Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chagas disease (CD) is a tropical zoonosis caused by the protozoan Trypanosoma cruzi. Severe autonomic dysfunction like reduced cardiac catecholamine-containing or acetylcholinesterase-positive innervation have been reported in CD. Renin-angiotensin system (RAS) seems to participate in the regulation of adrenal catecholamine secretion by adrenal medullary chromaffin cells, which might be dependent of nitric oxide (NO) pathways. To investigate the levels of RAS components in the adrenal gland during the acute infection with Y strain T. cruzi and in response to acute administration of an inhibitor of the enzyme NO synthase, L-NAME. Male Holtzman rats were inoculated intraperitoneally with Y strain T. cruzi and received L-NAME or tap water from one day before the infection until 13 or 17 days post-inoculation (dpi). The concentration of RAS molecules in the adrenal tissue was evaluated by ELISA immunoassay. Angiotensin converting enzyme 1 (ACE1) levels were significantly lower at 17 dpi when compared to 13 dpi. No significant differences were found compared with baseline, and no changes were detected in adrenal tissue levels of angiotensin converting enzyme 2 (ACE2), angiotensin II, or angiotensin-(1-7). Moreover, the treatment with L-NAME did not influence the levels of RAS components in adrenal tissue during the course of T. cruzi infection. We provided the first evidence that levels of RAS molecules change in the adrenal gland during acute phase of T. cruzi infection. Future studies are necessary to fully address the role of NO in RAS-associated adrenal gland function in CD.
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PMID:Renin angiotensin system molecules and nitric oxide local interactions in the adrenal gland of Trypanosoma cruzi infected rats. 3178 70

Nicotinamide (Nam, amide form of niacin acid or nicotinate), a precursor for nicotinamide adenine dinucleotide (NAD+), is important for normal physiological function of organisms. Nam also suppresses mobilization of Ca2+ from sarcoplasmic reticulum into cytoplasm through inhibiting ADP-ribose cyclase. Previously, we have demonstrated that a pharmacological dose of Nam normalizes maternal blood pressure in mouse models of preeclampsia, a pregnancy related hypertensive disorder. We hypothesized that Nam could decrease blood pressure in hypertensive conditions unrelated to pregnancy. Nam at a dose of 500 mg/kg/day was given to wild type (WT) mice treated with L-NAME, endothelial nitric oxide synthase (eNOS)-null and renin transgenic (Renin-Tg) mice via drinking water. Blood pressure was measured by tail-cuff at different stages of treatment. The function and structure of kidneys of WT mice with L-NAME were determined at the end of the study. The gene expression of markers of inflammation and fibrosis in the kidneys of WT mice with L-NAME was also measured. Nam effectively prevented increase in blood pressure in L-NAME treated mice and decreased elevated blood pressure in eNOS-null mice. However, it did not alter high blood pressure in Renin-Tg mice. Nam prevented increase in urinary albumin excretion and collagen deposit in kidneys of WT mice treated with L-NAME. In addition, Nam significantly decreased the mRNA levels of the markers of inflammation and fibrosis in the kidneys of WT mice treated with L-NAME. Nam may execute beneficial effects on hypertensive conditions associated with eNOS dysfunction via suppressing inflammation. Because Nam is generally regarded as safe in humans, it merits further evaluation for the tailored treatment for the subgroup of hypertensive cases associated with impaired eNOS system.
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PMID:Beneficial effects of nicotinamide on hypertensive mice with impaired endothelial nitric oxide function. 3290 9


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