AIDS, lupus, rheumatoid arthritis--hypertension?

W hat have these disease entities in common?There would be little argument among physicians and basic science investigators that an underlying defect in immunologic function is a major contributing factor in the etiology of acquired immunodeficiency syndrome, systemic lupus erythematosus, and rheumatoid arthritis.But immunologic dysfunction in hypertension is another matter.Physicians who treat hypertensive patients and researchers involved in the study of hypertension would quickly point to alterations in renal function, enhanced vascular smooth muscle reactivity, increased sympathetic tone or alterations in the renin-angiotensin system as major contributors to the development of hypertension.It would indeed be rare for immune function to be mentioned in discussions of this disease.Perhaps this should be reconsidered in light of the growing body of evidence that implicates altered immunologic function in the development of some forms of hypertension.The article by Tuttle and Boppana that appears in this volume should certainly help to bring the involvement of immune mechanisms in the pathogenesis of spontaneous hypertension in rats into focus.These investigators report that a single injection (5,000 units/kg) of human recombinant interleukin-2 (IL-2), given to young spontaneously hypertensive rats (SHR) before the development of hypertension, blocked the progressive elevation in arterial pressure as these animals grew to maturity.Furthermore, IL-2 administration to SHR with established hypertension lowered the elevated arterial pressure to control levels.This provocative finding, if verified by other laboratories, will certainly lend substance to the claim that immunologic dysfunction is a contributing factor in the development of hypertension in this model and might be implicated in human hypertension.For the past several years, a number of research groups, including our own, have been involved in studies linking altered immune function with the development of spontaneous hypertension.Takeichi et al 2 suggested that the SHR was immunologically