Purpose of Review Immune mechanisms exacerbate the severity of hypertension in humans and animal models of disease. This review summarizes recent mechanistic studies exploring the pathways whereby immunity influences salt-sensitive hypertension and renal disease. Recent Findings Emphasis is placed on the role of T cell subtypes, the mechanisms of T cell activation, and the identification of potential antigens or neoantigens. Summary Significant advancements have occurred in the search for pathways which activate the adaptive immune response. An enhanced understanding of the factors contributing to hypertension can lead to better therapies.

The present study assessed the importance of immunity in angiotensin (ANG) II (5 ng·kg·min iv)-mediated hypertension in Dahl salt-sensitive (SS) rats and SS rats deficient in T and B lymphocytes (SS) fed a 0.4% NaCl diet. Baseline mean arterial blood pressure (MAP) was not different between groups. ANG II infusion significantly increased MAP in both groups, although MAP increased more rapidly in SS rats, and the maximal MAP achieved was significantly greater in SS than SS rats (190 ± 3 vs. 177 ± 3 mmHg) after 12 days. Renal damage, as assessed by albumin excretion rate, was significantly increased after 12 days of ANG lI infusion in SS (from 32 ± 4 to 81 ± 9 mg/day) and SS (from 12 ± 2 to 51 ± 8 mg/day) rats; albumin excretion rate was significantly different between SS and SS rats at all points measured. After 9 days of recovery from ANG II, MAP was decreased to a greater extent in SS than SS rats (143 ± 5 vs. 157 ± 8 mmHg) compared with the peak MAP during ANG II infusion. At this same time point, albumin excretion rate was significantly lower in SS than SS rats (42 ± 8 vs. 66 ± 7 mg/day). Further studies demonstrated an increase in CD45 total leukocytes, CD11b/c macrophages/monocytes, and CD3 T cells in kidneys of ANG II- compared with vehicle-treated SS rats. The present data suggest that infiltrating T cells in the kidney exacerbate renal damage in ANG II-induced hypertension in SS rats maintained on a 0.4% NaCl diet, similar to results observed with a salt stimulus in SS rats.

Purpose: Clinical education is an integral component of the curriculum of all physical therapy (PT) entry-to-practice programmes in Canada. The literature indicates that working with and assessing students performing below expectations (SPBE) can be procedurally and emotionally difficult. Our study aimed to explore the experiences of clinical instructors (CIs) and the decision-making process involved when supervising SPBE in PT. Method: A total of 19 in-depth, semi-structured interviews were conducted with CIs, transcribed, and coded using qualitative thematic analysis. Results: Four factors appeared to be important for CIs when they were deciding how to assess SPBE: (1) features of student performance, (2) factors related to the CIs, (3) academic and clinical facility influencers, and (4) strategies and available resources. Concerns about safety and professional behaviour, a student’s clinical reasoning skills, and a lack of progression were key factors that CIs considered in recommending a final grade. CIs were more likely to recommend a failing grade if there was a series of repeated incidents rather than an isolated incident. Conclusions: We make several recommendations for the student, CI, and facilities to consider to better support and facilitate the process of working with SPBE in PT clinical education.