PARTIAL TRANSFER OF GENETIC-HYPERTENSION BY LYMPHOID-CELLS IN LYON RATS

Background and objective: The involvement of immune factors in a given disease is suggested by evidence that a disease can be prevented by i mmunosuppression and can be transferred by lymphoid cells. Because the first type of experimental result was achieved in Lyon hypertensive ( LH) rats, the present study was undertaken to determine whether hypert ension can be transferred to normotensive recipients. As a control, th e blood pressure effects of lymphoid cell grafts from renovascular hyp ertensive donors were also determined. Design and methods: Splenocytes and lymph node cells from LH and Lyon low-blood pressure (LL) rats wi th two-kidney Goldblatt hypertension were respectively injected into L H x Lyon normotensive (LN) F-1 hybrids and LL rats aged 7, 8, 9 and 10 weeks. Blood pressure was measured by plethysmography from age 6 to 1 3 weeks and an intra-arterial recording was performed in 14-week-old c onscious rats. Results: Lymphoid cell injections from LL rat donors wi th two-kidney hypertension did not modify the blood pressure of LL rat recipients. In contrast, lymphoid cell grafts from LH rat donors indu ced a significant increase in blood pressure in F-1 recipients compare d with control F-1 rats after the first injection. As confirmed by int ra-arterial recording, this blood pressure effect lasted until ape 14 weeks (145 +/- 1 versus 137 +/- 1 mmHg in grafted and ungrafted F-1, r espectively). It was not related to alterations in the acute role of t he renin-angiotensin and sympathetic nervous systems and was not assoc iated with increased presser responses to the vasoconstrictor drugs te sted. Conclusion: The present study demonstrates that genetic hyperten sion can be partially transferred by lymphoid cells in F-1 recipients. The effect seems to be specific to genetic hypertension because lymph oid cells from renovascular hypertensive donors failed to transfer thi s secondary form of hypertension. The present results support the hypo thesis that cellular immune reactions contribute to the pathogenesis o f hypertension and LH rats.