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Mol Cell Biochem. 2000 Jun;209(1-2):39-46.
MET-88, a gamma-butyrobetaine hydroxylase inhibitor, improves cardiac SR Ca2+ uptake activity in rats with congestive heart failure following myocardial infarction.

Hayashi Y, Ishida H, Hoshiai M, Hoshiai K, Kirimoto T, Kanno T, Nakano M, Tajima K, Miyake H, Matsuura N, Nakazawa H.

Pharmacology Research Laboratory, Taiho Pharmaceutical Co. Ltd., Tokushima, Japan.

We previously reported that MET-88, 3-(2,2,2-trimethylhydrazinium) propionate, improved left ventricular diastolic dysfunction induced by congestive heart failure (CHF) in rats. The present study was designed to investigate the mechanism by which MET-88 improved the cardiac relaxation impaired in CHF rats. The left coronary artery of the animals was ligated, and the rats were then orally administered vehicle (control), MET-88 at 50 or 100 mg/kg or captopril at 20 mg/kg for 20 days. Myocytes were isolated from the non-infarcted region in the left ventricle, and cell shortening and [Ca2+]i transients were measured with a video-edge detector and by fluorescence analysis, respectively. In CHF control rats, the diastolic phase of cell shortening was prolonged compared with that of the sham-operated (sham) rats. This prolongation was prevented by treatment with MET-88 at 100 mg/kg or captopril at 20 mg/kg. CHF control rats also showed an increase in the decay time of [Ca2+]i transients compared with sham rats. MET-88 at 100 mg/kg and captopril at 20 mg/kg attenuated the increase in decay time of [Ca2+]i transients. Ca2+ uptake activity of the sarcoplasmic reticulum (SR) isolated from the non-infarcted region in the left ventricle was measured, and Lineweaver-Burk plot analysis of the activity was performed. CHF control rats revealed a decrease in the Vmax for SR Ca2+ uptake activity without alteration in Kd. MET-88 at 100 mg/kg significantly prevented the decrease in Vmax, but had no effect on Kd. Also, treatment with MET-88 at 100 mg/kg improved myocardial high-energy phosphate levels impaired in CHF rats. These results suggest that one of the mechanisms by which MET-88 improved cardiac relaxation in CHF rats is based on the amelioration of [Ca2+]i transients through increase of SR Ca2+ uptake activity.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10942199&dopt=Abstract

J Nucl Med. 2000 Aug;41(8):1337-42.
Aspirin renography and captopril renography in the diagnosis of renal artery stenosis.

van de Ven PJ, de Klerk JM, Mertens IJ, Koomans HA, Beutler JJ.

Department of Nephrology and Hypertension, University Medical Center Utrecht, The Netherlands.

Preliminary data suggest that aspirin renography is more sensitive than captopril renography for indicating renal artery stenosis (RAS). Considering that aspirin, compared with captopril, reduces renal blood flow and, thus, tubular tracer delivery in poststenotic kidneys, aspirin renography is expected to be more useful, particularly if tubular tracers are used. METHODS: We prospectively compared aspirin renography (20 mg/kg orally) and captopril renography (25 mg orally) with 99mTc-mercaptoacetyltriglycine in 75 consecutive patients suspected of having RAS. RESULTS: RAS, diagnosed as stenosis of more than 50% on angiography, was found unilaterally in 34 patients and bilaterally in 17 patients. RAS was absent in 24 patients. The sensitivities for unilateral RAS or bilateral RAS (i.e., stenosis that was at least unilateral) were, respectively, 88% and 88% for captopril renography and 82% and 94% for aspirin renography (not significant). The overall specificity was 75% for captopril renography and 83% for aspirin renography (not significant). Tracer uptake ratios, time to peak activity, and percentage of 20-min tracer retention were also not significantly different for captopril and aspirin renography. Subgroup analysis of modest (50-75%) and severe (> or =75%) RAS, or of plasma creatinine greater than 120 micromol/L, also showed no difference between captopril and aspirin renography. CONCLUSION: We conclude that for identification of RAS, the usefulness of aspirin renography equals, but does not surpass, that of captopril renography.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10945524&dopt=Abstract

Mol Med. 2000 Apr;6(4):319-31.
Exclusion of angiotensin I-converting enzyme as a candidate gene involved in exudative inflammatory resistance in F344/N rats.

Jafarian-Tehrani M, Listwak S, Barrientos RM, Michaud A, Corvol P, Sternberg EM.

Section on Neuroendocrine Immunology and Behavior, National Institutes of Health, Bethesda, Maryland, USA.

BACKGROUND: Inbred LEW/N and F344/N rats respectively, are susceptible and relatively resistant to a broad range of inflammatory/autoimmune diseases. We recently identified a quantitative trait locus (QTL) on chromosome 10 that protects the F344/N rat from carrageenan-induced exudation in a dominant fashion. Angiotensin I-converting enzyme (ACE) is one of the candidate genes located in this QTL region that plays an important role in inflammation. MATERIALS AND METHODS: RNA was extracted from both LEW/N and F344/N rat strains and used to produce full length cDNA by reverse transcription polymerase chain reaction (RT-PCR). Both strands of the PCR products were entirely sequenced to determine nucleotide differences between strains. ACE activity was measured using the synthetic substrate 3H-hippuryl-glycylglycine. ACE protein levels were determined by Western blot using a specific ACE antibody. ACE kinetic and inhibition studies were performed using specific substrates (Hip-His-Leu and Acetyl-Seryl-Aspartyl-Acetyl-Lysyl-Proline) and inhibitors (lisinopril, captopril and quinaprilat) for each C- and N-terminal active site. Finally, the dose-effects of lisinopril treatment on carrageenen-induced exudate volume and ACE activity was studied. RESULTS: In this study, we report for the first time a missense mutation in the coding region of ACE cDNA at 5' 1021 from C to T, resulting in a Leu-341 to Phe substitution, close to the N-domain active site in the F344/N rats. Full characterization of soluble and tissue ACE in both LEW/N and F344/N rat strains showed that soluble ACE levels in serum and exudate were 1.5 fold higher in the F344/N rats than those in LEW/N rats. In addition, the soluble ACE level was inversely correlated with the exudate volume. However, the specific ACE activity and its catalytic properties were identical in both strains. Furthermore, the chronic inhibition of serum and exudate ACE levels by lisinopril treatment did not affect the exudate volume in F344/N rats, indicating that several factors besides ACE were involved in the control of carrageenan-induced exudation. CONCLUSIONS: This report describes a complete molecular, biochemical, enzymatic and pharmacologic study of a missense mutation in the ACE cDNA in F344/N rats, that taken together, excludes ACE as a candidate gene involved with resistance to carrageenan-induced exudation in F344/N rats.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10949912&dopt=Abstract

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