Drugs online research references
Proc Soc Exp Biol Med. 1991 Feb;196(2):175-7.
Local generation of angiotensin II as a mechanism of aldosterone secretion in rat adrenal capsules.
Oda H, Lotshaw DP, Franco-Saenz R, Mulrow PJ.
Department of Medicine, Medical College of Ohio, Toledo 43699.
Angiotensin-converting enzyme (ACE) is found in the adrenal gland, but the role of adrenal ACE in the formation of angiotensin II (AII) and subsequent stimulation of aldosterone is unclear. We examined the effect of adrenal ACE activity on aldosterone secretion by superfusing rat adrenal capsules with angiotensin I (AI) in the presence and absence of the ACE inhibitor, lisinopril. Angiotensin I (10 microM) stimulated aldosterone secretion from 914 +/- 41 to 1465 +/- 118 pg/min/capsule (P less than 0.05). Simultaneous superfusion of AI plus lisinopril (100 microM) inhibited the stimulation of aldosterone by 73% (P less than 0.05). Perfusion of the capsules with angiotensin II (1 microM) stimulated aldosterone from 893 +/- 180 to 1466 +/- 181 pg/min/capsule (P less than 0.01). In contrast, simultaneous superfusion of AII plus lisinopril (100 microM) did not inhibit the AII stimulation of aldosterone. The failure of lisinopril to inhibit AII stimulation of aldosterone argues against a toxic or nonspecific action of lisinopril. The inhibition of AI stimulation of aldosterone release by lisinopril is mostly due to lisinopril inhibition of ACE and resulting decreased conversion of AI to AII. These results demonstrate that adrenal ACE may generate AII from AI in the adrenal gland, and this locally produce AII stimulates aldosterone.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1846675&dopt=Abstract
enzyme.chem.msu.su
Inhibition of bovine lung and testicular angiotensin-converting enzyme (ACE) by some well-known ACE inhibitors (lisinopril, captopril, enalapril), new substances (Nalpha-carboxyalkyl dipeptides PP-09, PP-35, and PP-36), and phosphoramidon was investigated using Cbz-Phe-His-Leu and FA-Phe-Phe-Arg (C-terminal analogs of angiotensin I and bradykinin, respectively) as the substrates. The somatic (two domains) and testicular (single domain) isoenzymes demonstrated different kinetic parameters for hydrolysis of these substrates. All of the inhibitors were competitive inhibitors of both ACE isoforms, and the Ki values were substrate-independent. The relative potencies of the inhibitors for both enzymes were: lisinopril > captopril > PP-09 > enalapril > PP-36 > PP-35 > phosphoramidon. The inhibition efficiency of PP-09 was comparable with those of the well-known ACE inhibitors. Captopril was more effectively bound to the somatic ACE (Ki = 0.5 nM) than to the testicular isoform (Ki = 6.5 nM).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10498812&dopt=Abstract
cyberg.it
Experimental data consistently indicate that renal disease progression is fully prevented in proteinuric glomerulopathies by long-enough angiotensin-converting enzyme (ACE) inhibition therapy. Whether regression of established proteinuria to normal can be achieved is, however, ill defined. The current study was designed with the aim to clarify whether ACE inhibition may induce regression of established proteinuria and renal structural damage in MWF rats, a genetic model of progressive proteinuria and renal injury. Animals treated with the ACE inhibitor lisinopril from 20 weeks of age (time when proteinuria is already important) and age-matched untreated rats were followed for 10 weeks. ACE inhibition normalized systolic blood pressure and progressively reduced proteinuria (from 172 +/- 79 to 81 +/- 23 mg/24 hours). In these animals, a highly significant correlation was obtained between baseline proteinuria and antiproteinuric response. At variance in untreated rats, proteinuria showed a marked increase in the 10-week follow-up period (from 165 +/- 57 to 325 +/- 86 mg/24 hours). Lisinopril prevented the progression of renal damage, as documented by a significantly lower incidence of glomeruli affected by sclerotic lesions (P < 0.01) than in untreated animals after the 10-week study period. Kidney tissue damage was comparable in lisinopril-treated rats and in untreated animals at 20 weeks of age, indicating that structural changes were arrested by the treatment. Thus, in proteinuric MWF rats, late-onset ACE inhibition normalized blood pressure, effectively and progressively restored high protein excretion rate toward normal values, and arrested progression of tissue damage.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10516341&dopt=Abstract
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