Ma X Y, Sun G Q, He R R
Department of Physiology, Institute of Basic Medicine, Hebei Medical College, Shijiazhuang.
Sheng Li Xue Bao. 1997 Feb;49(1):54-60.
The effects of intraventricular injection of adenosine and its analogues on renal sympathetic nerve activity (RSNA) were examined in sinoaortic denervated and vagotomized anesthetized rats. In response to intraventricular bolus injection of adenosine, RSNA was increased by 41.9 +/- 6.08% (P < 0.001), mean arterial pressure (MAP) was initially increased by 1.39 +/- 0.19 kPa (P < 0.001) and subsequently decreased by 3.74 +/- 0.64 kPa (P < 0.001), and heart rate (HR) was reduced by 95 +/- 14 bpm (P < 0.001). To determine the adenosine-receptor subtype which mediates the response of RSNA to adenosine, we used selective A1-receptor agonist (R-PIA) and A2-receptor agonist (NECA) and found that MAP and HR were reduced by R-PIA and NECA. The effects lasted significantly longer than those of adenosine. R-PIA induced an increase in RSNA by 31.6 +/- 5.21% (P < 0.001), while NECA showed no effect on RSNA. The renal sympathoexcitatory response to intraventricular injection of adenosine was completely inhibited by pretreatment with a selective A1-receptor antagonist (DPCPX). Following the bilateral stellate ganglionectomy, intraventricular injection of adenosine failed to induce the increase in RSNA. The results indicate that adenosine may activate cardiac sympathetic afferents through A1-receptor, resulting in a reflex augmentation of RSNA.