In addition increased responsiveness of α1B-adrenoreceptors to NA, PE and ME may be attributed to the local vasodilation in the kidney by the upregulation of CSE/H2S and eNOS/NO/cGMP pathways, which is supported by a previous study in which α1B-adrenoreceptor subtype mediated the renal vasoconstriction in a rat model of chronic renal disease induced with cisplatin [59]. Here, NOS3 is linked to chronic kidney disease.