Renin-angiotensin system in two genetically normotensive strains of Lyon rats

Compared to the Lyon normotensive (LN) controls, adult Lyon hypertensive ra ts (LH) exhibit a renin-angiotensin system (RAS) dependent hypertension des pite a low renin secretion. This discrepancy could be explained by the elev ated slow presser response to angiotensin II (AII) found in LH rats compare d to LN controls. To evaluate more precisely the pathophysiological importa nce of this increased response, the present work aimed at determining wheth er the characteristics of the RAS were identical in LN and low blood pressu re (LL) rats, the other normotensive control strain simultaneously selected with LH rats. Plasma and kidney renin and prorenin were measured in Ii-wee k-old LN and LL rats. Aortic blood pressure (BP) was recorded at 15 weeks o f age in freely moving rats of both strains either untreated or having rece ived an angiotensin converting enzyme inhibitor, perindopril (3 mg/kg/day o rally) since the age of 3 weeks. Acute dose-response curves were constructe d for AII and norepinephrine (NE). The long-term presser effects of AII (20 0 ng/kg/min) and NE (1000 ng/kg/min) were measured after chronic infusions in perindopril-treated LN and LL rats. LN and LL rats exhibited similar mea n BP level before (114 +/- 2 and 117 +/- 2 mm Hg, respectively) and after p erindopril treatment (91 +/- 3 and 93 +/- 1 mm Hg, respectively). Plasma an d kidney renin and prorenin were decreased in LL rats. In acute conditions, LL rats exhibited an unspecific hypersensitivity to AII and NE. Chronicall y given AII exerted a greater presser effect in LL than in LN rats after 4 weeks (113 +/- 3 v 97 +/- 5 mm Hg in LL and LN rats respectively, P < .05) and, even more, after 8 weeks of infusion (144 +/- 9 v 124 +/- 4 mm Hg in L L and LN rats respectively, P < .05). The NE was devoid of chronic presser effects. In conclusion, 1) the increased slow presser response to AII may n ot be a critical pathogenetic factor in the development of hypertension, as it also exists in normotensive LL rats; 2) LN and LL rats have the same no rmal BP despite marked differences in their RAS, thus suggesting that there could be several forms of normotension as known for hypertension; and 3) t he simple comparison between one genetically hypertensive strain and one si ngle normotensive control strain does not allow one to conclude that a phen otypic difference is of pathophysiological significance. Am J Hypertens 200 0;13:283-289 (C) 2000 American Journal of Hypertension, Ltd.