Sh. Ye et al., Interleukin-1 beta and neurogenic control of blood pressure in normal ratsand rats with chronic renal failure, AM J P-HEAR, 279(6), 2000, pp. H2786-H2796
Citations number
50
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Increased sympathetic nervous system (SNS) activity plays a role in the gen
esis of hypertension in rats with chronic renal failure (CRF). The rise in
central SNS activity is mitigated by increased local expression of neuronal
nitric oxide synthase (NOS) mRNA and NO2/NO3 production. Because interleuk
in (IL)-1 beta may activate nitric oxide in the brain, we have tested the h
ypothesis that IL-1 beta may modulate the activity of the SNS via regulatio
n of the local expression of neuronal NOS (nNOS) in the brain of CRF and co
ntrol rats. To this end, we first found that administration of IL-1 beta in
the lateral ventricle of control and CRF rats decreased blood pressure and
norepinephrine (NE) secretion from the posterior hypothalamus (PH) and inc
reased NOS mRNA expression. Second, we observed that an acute or chronic in
jection of an IL-1 beta -specific antibody in the lateral ventricle raised
blood pressure and NE secretion from the PH and decreased NOS mRNA abundanc
e in the PH of control and CRF rats. Finally, we measured the IL-1 beta mRN
A abundance in the PH, locus coeruleus, and paraventricular nuclei of CRF a
nd control rats by RT-PCR and found it to be greater in CRF rats than in co
ntrol rats. In conclusion, these studies have shown that IL-1 beta modulate
s the activity of the SNS in the central nervous system and that this modul
ation is mediated by increased local expression of nNOS mRNA.