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We investigated sodium-proton (Na(+)-H+) exchange activity in transgenic TGR(mRen-2)27 rats, a strain showing fulminant hypertension after the mouse Ren-2d renin gene has been integrated into its genome, in age-matched normotensive Sprague-Dawley (SD) rats, in spontaneously hypertensive rats (SHR) from the Münster strain, and in normotensive Wistar-Kyoto (WKY) rats. From each strain Na(+)-H+ exchange activity was determined 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 (pHi) after intracellular acidification. Resting pHi was not significantly different in transgenic rats (n = 10) compared with SD rats (n = 10) (7.305 +/- 0.038 versus 7.337 +/- 0.031; mean +/- SEM), but resting pHi was significantly lower in lymphocytes from SHR (n = 12) compared with their normotensive WKY counterparts (n = 12) (7.232 +/- 0.030 versus 7.377 +/- 0.022; P &lt; .01). Na(+)-H+ exchange activity was significantly lower in lymphocytes from transgenic rats compared with SD rats (5.102 +/- 0.561 versus 7.385 +/- 0.491 x 10(-3) dpHi/s; P &lt; .01), whereas Na(+)-H+ exchange was significantly enhanced in lymphocytes from SHR compared with WKY rats (5.564 +/- 0.432 versus 3.921 +/- 0.433 x 10(-3) dpHi/s; P &lt; .05). The apparent half-maximal activation of Na(+)-H+ exchange was not significantly different in the strains tested. The present study indicates that hypertension in transgenic rats is not related to Na(+)-H+ exchange overactivity.

Reduced sodium-proton exchange activity in lymphocytes from transgenic rats.