We investigated sodium-proton (Na+-H+) exchange activity in transgenic
TGR(mRen-2)27 rats, a strain showing fulminant hypertension after the
mouse Ren-2(d) renin gene has been integrated into its genome, in age
-matched normotensive Sprague-Dawley (SD) rats, in spontaneously hyper
tensive rats (SHR) from the Munster strain, and in normotensive Wistar
-Kyoto (WKY) rats. From each strain Na+-H+ exchange activity was deter
mined in lymphocytes using the pH-sensitive fluorescent dye 2',7'-bis(
2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM)
by measuring the recovery rate of cytosolic pH (pH(i)) after intracel
lular acidification. Resting pH(i) was not significantly different in
transgenic rats (n=10) compared with SD rats (n=10) (7.305+/-0.038 ver
sus 7.337+/-0.031; mean+/-SEM), but resting pH(i) was significantly lo
wer in lymphocytes from SHR (n=12) compared with their normotensive WK
Y counterparts (n=12) (7.232+/-0.030 versus 7.377+/-0.022; P<.01). Na-H+ exchange activity was significantly lower in lymphocytes from tran
sgenic rats compared with SD rats (5.102+/-0.561 versus 7.385+/-0.491x
10(-3) dpH(i)/s; P<.01), whereas Na+-H+ exchange was significantly enh
anced in lymphocytes from SHR compared with WKY rats (5.564+/-0.432 ve
rsus 3.921+/-0.433x10(-3) dpH(i)/s; P<.05). The apparent half-maximal
activation of Na+-H+ exchange was not significantly different in the s
trains tested. The present study indicates that hypertension in transg
enic rats is not related to Na+-H+ exchange overactivity.