Immune system dysfunction contributes to the aetiology of spontaneous hypertension

Spontaneously hypertensive rats (SHRs) have a depressed T lymphocyte system, especially a reduced activity of the suppressor T cells, and it has been postulated that an auto-immune defect may be important in the aetiology of hypertension in these rats. In an earlier study we demonstrated that chronic immunosuppressive therapy prevents approximately 50% of the hypertension in the SHR. In the present study, an attempt was made to correct the immune imbalance by implanting thymic tissue from normotensive rats into SHRs. Weekly thymic implants from Wistar donor rats into 16-week-old SHRs produced a maximal reduction (P less than 0.05) in the tail-cuff pressure, after 4 weeks, to a level of 156 +/- 2.3 mmHg (n = 8) in thymus-implanted SHRs versus 189 +/- 2.5 mmHg (n = 6) in sham-implanted SHRs. Also, neonatal thymic implants delayed development of spontaneous hypertension and attenuated the final hypertensive state. Mean arterial pressure averaged 186 +/- 2.8 mmHg in 22-week-old, neonatally sham-implanted SHRs, while it was reduced (P less than 0.05) to 164 +/- 4.2 mmHg in the neonatally thymus-implanted SHRs at this time. The thymic implants had little effect on total T cell, helper T cell or suppressor T cell counts. However, the antihypertensive effect of the thymic implants was associated with a substantial increase in the blastogenic responsiveness of suppressor T cells from the SHRs. These results support the hypothesis that immunological dysfunction plays an important role in the aetiology of spontaneous hypertension.