Drugs online research references
Arch Biochem Biophys. 1989 Apr;270(1):255-66.
A peptidyl dipeptidase-4 from Pseudomonas maltophilia: purification and properties.
Dasarathy Y, Stevens J, Fanburg BL, Lanzillo JJ.
Department of Medicine, New England Medical Center, Boston, Massachusetts 02111.
A peptidyl dipeptidase-4 (bacterial PDP-4) was purified to near homogeneity from a supernatant of Pseudomonas maltophilia extracellular medium. Bacterial PDP-4 is a single-polypeptide-chain enzyme, 82 kDa, with an alkaline isoelectric point. Peptides susceptible to hydrolysis by bacterial PDP-4 include angiotensin 1, bradykinin, enkephalins, atriopeptin 2, and smaller synthetic peptides. N-acylated tripeptides are hydrolyzed, but free tripeptides are not. A free carboxy terminus is required for hydrolysis. Peptides with ultimate and penultimate Pro residues are not hydrolyzed. The enzyme does not require an anion for activity. Bacterial PDP-4 was inhibited by EDTA and the dipeptide Phe-Arg. Thiorphan was an inhibitor only at levels well above those required for inhibition of neutral metalloendopeptidase (NEP), an enzyme for which thiorphan is specific. A second NEP and thermolysin inhibitor, phosphoramidon, did not inhibit bacterial PDP-4. The potent angiotensin-converting enzyme inhibitor lisinopril was not inhibitory. Bacterial PDP-4 is distinguished from a similar enzyme from Escherichia coli, which is not susceptible to EDTA inhibition, and one from Corynebacterium equi, which hydrolyzes free tripeptides. These data indicate that the bacterial PDP-4 catalytic site is unlike those of other enzymes that function either wholly or in part as peptidyl dipeptidases.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2539048&dopt=Abstract
Scand J Urol Nephrol. 1988;22(4):317-25.
Delayed tolerance to furosemide diuresis. Influence of angiotensin converting enzyme inhibition by lisinopril.
Sjostrom PA, Beermann BA, Odlind BG.
Department of Internal Medicine, Orebro Medical Center Hospital, Sweden.
The role of the renin-angiotensin-aldosterone system in the development of tolerance to the diuretic effect of furosemide was investigated in 12 healthy male volunteers. Furosemide in a dose of 40 mg daily for one week had a brisk acute diuretic effect, but did not lead to dehydration, hyponatremia or fall in blood pressure. The reason for this was a reduction in sodium excretion between doses (rebound effect) and a decrease in sensitivity to furosemide from day 1 to day 7. The latter phenomenon is referred to as delayed tolerance to furosemide. Inhibition of angiotensin converting enzyme with lisinopril 20 mg daily did not change the renal furosemide excretion rate, the renal sensitivity to furosemide or the tolerance development. Thus, delayed tolerance to furosemide diuresis was not related to dehydration or activation of the renin-angiotensin-aldosterone system. Other mechanisms, probably intrarenal, will have to be looked for.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2853446&dopt=Abstract
Free Radic Res Commun. 1993;18(2):107-13.
Oxidant stress and glomerular prostanoid production: influence of angiotensin converting enzyme inhibition.
Clayton L, Hiley C, D'Souza RJ, Jones PW, Davies SJ, Strange RC, Aber GM.
Renal Laboratory, School of Postgraduate Medicine, University of Keele, England.
1. The effect of H2O2 (4.7 x 10(-9) -4.7 x 10(-3) M) on prostanoid production by isolated glomeruli from normotensive (WKY) and, spontaneously hypertensive rats (SHR) has been studied. 2. Oxidant stress significantly increased synthesis of prostaglandin E2 (PGE2), I2 (PGI2) and thromboxane A2 (TxA2) by glomeruli from both strains whereas the ratio (PGE2 + PGI2)/TxA2 increased in only SHR. 3. Pre-incubation of glomeruli with the angiotensin converting enzyme inhibitors captopril or lisinopril, had virtually no effect on H2O2-induced synthesis of individual prostanoids nor on the ratio (PGE2 + PGI2)/TxA2 by glomeruli from either WKY or SHR. 4. The findings suggest that H2O2-induced changes in glomerular function may be mediated, in part, by PGs but fail to support the suggestion that the ability of ACEI to protect glomeruli from H2O2-induced damage is determined by PGs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8386683&dopt=Abstract
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