Drugs online research references
J Exp Zool. 1989 Apr;250(1):109-15.
Localization of angiotensin-converting enzyme in the trout gill.
Olson KR, Lipke DW, Kullman D, Evan AP, Ryan JW.
South Bend Center, Indiana University School of Medicine, Indianapolis.
Angiotensin-converting enzyme (ACE) was localized in perfused trout gills by measuring gill extraction of two radiolabeled ACE inhibitors, 125I-351A (an iodinated derivative of lisinopril) and 3H-RAC-X-65, and by autoradiography of gills perfused with 125I-351A. A 125I-351A pulse was preferentially extracted by the arterio-arterial (AA) pathway (61.7% +/- 1.8% extraction; mean +/- SE, N = 4); the arteriovenous (AV) pathway extracted an additional 10%. Extraction by either pathway was reduced by simultaneous perfusion with 10(-5) M unlabeled lisinopril. AA extraction of RAC-X-65 during continuous perfusion was maximal (75% +/- 5%, N = 6) during the first few minutes of perfusion and decreased steadily to 38% +/- 9% by 20 min and to less than 10% by 40 min. AV extraction of RAC-X-65 was negligible. Autoradiography of gills continuously perfused with 125I-351A showed that the radiolabel was concentrated in the respiratory lamellae. The highest grain density was associated with the pillar cells nearest the medial (inner) lamellar margin. Afferent filamental arteries and afferent lamellar arterioles were labeled to a lesser extent. Relatively little label was found on the efferent lamellar arterioles or efferent filamental arteries. 125I-351A binding was not evident in AV vessels. These findings support the hypothesis that the gill is an important site for formation of plasma angiotensin II and they suggest that enzymes associated with mammalian endothelial cells are also common to gill pillar cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2542430&dopt=Abstract
Kidney Int. 1988 Mar;33(3):652-5.
Partial protein sequence of mouse and bovine kidney angiotensin converting enzyme.
Bernstein KE, Martin BM, Striker L, Striker G.
Renal Cell Biology Group, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland.
Angiotensin converting enzyme (ACE) plays an important role in the regulation of renal blood pressure by the hydrolysis of the inactive precursor peptide angiotensin I to the potent vasopressor angiotensin II. Renal ACE is a surface membrane protein of both endothelium and tubular epithelium. Enzymatically active ACE was isolated from renal homogenates by chromatography using an affinity column constructed by linking an ACE inhibitor, lisinopril, to Affi-Gel 15. Analysis of eluates from this column showed that ACE activity was increased greater than 500-fold. SDS-polyacrylamide gel electrophoresis demonstrated a single band of molecular weight 144 kD (mouse) and 149 kD (bovine). N-terminal amino acid sequence analysis revealed: (formula; see text) Though bovine ACE has one additional N-terminal amino acid, these two partial sequences are highly homologous (16 of 20 positions are identical). Mouse ACE was digested with trypsin and the peptides were isolated by reverse phase HPLC. Analysis of the amino acid sequences showed that these tryptic peptides were unique to ACE. Thus, we were able to isolate ACE from bovine and mouse kidneys and show that they had substantial structural homology. They were also quite similar to that from rabbit lung.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2835538&dopt=Abstract
Acta Diabetol. 1993;30(1):46-8.
Rapid reversal of a motor nerve conduction deficit in streptozotocin-diabetic rats by the angiotensin converting enzyme inhibitor lisinopril.
Cameron NE, Cotter MA, Robertson S.
Department of Biomedical Sciences, University of Aberdeen, Marischal College, UK.
The effect of treatment of rats with the angiotensin converting enzyme inhibitor lisinopril after 5 weeks of untreated streptozotocin-diabetes was examined by daily monitoring of sciatic motor conduction velocity to tibialis anterior muscle. Diabetes produced a 31.5% decrease in conduction velocity (P < 0.001). Lisinopril treatment caused a progressive improvement which was significant after 3 days (P = 0.002), full normalization being achieved by 6 days (P < 0.0001). After 7 days of treatment there followed a 7-day washout period in which no lisinopril was given. During this time conduction velocity declined to untreated diabetic levels over 3 days. A subsequent treatment period resulted in complete normalization of conduction velocity within 2 days (P < 0.0001). Thus, the marked functional effects seen for vasodilator treatment with lisinopril suggest that angiotension converting enzyme inhibitors may have potential therapeutic value in the treatment of diabetic neuropathy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8392403&dopt=Abstract
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