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Biomedical subjects

Carol Moreno

Publications and source records attributed to Carol Moreno.

21 records · Page 2Linked to original sources

Changes in NOS activity and protein expression during acute and prolonged ANG II administration.

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 x min(-1) x g wet wt(-1)) 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.

Angiotensin II↗

Role of Cyclooxygenase-2-Derived Metabolites and NO in Renal Response to Bradykinin.

-It has been reported that bradykinin (BK) can induce or activate both cyclooxygenase (COX) isoforms and that the renal effects of BK seem to be mediated by prostaglandins and NO. The first objective of this study was to evaluate the relative contribution of both COX isoforms in mediating the renal response to BK in anesthetized dogs. The second objective was to examine whether COX-2 inhibition potentiates the renal effects induced by NO reduction during BK administration. Intrarenal BK infusion (8 ng. kg(-1). min(-1), n=6) elicited a significant increment in renal blood flow, sodium excretion, urine volume, and the fractional excretion of lithium. COX-2 inhibition (nimesulide, 5 µg. kg(-1). min(-1), n=6) reduced the renal vasodilatation but did not significantly modify the natriuresis or diuresis secondary to BK. Administration of a nonspecific isozyme COX inhibitor (meclofenamate, 5 µg. kg(-1). min(-1); n=6) did not induce greater effects than those produced by nimesulide. NO synthesis reduction (N:(G)-nitro-L-arginine methyl ester [L-NAME], 3 µg. kg(-1). min(-1)) prevented the renal vasodilatation and the increment in the fractional excretion of lithium induced by BK but did not affect the natriuretic or diuretic response. Simultaneous nimesulide infusion did not modify the renal effects of L-NAME during BK infusion (n=6). Finally, inhibition of both COX isoforms with meclofenamate, in dogs treated with L-NAME (n=6), completely prevented the vasodilator and excretory actions of BK. The results of this study suggest that (1) NO and prostanoids dependent on COX-2 seem to be involved in the renal vasodilatation induced by BK, and (2) there is an interaction between NO and COX-1-derived metabolites in mediating the natriuretic and diuretic response to BK.

Journal Article↗

Increased diagnosis of asthma in hospitalized infants: the next target population for care management?

Hospitalization of children with asthma declined at our institution between 1996 and 2000, before stabilizing for the past 5 years. The ages of children hospitalized since 2000 were examined to see if the demographics of the hospitalized population have changed to better understand why the hospitalization rate has remained the same despite continued, aggressive screening and education efforts. Data were gathered for our hospital through the Department of Defense Medical Health System Management Analysis and Reporting System (M2). The mean age (+/- SD) of children hospitalized in 2003 (2.84 +/- 2.53) was less than the mean age for 2000 and 2002 (4.85 +/- 3.7 and 4.61 +/- 4.45), respectively (p < 0.05), and more infants less than 2 years of age were hospitalized in 2003 (33/60, 55% p < 0.01) and 2004 (32/68, 47% p < 0.05) than in 2000 (19/70, 27%). The diagnosis of asthma in hospitalized infants and young children has increased over the past 5 years, suggesting better recognition and providing a new target population for intervention with early asthma controller therapy.

Age Factors↗