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and neurogenic control of blood pressure in
normal rats and rats with chronic renal failure
Division of Nephrology, Department of Medicine, University of Southern California, Los Angeles, California 90033
Increased sympathetic
nervous system (SNS) activity plays a role in the genesis 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 interleukin
(IL)-1
may activate nitric oxide in the brain, we have tested the
hypothesis that IL-1 may modulate the activity of the SNS via
regulation of the local expression of neuronal NOS (nNOS) in the brain
of CRF and control rats. To this end, we first found that
administration of IL-1 in the lateral ventricle of control and CRF
rats decreased blood pressure and norepinephrine (NE) secretion from
the posterior hypothalamus (PH) and increased NOS mRNA expression.
Second, we observed that an acute or chronic injection of an
IL-1-specific antibody in the lateral ventricle raised blood
pressure and NE secretion from the PH and decreased NOS mRNA abundance
in the PH of control and CRF rats. Finally, we measured the IL-1
mRNA abundance in the PH, locus coeruleus, and paraventricular nuclei of CRF and control rats by RT-PCR and found it to be greater in CRF
rats than in control rats. In conclusion, these studies have shown that
IL-1 modulates the activity of the SNS in the central nervous system
and that this modulation is mediated by increased local expression of
nNOS mRNA.
sympathetic nerve activity; nitric oxide; nitric oxide synthase; posterior hypothalamus
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