Transfer of renovascular hypertension and coronary heart disease by lymphoid cells from SLE-prone mice.

Among early life SLE mice, the male F1 hybrids of NZW X BXSB crosses are unique by their much earlier onset of glomerulonephritis (GN) (evident by 2 1/2 months of age), progressive hypertension, and high frequency of degenerative cardiovascular disease (CVD) with myocardial infarcts. In contrast, their female counterparts and the other kinds of SLE mice have later onset of GN, minimal hypertension, and lower incidence of CVD. The etiopathogenesis of these F1 males' disease was investigated by reciprocally transferring syngeneic lymphoid cells into lethally irradiated F1 male and female mice. As a result, female recipients of male lymphoid cells developed accelerated GN, hypertension, and severe CVD, but the male recipients of female lymphoid cells (at comparable ages) had delayed SLE, remained normotensive, and were spared coronary or myocardial damage. These findings strongly indicate that the hypertension and CVD of these F1 males originate from immunologic abnormalities rather than from other nonlymphoid factors.