Emotional reactivity to social rejection and negative evaluation among persons with borderline personality features.

The present study examined the emotional reactivity of persons with heightened borderline personality (BP) features to social rejection and negative evaluation in the laboratory. Individuals with high levels of BP features (n = 30) and controls with low levels of BP features (n = 44) were randomly assigned to a condition involving negative evaluation based on writing (negative evaluation/academic), or a condition involving negative evaluation based on personal characteristics as well as social rejection (negative evaluation/social rejection). Hypothesis 1 was that high-BP individuals, but not low-BP controls, would show greater emotional reactivity to the negative evaluation/social rejection stressor, compared with the negative evaluation/academic (writing) stressor.

Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism.

Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature.

Renal cortical vasoconstriction contributes to development of salt-sensitive hypertension after angiotensin II exposure.

Rats that are administered angiotensin II (AngII) for 2 wk develop persistent salt-sensitive hypertension, which can be prevented by the immunosuppressor mycophenolate mofetil (MMF) given during the AngII infusion. This study examined the contribution of glomerular hemodynamics (GFR dynamics) in the post-AngII hypertensive response to a high-salt diet (HSD) and the effect of MMF treatment. During AngII administration, rats developed severe hypertension (systolic BP [SBP], 185 +/- 3.

Protective role of nitric oxide in a model of thrombotic microangiopathy in rats.

Anew model of thrombotic microangiopathy (TMA) was previously developed, and it was demonstrated that endothelial nitric oxide (NO) synthase (NOS) is upregulated in glomeruli in this model. It was hypothesized that the synthesis of NO, a potent vasodilator and platelet inhibitory factor, is induced as a defense mechanism. The goal of this study was to clarify the role of NO in this model.

Impaired angiogenesis in the remnant kidney model: I. Potential role of vascular endothelial growth factor and thrombospondin-1.

Few studies have examined the role of the microvasculature in progressive renal disease. It was hypothesized that impaired angiogenesis might occur in the diseased kidney and could contribute to renal scarring. Progressive renal disease was induced in rats by 5/6 renal ablation and those rats were compared with sham-operated control animals at multiple time points, for examination of changes in the microvasculature and the expression of angiogenic factors.