This study aimed to examine whether lipopolysaccharide (LPS)-induced increase in tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) gene transcription was regulated by beta-adrenoceptor activation and whether TNF-alpha and IL-6 gene transcription was regulated by angiotensin II in rat renal resident macrophage cells. The cells were transfected with a fusion gene with the 5'-flanking region of rat TNF-alpha or IL-6 genes linked to a luciferase coding sequence as a reporter. The stimulatory effect of LPS on TNF-alpha transcription was suppressed by isoproterenol (10(-8)-10(-5)M) in a dose-dependent manner, whereas IL-6 transcription was only decreased by the high concentration (10(-5)M) of isoproterenol. The addition of beta(2)-adrenoceptor antagonist (ICI118,551), but not a beta(1)-adrenoceptor antagonist (atenolol), blocked the inhibitory effect of isoproterenol. By contrast, angiotensin II (10(-8)-10(-5)M) enhanced IL-6 gene transcription in the cells in a dose-dependent manner which was inhibited by type 1 angiotensin II receptor antagonist (CV11,974). TNF-alpha and IL-6 secretion from the cells was altered with beta(2)-adrenoceptor agonists (terbutaline, formoterol) and angiotensin II corresponding to changes of TNF-alpha and IL-6 gene transcription. Angiotensin II had no effect on TNF-alpha secretion and gene transcription. These findings suggested that beta(2)-adrenoceptor agonist and angiotensin II potentially could influence renal immune function through the regulation of TNF-alpha and IL-6 gene transcription by the renal resident macrophage cells.