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1 Department of Physiology, University of Murcia School of Medicine, E-30100 Murcia; 2 Fundación Jiménez Díaz, E-28040 Madrid; and 3 Department of Medical Sciences, University of Castilla-La Mancha, E-02071 Albacete, Spain
The aim of this study was to
assess the effects of acute or prolonged increases of ANG II on nitric
oxide synthase (NOS) activities and protein expression in mesenteric
resistance vessels, left ventricle, renal cortex, and renal medulla.
The response of NOS activities to ANG II is compared with that induced
by phenylephrine. ANG II or phenylephrine were infused over either
3 h or 3 days to conscious rats. NOS activity was examined by
measuring the rate of conversion of
L-[14C]arginine to
L-[14C]citrulline. Protein levels of
endothelial (e) and neuronal (n) NOS were determined by Western blot
analysis. Arterial pressure (AP) increased (P < 0.05)
during acute and prolonged ANG II infusion. Ca2+-dependent
NOS activity values (pmol of
citrulline · min
1 · g wet
wt1) for control rats were 21 ± 9 in mesenteric
arteries, 13 ± 7 in left ventricle, 14 ± 8 in renal cortex,
and 411 ± 70 in renal medulla. Acute ANG II infusion increased
(P < 0.05) Ca2+-dependent NOS activity in
renal cortex and renal medulla (81 ± 18 and 611 ± 48, respectively), but no differences were found in mesenteric arteries and
left ventricle with respect to control rats. In contrast to the renal
changes in NOS activity, acute ANG II infusion did not modify eNOS or
nNOS expression in any of the tissues examined. Prolonged ANG II
infusion increased (P < 0.05)
Ca2+-dependent NOS activity in mesenteric arteries (70 ± 17), renal cortex (104 ± 31), and left ventricle (49 ± 8) and did not elicit changes in renal medulla. After a prolonged ANG
II infusion, eNOS and nNOS levels increased in all tissues examined
with the exception of eNOS in the mesenteric arteries and nNOS in the
left ventricle, which were not altered. Acute and prolonged
phenylephrine infusion elevated AP to a similar extent as ANG II but
only elicited significant increments of Ca2+-dependent NOS
activity in renal cortex. These data indicate that acute and prolonged
elevations in ANG II upregulate Ca2+-dependent NOS activity
and protein expression in different tissues related to the control of
blood pressure. However, these ANG II effects are heterogeneous with
respect to the tissue implicated, the time course of the stimulation,
and the NOS isoform involved. Phenylephrine only induces a significant
elevation of Ca2+-dependent NOS activity in renal cortex.
heart; mesenteric arteries; nitric oxide synthase; phenylephrine renal cortex; renal medulla
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