P. Lantelme et al., MECHANISMS OF SPONTANEOUS BAROREFLEX IMPAIRMENT IN LYON HYPERTENSIVE RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 44(3), 1998, pp. 920-925
This experiment aimed at 1) comparing the spontaneous baroreflex sensi
tivity (SBRS) in Lyon genetically hypertensive (LH), normotensive (LN)
, and low blood pressure (LL) rats and 2) assessing some aspects of th
e mechanisms of its impairment in LH rats. Baroreflex was studied in c
ontrol animals after an early chronic converting enzyme inhibition wit
h perindopril and after a 4-wk infusion of ANG II in perindopril-treat
ed rats. The SBRS was determined with a previously validated method, u
sing statistical dependence between blood pressure (BP) and heart rate
values recorded in freely moving animals. LH rats exhibited high BP,
cardiac hypertrophy, and decreased SBRS (LH, 1.3 +/- 0.2; LN, 2.5 +/-
0.4; LL, 2.2 +/- 0.4 beats .min(-1).mm.Hg-1). Perindopril prevented th
e development of hypertension and cardiac hypertrophy and normalized S
BRS. BP rose in LH and LL rats after ANG II infusion, but only LH rats
, which developed a cardiac hypertrophy, had an impaired SBRS (LH, 1.1
+/- 0.2; LN, 2.5 +/- 0.2; LL, 2.8 +/- 0.3 beats.min(-1).mm.Hg-1). Thi
s impairment was partially reversed by an acute ANG II blockade with l
osartan. These results demonstrate that high BP does not account for t
he decreased SBRS in LH rats. SBRS impairment could result either from
cardiac hypertrophy or from the direct effect of ANG II on the barore
flex loop.