Drugs online research references
Neuropeptides. 1995 Mar;28(3):137-45.
Substrate- and inhibitor-specificity of a non-endothelial enzyme which forms [Met5]-enkephalin from [Met5]-enkephalin-Arg6,Phe7 in isolated rabbit ear artery: pharmacological characterization.
Ronai AZ, Feher E, Botyanszki J, Hepp J, Magyar A, Medzihradszky K.
Institute of Organic Chemistry, L. Eotvos University, Budapest, Hungary.
The captopril-inhibited enzyme which forms [Met5]-enkephalin from [Met5]-enkephalin-Arg6,Phe7 in isolated rabbit ear artery was characterized further by using various natural substrate candidates/analogues ([Met5]-enkephalin-Arg6,Phe7 and its amide, [Met5]-enkephalin, angiotensin I and bradykinin), peptidase inhibitors such as captopril, enalaprilate and thiorphan and by endothelial removal. 10(-5) and 10(-4) M but not 10(-6) M captopril reduced the effectiveness of [Met5]-enkephalin-Arg6,Phe7 and potentiated the effect of bradykinin but did not affect markedly the action of the other peptides. Of the inhibitors, enalaprilate was less effective than captopril, and thiorphan had no effect. The [Met5]-enkephalin-Arg6,Phe7-->[Met5]-enkephalin conversion was not affected by endothelial removal. The substrate and inhibitor spectrum of this non-endothelial enzyme activity bears no relationship in other, hitherto characterized dipeptidylcarboxypeptidases/endopeptidases known to be involved in the metabolism of the tested peptides.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7791957&dopt=Abstract
J Cardiovasc Pharmacol. 1993;22 Suppl 5:S17-22.
Different effects of angiotensin-converting enzyme inhibition in human arteries and veins.
Yang Z, Arnet U, von Segesser L, Siebenmann R, Turina M, Luscher TF.
Department of Medicine, University Hospitals Basel, Switzerland.
The renin-angiotensin system (RAS) participates in the regulation of vascular tone; its effects were studied in human internal mammary artery (IMA) and saphenous vein (SV) suspended in organ chambers for isometric tension recording. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine. The contractions to angiotensin I (Ang I; 10(-7) M) were markedly inhibited by enalaprilat (10(-7) M) in SV (control: 34 +/- 6% of 100 mM KCl; treatment: 18 +/- 6%; n = 7; p < 0.05) but not in IMA (control: 33 +/- 4%; treatment: 30 +/- 6%; n = 7; NS) and abolished by the Ang II receptor antagonist DuP 753 (10(-7) M) in both blood vessels. Ang II (10(-7) M) induced more pronounced contractions than Ang I in IMA (63 +/- 4%) and SV (63 +/- 5%; n = 5-6; p < 0.05 vs. Ang I), which was markedly inhibited by DuP 753 (10(-7) M; IMA: 21 +/- 5%; SV: 32 +/- 5%; p < 0.05). Thus, in SV but not IMA, ACE inactivates bradykinin and thereby blunts endothelium-dependent relaxations to the peptide and converts Ang I to Ang II.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7508047&dopt=Abstract
Eur J Pharmacol. 1994 Jun 23;259(1):27-36.
Renal actions of the angiotensin AT2 receptor ligands CGP 42112 and PD 123319 after blockade of the renin-angiotensin system.
Macari D, Whitebread S, Cumin F, De Gasparo M, Levens N.
Ciba-Geigy Ltd., Basel, Switzerland.
The purpose of this study was to investigate whether the selective angiotensin AT2 receptor ligands, CGP 42112B (Nic-Tyr-(N alpha-benzoyloxycarbonyl-Arg)Lys-His-Pro-Ile-OH) and PD 123319 ((s)-1-[[4-(dimethylamino)-3-methyl-phenyl]methyl]-5-(diphenylacetyl+ ++)-4,5,6,7-tetrahydro-1H-imidazo[4,5-c]-pyridine-6-carboxylic acid) are agonists at angiotensin receptors influencing blood pressure and renal function in the enalaprilat-treated anesthetized rat. The agonist angiotensin II significantly increased blood pressure and renal vascular resistance. Glomerular filtration rate was unchanged by angiotensin II. Effective renal blood flow decreased significantly in response to angiotensin II leading to a significant increase in filtration fraction. Angiotensin II did not induce significant change in urinary potassium excretion or free water formation but significantly increased both urine volume and urinary sodium excretion. At doses up to 3 orders of magnitude greater than angiotensin II, CGP 42112B also significantly increased blood pressure, filtration fraction, glomerular filtration rate, urine volume and urinary sodium excretion, but did not significantly affect effective renal blood flow or renal vascular resistance. The selective angiotensin AT2 receptor ligand PD 123319 had no significant effects on blood pressure nor any measured parameter of renal function. The changes in blood pressure and renal function produced by angiotensin II and CGP 42112B could be completely blocked by the angiotensin AT1 receptor antagonist losartan. The results therefore only support a role for angiotensin AT1 receptors and not angiotensin AT2 receptors in the control of renal function in the rat and demonstrate that at high doses the angiotensin AT2 selective ligand CGP 42112B behaves as an agonist at angiotensin AT1 receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7957590&dopt=Abstract
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