The physiological effects of angiotensin II (ANG II) on the kidney are mediated primarily by the ANG II type 1 (AT1) receptor. Two highly similar AT1 receptor subtypes have been identified in the rat by molecular cloning techniques, namely AT1A and AT1B. The intrarenal localization of the AT1A and AT1B receptor subtypes has not been studied by hybridization methods with subtype-specific receptor probes. Using radiolabeled probes from the 3' noncoding region of the AT1A and AT1B cDNAs, we localized AT1 mRNA in rat kidney by in situ hybridization. Specificity of the 3' noncoding region probes was tested by Northern blot and solution hybridization methods. AT1A mRNA levels were highest in the liver, kidney, and adrenal. In contrast, AT1B mRNA levels were highest in the adrenal and pituitary and low in kidney. Autoradiographic localization of 125I-[Sar1,Ile8]ANG II binding indicated that the highest levels of AT1 receptors were found in glomeruli and vascular elements. In situ hybridization with a nonselective AT1 receptor riboprobe indicated that the highest levels of AT1 mRNA were in the outer medullary vasa recta and cortical glomeruli with additional diffuse labeling of the cortex and outer medulla, consistent with labeling of tubular elements. In contrast, in situ hybridization with the AT1 subtype selective probes revealed that AT1A receptor mRNA was primarily localized to the vasa recta and diffusely to the outer stripe of the outer medulla and the renal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

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Byproduct formation (chlorate, bromate, organic halogen, etc.) during sulfate radical (SO4 •–)-based processes like ultraviolet/peroxymonosulfate (UV/PMS) has aroused widespread concern. However, hypohalous acid (HOCl and HOBr) can form via two-electron transfer directly from PMS, thus leading to the formation of organic halogenated byproducts as well. This study found both PMS alone and UV/PMS can increase the toxicity to mammalian cells of wastewater, while the UV/H2O2 decreased the toxicity. Cytotoxicity of two wastewater samples increased from 5.6–8.3 to 15.7–29.9 mg-phenol/L, and genotoxicity increased from 2.8–3.1 to 5.8–12.8 μg 4-NQO/L after PMS treatment because of organic halogen formation. Organic halogen formation from bromide rather than chloride was found to dominate the toxicity increase. The SO4 •–-based process UV/PMS led to the formation of both organic halogen and inorganic bromate and chlorate. However, because of the very low concentration (<20 μg/L) and relatively low toxicity of bromate and chlorate, contributions of inorganic byproducts to toxicity increase were negligible. PMS would not form chlorate and bromate, but it generated a higher concentration of total organic halogen, thus leading to a more toxic treated wastewater than UV/PMS. UV/PMS formed less organic halogen and toxicity because of the destruction of byproducts by UV irradiation and the removal of byproduct precursors. Currently, many studies focused on the byproducts bromate and chlorate during SO4 •–-based oxidation processes. This work revealed that the oxidant PMS even needs more attention because it caused higher toxicity due to more organic halogen formation.