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Recent studies have indicated that urotensin II (UII), a cyclic peptide, is vasoactive and may be involved in cardiovascular dysfunctions. It remains unknown, however, whether UII plays a role in the control of renal vascular tone and tubular function. In the present study, a continuous infusion of synthetic human UII (hUII) into the renal artery (RA) in anesthetized rats was found to increase renal blood flow (RBF) and urinary water and sodium excretion (UV and [U.sub.Na.]V) in a dose-dependent manner. At a dose of 20 ng*[kg.sup.-1]. [min.sup.-1], it increased RBF by 20% and UV and [U.sub.Na]V by 94 and 109%, respectively. Nitric oxide (NO) synthase inhibitor [N.sup.G]-nitro-L-arginine methyl ester (L-NAME) completely abolished hUII-induced increases in RBF and water/sodium excretion. In isolated, pressurized, and phenylephrine-precontracted small RA with internal diameter of ~200 [micro]m, hUII produced a concentration-dependent vasodilation with a maximal response of 55% at 1.5 [micro]M. L-NAME significantly blocked this hUII-induced vasodilation by 60%. In denuded RA, hUII had neither vasodilator nor vasoconstrictor effect. With the use of 4,5-diaminofluorescein diacetate-based fluorescence imaging analysis of NO levels, hUII (1 [micro]M) was shown to double the NO levels within the endothelium of freshly dissected small RA, and L-NAME blocked this UII-induced production of endothelial NO. These results indicate that UII produces vasodilator and natriuretic effects in the kidney and that UII-induced vasodilation is associated with increased endothelial NO in the RA. natriuretic factor; renal circulation; sodium reabsorption; renal tubule; renal hemodynamics

A membrane-permeable SOD mimetic, 4-hydroxytetramethyl-piper-idine-1-oxyl (tempol), has been used as an antioxidant to prevent hypertension. We recently found that this SOD mimetic could not prevent development of hypertension induced by inhibition of renal medullary SOD with diethyldithiocarbamic acid. The present study tested a hypothesis that increased [H.sub.2][0.sub.2] counteracts the effects of tempol on renal medullary blood flow (MBF) and Na+ excretion ([U.sub.Na]V), thereby restraining the antihypertensive effect of this SOD mimetic. By in vivo microdialysis and Amplex red [H.sub.2][0.sub.2] microassay, it was found that interstitial [H.sub.2][0.sub.2] levels in the renal cortex and medulla in anesthetized rats averaged 55.91 [+ or -] 3.66 and 102.18 [+ or -] 5.16 nM, respectively. Renal medullary interstitial infusion of tempol (30 [micro]mol*[min-sup.1]*[kg.sup.-1]) significantly increased medullary [H.sub.2][0.sub.2] levels by 46%, and coinfusion of catalase (10 mg*[min.sup.-1]*[kg.sup.-1]) completely abolished this increase. Functionally, removal of [H.sub.2][0.sub.2] by catalase enhanced the tempol-induced increase in MBF, urine flow, and [U.sub.Na]V by 28, 41, and 30%, respectively. Direct delivery of [H.sub.2][0.sub.2] by renal medullary interstitial infusion (7.5-30 nmol*[min.sup.-1]*[kg.sup-1]) significantly decreased renal MBF, urine flow, and [U.sub.Na]V, and catalase reversed the effects of [H.sub.2][0.sub.2]. We conclude that tempol produces a renal medullary vasodilator effect and results in diuresis and natriuresis. However, this SOD mimetic increases the formation of [H.sub.2][0.sub.2], which constricts medullary vessels and, thereby, counteracts its vasodilator actions. This counteracting effect of [H.sub.2][0.sub.2] may limit the use of tempol as an antihypertensive agent under exaggerated oxidative stress in the kidney. free radicals; renal hemodynamics; renal medulla; kidney; rat

