Drugs online research references
Neuroscience. 1991;42(2):483-95.
Angiotensin converting enzyme in the monkey (Macaca fascicularis) brain visualized by in vitro autoradiography.
Chai SY, McKinley MJ, Paxinos G, Mendelsohn FA.
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.
Angiotensin converting enzyme is localized in the monkey (Macaca fascicularis) brain by in vitro autoradiography using the radiolabelled inhibitor, [125I]351A. This radioligand binds with high affinity and specificity to monkey cortical sections. Specific inhibitors of converting enzyme, lisinopril and perindoprilat complete for the radioligand binding to monkey cortex sections with inhibitory constants of 10 nM. High concentrations of angiotensin converting enzyme occur in most components of the basal ganglia including the caudate nucleus, putamen, the internal and external globus pallidus, nucleus accumbens, ventral pallidum and the reticular part of the substantia nigra. The distribution of converting enzyme in the caudate nucleus and putamen is heterogeneous, with prominent patches of higher activity. The patches in the caudate nucleus correspond closely with the acetylcholinesterase-poor striosomes. In the hypothalamus, very high levels of angiotensin converting enzyme occur in the median eminence and the pituitary stalk and high concentrations occur in the supraoptic and suprachiasmatic nuclei. Moderate, diffuse binding is observed in the median preoptic nucleus, the medial preoptic area, and in the anterior, lateral, ventromedial, posterior and arcuate nuclei. In the circumventricular organs, the subcommissural and subfornical organs exhibit high levels of angiotensin converting enzyme. The organum vasculosum of the lamina terminalis and the pineal body display moderate enzyme activities whereas the area postrema is devoid of labelling. The interpeduncular nucleus and, in the hippocampal formation, the molecular layer of the dentate gyrus are also intensely labelled. High levels of angiotensin converting enzyme activity are also detected throughout the cerebral cortex with laminations of higher activity corresponding to cell dense layers of the cortex. Layered binding is also present in the cerebellar cortex, with the most intense labelling in the molecular layer. Moderate concentrations of converting enzyme also occur in the paraventricular, medial habenula, lateral habenula and central median nuclei of the thalamus, the amygdala, the central gray, the locus coeruleus, the parabrachial nucleus and dorsal tegmental nucleus. The dorsal vagal complex, inferior olivary nucleus and the caudal subnucleus of the spinal trigeminal nucleus all display high levels of binding. Moderate, diffuse labelling is found throughout the reticular region and is also present in the gracile and cuneate nuclei. Although the overall distribution of angiotensin converting enzyme in the monkey brain resembles that in the rat, there are some striking differences. These include the high levels of binding throughout the monkey cerebral cortex and in the interpeduncular and suprachiasmatic nuclei.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1654536&dopt=Abstract
Kidney Int. 1994 Jun;45(6):1614-21.
Regulation of the renal angiotensin II receptor gene in acute unilateral ureteral obstruction.
Pimentel JL Jr, Wang S, Martinez-Maldonado M.
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
We have shown that acute (24-hr) unilateral ureteral obstruction (UUO) induces the genes encoding for renin, in juxtaglomerular apparatuses and in tubules, for angiotensin converting enzyme in vascular endothelial cells, and for angiotensinogen in perivascular fat. These molecular changes occur in temporal association to marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR), suggesting that angiotensin II (Ang II) is at least partly responsible for the renal vasoconstriction. We tested the hypothesis that down-regulation of the Ang II type-1 receptor (AT1-R) gene occurs in UUO in response to Ang II, by examining the effects of an ACE inhibitor [lisinopril (Li), 5 mg/kg/day] and of the specific nonpeptidic AT1-R blocker, losartan (Lo) (10 mg/kg/day). UUO or sham operated (which included manipulation but not obstruction of the ureter) rats (S) were studied. Northern blot analysis of the steady state concentration of AT1-R mRNA corrected for GAPDH mRNA showed a marked decrease in receptor expression (-77%, N = 4, P < 0.01) in the obstructed kidney (UUO) compared to S; sham diminished gene expression modestly compared to the contralateral kidneys (C) of UUO. In situ hybridization for AT1-R mRNA also showed diminished expression in UUO compared to C kidneys (N = 4). Treatment of UUO rats (N = 4) with Lo increased AT1-R mRNA five times above the levels in UUO rats receiving vehicle; the increase induced by Li was 50% that of Lo; S (N = 4) and C (N = 4) did not change. Losartan, but not vehicle treatment increased RBF (sixfold) and GFR (fivefold) in the UUO kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7933808&dopt=Abstract
J Cardiovasc Pharmacol. 1991 Oct;18(4):478-86.
Angiotensin converting enzyme inhibition in heart, kidney, and serum studied ex vivo after administration of zofenopril, captopril, and lisinopril.
Sun Y, Mendelsohn FA.
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.
Angiotensin converting enzyme inhibition in heart, kidney, and serum were studied ex vivo after oral administration of lisinopril (10 mg/kg), zofenopril (10 mg/kg), and captopril (30 mg/kg) to rats to study the time course, degree, and sites of inhibition of ACE by a quantitative in vitro autoradiography and enzymatic assay. ACE activity in all regions of the heart, kidney, and serum was markedly reduced 4 h after administration of lisinopril and zofenopril and only partially recovered toward control levels at 24 h. After captopril treatment, ACE activity was partially inhibited in heart, kidney, and serum at 1 h and fully recovered toward control levels in most regions at 24 h. These results suggest that these inhibitors reduce ACE in all regions of the heart and kidney without regional selective inhibition. Lisinopril and zofenopril at these doses produced longer-lasting ACE inhibition than captopril. ACE recovery after ACE inhibitor treatment in serum was faster than in heart or kidney.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1724523&dopt=Abstract
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