of sympathectomy,
if any, was related or not to the prevention of structural vascular
changes. Neonatally-sympathectomized and sham-sympathectomized male
Sprague-Dawley rats received 100 or 200 ng/kg.min-1 ANG II ip for 7
-10 days, or 200 ng/kg.min-1 ANG II sc for 4 weeks. Sham-treated
sympathectomized and sham-sympathectomized rats were controls.
Vasoconstrictor responses to ANG II, norepinephrine (NE), arginine
-vasopressin and periarterial nerve stimulation were measured in the
mesentery of rats and, thereafter, in the chronically treated rats,
mesenteric resistance arteries were fixed in situ for morphometric
measurements. In ANG II-treated sham-sympathectomized rats: 1) tail
systolic BP was unchanged after 7-10 days and increased by 23 mmHg at
4 weeks (p<0.001); 2) vasoconstrictor responses were selectively
increased to ANG II (autopotentiation) (p=0.026) and nerve
stimulation (p=0.031) at 7-10 days, and non-selectively increased to
all stimuli at 4 weeks (p<0.05 to <0.01); and 3) after 4
weeks, the wall-to-lumen ratio of resistance arteries was increased
(p<0.02). In ANG II-treated sympathectomized rats, there were no
changes in systolic BP or vasoconstrictor responses at either 7-10
days or 4 weeks, but structural vascular changes developed to the
same extent as in sham-sympathectomized, ANG II-treated rats.
Autopotentiation of vasocontrictor responses appears to be due to an
interaction between ANG II and the sympathetic nervous system,
because it is prevented by sympathectomy. The dissociation of
function and structure in the chronic stage of ANG II administration
to sympathectomized rats suggests that structural vascular changes by
themselves are insufficient to cause hypertension, but increased
vascular reactivity or vasoconstrictor input are also needed.
Received 13 June 1996; accepted in final form 13 August 1996.
APS Manuscript Number H526-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996