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 transmission in the tail artery of hypertensive rats transgenic for the mouse renin gene Ren-2 (TGR) in comparison with its control, the Sprague-Dawley (SD) rat. 2 Electrical field stimulation (EFS) of vascular segments produced frequency-dependent vasoconstrictions that were significantly greater in TGR arteries. 3 These contractions were abolished by tetrodotoxin (0.1 mu M). Phentolamine (50 nM) and prazosin (1-10 nM) produced an inhibition of these responses that was significantly greater in SD arteries, whereas that produced by yohimbine (0.5-1 mu M) was higher in TGR arteries. In both strains, propranolol (1 mu M) potentiated the responses to EFS, and this increase was observed at lower frequencies in TGR arteries. 4 The EFS-evoked [H-3]-noradrenaline (NA) release 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) increased the tritium outflow to a similar degree in both strains. 5 Exogenous NA also induced greater vasoconstriction in TGR arteries. 6 These 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.