James P. Fisher

TL;DR: A perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension is provided.

TL;DR: The goal is to provide a detailed review of the parasympathetic and sympathetic changes that occur with exercise distinguishing between the onset of exercise and steady-state conditions, when appropriate.

TL;DR: ET and SIT were equally effective at decreasing arterial stiffness and increasing skeletal muscle capillarisation and eNOS content, suggesting that both training modes improve skeletal muscle microvascular and macrovascular function.

TL;DR: This review will specifically focus on central sympathetic overactivity and highlight three main areas of interest: 1) the pathological consequences of excessive sympathetic nerve activity; 2) the potential role of centrally derived nitric oxide in the genesis of neural dysregulation in disease; and 3) the promise of several novel therapeutic strategies targeting central sympatheticOveractivity.

TL;DR: During exercise the reduction of arterial baroreceptor reflex sensitivity at the operating point was a result of vagal withdrawal rather than an increase in sympathetic activity, suggesting that the two dynamic methods applied to evaluate arterialbaroreflex (ABR) function provide the same information as the modelled GOP.