Acidosis modulates physiologic and pathophysiologic processes but the mechanism of acidotic vasodilatation remains unclear. We therefore explored this in aortic rings from normal and streptozotocin-induced diabetic Sprague-Dawley rats. Phenylephrine (PE)-induced contraction in endothelium-intact and -denuded rings were recorded under normal and acidotic pH with or without drug probes. Acidosis exerted a relaxant effect in endothelium-intact and -denuded euglycaemic and diabetic tissues. l-NAME or methylene blue partially inhibited acidotic relaxation in these endothelium-intact but not the -denuded tissues, with greater inhibition in the diabetic tissues, indicating that acidosis induces relaxation by endothelium-dependent and -independent mechanisms, the former being EDNO-cGMP mediated. Indomethacin had no effect on the tissues, indicating that cyclooxygenase products are neither involved in acidosis-induced vasodilatation nor in the modulation of phenylephrine-contraction. In euglycaemic tissues under normal pH, no K(+) channel blocker altered phenylephrine-contraction, but all (except glibenclamide) enhanced diabetic tissue contraction, indicating that normally, these channels (K(ir), K(V), BK(Ca), K(ATP)) do not modulate phenylephrine-contraction, but they (except K(ATP)) are expressed in diabetes where they attenuate phenylephine-induced contraction and modulate acidosis. Only the K(ir) channel modulates acidotic relaxation in euglycaemic tissues. Only tetraethylammonium and iberiotoxin enhanced phenylephrine-induced contraction in endothelium-denuded diabetic tissues indicating that BK(Ca) attenuates phenylephrine-contraction and that acidotic relaxation in this condition is modulated by a tetraethylammonium-sensitive mechanism. In conclusion, acidosis causes vasodilatation in normal and diabetic tissues via endothelium-dependent and -independent mechanisms differentially modulated by a combination of a NO-cGMP process and K(+) channels, some of which are dormant in the normal state but activated in diabetes mellitus.
Wastewater treatment has been regarded as an effective solution in lowering the potential environmental hazards caused by palm oil mill effluent (POME). To ensure the efficient remediation of POME, the implementation of a promising strategy is necessary to overcome the limitations of conventional water treatment methods for the treatment of this pollutant. In this study, the synthesis of carbon, nitrogen codoped titanium dioxide nanoparticles (C, N-TiO2 NPs) was successfully performed by a sol-gel approach for the treatment of POME as a model pollutant under solar light irradiation. The synthesized C, N-TiO2 NPs displayed unique characteristics including an anatase phase with an average crystallite size of 11.35 nm and irregular spherical structures. Additionally, C, N-TiO2 possessed a lower band gap energy of 2.95 eV than 3.2 V of bulk anatase TiO2 and slower electron-hole (e--h+) pair recombination rate as evidenced by photoluminescence (PL) studies. The adsorption isotherm study of POME was most compatible with the Langmuir isotherm model, and the POME degradation kinetics proceeded according to first-order kinetics. Accordingly, the photocatalytic degradation of POME displayed a maximum degradation efficiency of 100% under the optimum condition of pH 7 in the presence of 0.12 g of the C, N-TiO2 photocatalyst within 150 min. The scavenging study showed that the superoxide radical (•O2 -) was the primary active species in the POME photodegradation. Finally, the reusability analysis confirmed that the C, N-TiO2 NPs could be reused for a maximum of five cycles, making them promising photocatalysts for wastewater treatment.