The Role Of AT₁ Receptor In Natriuresis Induced By Brain Cholinergic Stimuli And The Change Of TH-IR In Lc And Sol

Aim and Methods : In the present study, we investigated the natriuresis induced by brain cholinergic stimuli and the TH-IR in locus coeruleus (LC) and nucleus of solitary tract (Sol), and the expression of angiotensin AT1 receptor in LC by immunohistochemistry in conscious rats. Meanwhile the influence on above effect of blocking AT1 receptor was also observed. Results: Intracerebroventricular injection of carbachol induced potent natriuresis. The natriuretic effect was partially inhibited by pretreatment of losartan, a specific blocker of angiotensin AT1 receptor. Both mean grey and number of TH-IR and AT1-IR positive neurons were markedly increased in LC and Sol after 40 minutes of i.c.v. injection of carbachol (0.5μg) (P﹤0.05). The enhancement was significantly reduced by i.c.v. injection of losartan (P﹤0.05). We also observed the clearance of inulin and PAH in rats. Intracerebroventricular injection of carbachol and losartan had no effect on GFR and RPF (P﹤0.05). Conclusion: The results above suggest that i.c.v. injection of cholinergic agonist carbachol can induced natriuresis and enhance the activity of adrenergic neurons in LC and Sol, and the expression of AT1 receptor in LC. The blockade of AT1 receptor may down regulate the above action. However GFR and RPF remained no change in the whole process. We postulate that brain adrenergic and angiotensinergic pathway jointly modulate the natriuresis induced by brain cholinergic stimuli. Moreover the angiotensinergic neurons and adrenergic neurons may interact in LC. And the above effects could not act through the change of renal plasma flow and glomerular filtration rate, but through the renal tubule by neural and humoral mechanism.