cADP ribose (cADPR) serves as second messenger to activate the ryanodine receptors (RyRs) of the sarcoplasmic reticulum (SR) and mobilize intracellular [Ca.sup.2+] in vascular smooth muscle cells. However, the mechanisms mediating the effect of cADPR remain unknown. The present study was designed to determine whether FK-506 binding protein 12.6 (FKBP12.6), an accessory protein of the RyRs, plays a role in cADPR-induced activation of the RyRs. A 12.6-kDa protein was detected in bovine coronary arterial smooth muscle (BCASM) and cultured CASM cells by being immunoblotted with an antibody against FKBP12, which also reacted with FKBP12.6. With the use of planar lipid bilayer clamping techniques, FK-506 (0.01-10 [micro]M) significantly increased the open probability (N[P.sub.o]) of reconstituted RyR/[Ca.sup.2+] release channels from the SR of CASM. This FK-506-induced activation of RyR/[Ca.sup.2+] release channels was abolished by pretreatment with anti-FKBP12 antibody. The RyRs activator cADPR (0.1-10 [micro]M) markedly increased the activity of RyR/[Ca.sup.2+] release channels. In the presence of FK-506, cADPR did not further increase the N[P.sub.o] of RyR/[Ca.sup.2+] release channels. Addition of anti-FKBP12 antibody also completely blocked cADPR-induced activation of these channels, and removal of FKBP12.6 by preincubation with FK-506 and subsequent gradient centrifugation abolished cADPR-induced increase in the N[P.sub.o] of RyR/ [Ca.sup.2+] release channels. We conclude that FKBP12.6 plays a critical role in mediating cADPR-induced activation of RyR/ [Ca.sup.2+] release channels from the SR of BCASM. second messenger; [Ca.sup.2+] mobilization; sarcoplasmic reticulum; nucleotide

Chen, Ya-Fei, Pin-Lan Li, and Ai-Ping Zou. Oxidative stress enhances the production and actions of adenosine in the kidney. Am J Physiol Regulatory Integrative Comp Physiol281: R1808-R1816, 2001.--The purpose of this study was to determine whether superoxide anions ([O.sub2].) activate 5'-nucleotidase (5'-ND), thereby increasing the production of renal adenosine and regulating renal function. Using HPLC analysis, we found that incubation of renal tissue homogenate with the [O.sup.-.sub.2], donor K[O.sub.2] doubled adenosine production and increased the maximal reaction velocity of 5'-ND from 141 to 192 nmol.[min.sup.-1].mg [protein.sup.-1]. The [O.sup.-.sub.2].-generating system, xanthine/xanthine oxidase increased the maximal reaction velocity of 5'-ND from 122 to 204 nmol .[min.sup.-1].mg [protein.sup.-1]. Superoxide dismutase (SOD) with catalase produced a concentration-dependent reduction of 5'-ND activity in renal tissue homogenate, while the SOD inhibitor diethyl-dithiocarbamic acid significantly increased 5'-ND activity. Inhibition of disulfide bond formation by thioredoxin or thioredoxin reductase significantly decreased xanthine/xanthine oxidase-induced activation of renal 5'-ND. In in vivo experiments, inhibition of SOD by diethyldithiocarbamic acid (0.5 mg.[kg.sup.-1], .[min.sup.-1] iv) enhanced renal vasoconstriction induced by endogenously produced adenosine and increased renal tissue adenosine concentrations under control condition and in ischemia and reperfusion. We conclude that oxidative stress activates 5'-ND and increases adenosine production in the kidney and that this redox regulatory mechanism of adenosine production is important in the control of renal vascular tone and glomerular perfusion. redox signaling; renal hemodynamics; reactive oxygen species; nucleotide Received 5 February 2001; accepted in final form 25 July 2001

The focus of this work was to investigate the pyrolysis and combustion behaviors of heavy oil and its low temperature oxidation products by TG/DSC techniques. The results indicated that coke had similar reaction paths and sequences during pyrolysis and combustion process. The pyrolysis of samples mainly showed endothermic effect, while two major exothermic stages (LTO and HTO) were obviously identified on the combustion DSC curves. The magnitudes difference of the remaining mass and activation energy of the samples revealed the difference in the types of substances involved and molecular reactive sites during the pyrolysis and combustion processes. [ABSTRACT FROM AUTHOR]