Summary In the search for a functional role for the polarized glycoconjugates of rat collecting duct epithelial cells, the relation between binding of various lectins and expression of cellular transport enzyme profile of the cells was studied. For this purpose, principal and intercalated cells of rat kidney collecting duct were identified by morphological criteria and by their immunocytochemically determined content of (Na++K+)-ATPase and carbonic anhydrase (CA II), respectively. VariousN-acetylgalactosamine-specific lectins such as those fromHelix pomatia andMaclura pomifera revealed heterogeneity among both principal and intercalated cells, whereas -N-acetylgalactosa nine-specific lectin fromDolichos biflorus andVicia villosa bound preferentially to principal cells. Still another lectin fromArachis hypogaea reacted with most collecting duct cells in the cortex and outer medulla, but only with a subpopulation of cells in the inner medulla. Interestingly, some lectins reacted exclusively with the apical aspect of the collecting duct epithelial cells, whereas others revealed both an apical and basolateral distribution of lectin reactive glycoconjugates. The results thus show subtle differences in the glycocalyx structure of principal and intercalated cells and differences in the intracellular polarization of glycoconjugates of these cells. Thus, lectins may be useful tools in the study of the molecular mechanisms which establish and maintain the polarized functions of principal and intercalated cells. 相似文献
Histamine caused a triphasic response of human pulmonary artery strips in vitro, consisting of a small initial contraction followed by pronounced relaxation preceding a second contractile response. These characteristics were not seen with other contractile stimuli including 5-hdyroxytryptamine, leukotriene D4, and KC1. The relaxant component of this response was ablated by removal of endothelium from the vascular strips or by pretreatment of the tissues with 1μM indomethacin. Measurement of the PGI2 degradation product 6-keto-PGF1α in supernatants from histamine-challenged tissues confirmed the synthesis of PGI2. Supernatants from unstimulated or leukotriene-challenged tissues contained no detectable amounts of 6-keto-PGF1α. The histamine H1 antagonist diphenhydramine inhibited both the contractile and relaxant responses to histamine whereas the H2 antagonist cimetidine affected neither component. The released PGI2 significantly altered the dose-respons curve to histamine without inhibiting the maximal contractile responses. We conclude that histamine induces PGI2 formation from pulmonary arterial endothelium via an H1 receptor. 相似文献
Three new furanoditerpenoids of the caesalpin-type have been isolated from the roots of Caesalpinia pulcherrima. The structures of these compounds, vouacapen-5α-ol, 6β-cinnamoyl-7β-hydroxy-vouacapen-5α-ol and 8,9,11,14-didehydrovouacapen-5α-ol, were elucidated through interpretation of their spectral data. Sitosterol was also obtained. 相似文献
The polyether bridged diphosphines, (n = 1,2) have been prepared in 60–70% yield by reduction of the corresponding diphosphinedioxides with Si2Cl6 or (i-Bu)2AlH. These diphosphinedioxides have been prepared in 75–90% yield by reaction of two equivalents of the appropriate with one equivalent of di- and triethylene glycol ditosylate.In general, reaction between the diphosphines, Rh(COD)acac and HClO4 gives a mixture of species, cis-[Rh(COD)()] [ClO4] being the main complex. This complex reacts with CO to η3-trans- [)] [ClO4]. 相似文献
To determine whether agents which inhibit cytochrome P-450 enzymes also inhibit lipoxygenase, the effects of metyrapone and SKF 525-A were assessed on soybean lipoxygenase using a spectrophotometric technique which allows for measurement of both the rate and magnitude of product formation. Both SKF 525-A and metyrapone inhibited the rate of product formation and the final amount of product formed in 5 min incubations SKF 525-A was 5 to 6 times more potent than metyrapone, with the IC50 for SKF 525-A 40 uM and for metyrapone between 150 and 200 uM as determined by the total product formation in 5 minutes. Analysis of the reduced product by HPLC confirmed that the substances monitored were those generated by the 15-lipoxygenase enzyme. 相似文献
Sprague-Dawley albino rats or Long-Evans pigmented rats were exposed during the dark phase of the daily light:dark cycle to various intensities of a sunlight-stimulating white fluorescent light (0.022, 0.044, 0.110, 0.220, 0.440 or 2.200 μW/cm2) for 30 min; pineal glands and trunk blood samples were then collected and assayed for melatonin by radioimmunoassay. Albino rats exposed to irradiances of 0.110 μW/cm2 or less had pineal melatonin levels that were not significantly different from those of unexposed animals; higher irradiances significantly (P < 0.001) reduced melatonin levels. In contrast, as little as 0.022 μW/cm2 significantly (P < 0.02) reduced pineal and serum melatonin levels in the pigmented rats. These results suggest that something other than the simple presence or absence of eye pigmentation is the critical factor in determining the sensitivity of the rat's pineal to retinal-mediated photic suppression of melatonin synthesis. 相似文献
Apolipoprotein B (apoB) of plasma low density lipoproteins (LDL) binds to high affinity receptors on many cell types. A minor subclass of high density lipoproteins (HDL), termed HDL1, which contains apoE but lacks apoB, binds to the same receptor. Bound lipoproteins are engulfed, degraded, and regulate intracellular cholesterol metabolism and receptor activity. The HDL of many patients with liver disease is rich in apoE. We tested the hypothesis that such patient HDL would reduce LDL binding and would themselves regulate cellular cholesterol metabolism. Normal HDL had little effect on binding, uptake, and degradation of 125I-labeled LDL by cultured human skin fibroblasts. Patient HDL (d 1.063-1.21 g/ml) inhibited these processes, and in 15 of the 25 samples studied there was more than 50% inhibition at 125I-labeled LDL and HDL protein concentrations of 10 micrograms/ml and 25 micrograms/ml, respectively. There was a significant negative correlation between the percentage of 125I-labeled LDL bound and the apoE content of the competing HDL (r = -0.54, P less than 0.01). Patient 125I-labeled HDL was also taken up and degraded by the fibroblasts, apparently through the LDL-receptor pathway, stimulated cellular cholesterol esterification, increased cell cholesteryl ester content, and suppressed cholesterol synthesis and receptor activity. We conclude that LDL catabolism by the receptor-mediated pathway may be impaired in liver disease and that patient HDL may deliver cholesterol to cells. 相似文献