Sex differences in blood pressure control: are T lymphocytes the missing link?

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See related article, pp 384–390 There is an ever expanding literature base implicating T lymphocytes in the development and progression of numerous cardiovascular diseases, including hypertension. T lymphocytes contribute to the development of hypertension in genetic, angiotensin II (Ang-II), and salt-sensitive male experimental animals.1 Among the most definitive studies implicating T lymphocytes in hypertension are studies conducted in Rag-1−/− mice, which lack B and T lymphocytes. Guzik et al2 were the first to demonstrate that these mice have a blunted hypertensive response to Ang-II infusion. Adoptive transfer of T lymphocytes into male Rag−/− mice restored the hypertensive response to Ang-II; adoptive transfer of B lymphocytes did not alter the blood pressure (BP) response. Although low-grade inflammation, and T lymphocytes in particular, are now a recognized hallmark of hypertension, the majority of basic science literature in this field has been conducted exclusively in males, despite the fact that females account for ≈50% of all hypertensive cases in the United States. Therefore, it was with great interest that we read the study by Pollow et al3 in the current issue of Hypertension , which was designed to determine (1) whether there are sex differences in the ability of T lymphocytes to induce Ang-II–dependent hypertension and (2) whether sex affects central or renal T lymphocytes infiltration after Ang-II hypertension. Of particular interest, they found that male mice exhibited a significant increase in BP and renal damage to Ang-II after the adoptive transfer of CD3+ T lymphocytes from wild-type male mice. In contrast, BP responses and renal injury to Ang-II were not significantly altered in female Rag−/− mice after adoptive transfer of T lymphocytes from males. Male Rag−/− mice also had greater renal CD3+, CD4+, CD8+, and T-regulatory cells (Tregs) …