NORADRENERGIC TRANSMISSION IN THE TAIL ARTERY OF HYPERTENSIVE RATS TRANSGENIC FOR THE MOUSE RENIN GENE REN-2

1 The aim of the present study was to analyse the noradrenergic transm ission in the tail artery of hypertensive rats transgenic for the mous e renin gene Ren-2 (TGR) in comparison with its control, the Sprague-D awley (SD) rat. 2 Electrical field stimulation (EFS) of vascular segme nts produced frequency-dependent vasoconstrictions that were significa ntly greater in TGR arteries. 3 These contractions were abolished by t etrodotoxin (0.1 mu M). Phentolamine (50 nM) and prazosin (1-10 nM) pr oduced an inhibition of these responses that was significantly greater in SD arteries, whereas that produced by yohimbine (0.5-1 mu M) was h igher in TGR arteries. In both strains, propranolol (1 mu M) potentiat ed the responses to EFS, and this increase was observed at lower frequ encies in TGR arteries. 4 The EFS-evoked [H-3]-noradrenaline (NA) rele ase was significantly greater in TGR than in SD rats. However, NA (10 nM-10 mu M) reduced and yohimbine and phentolamine (10 nM-10 mu M) inc reased the tritium outflow to a similar degree in both strains. 5 Exog enous NA also induced greater vasoconstriction in TGR arteries. 6 Thes e results suggest the existence in TGR tail artery of an increase in: (a) NA-release and alpha(2)-adrenoceptor-mediated contractions, which could contribute to the elevated blood pressure in these rats; and (b) beta-adrenoceptor-mediated vasodilatations, which may be a mechanism to counteract high blood pressure.