Sir George Johnson FRCP (1818-96), high blood pressure and the continuing altercation about its origins.

The widely promulgated notion that long-term elevation in mean arterial blood pressure (MAP) can be caused by raised peripheral vascular resistance remains a subject of vigorous debate. According to the 1967 mathematical model of Guyton and Coleman, such a causal relationship is impossible, kidney function being the determining factor. We explore this altercation starting with Sir George Johnson's 19th-century renal vascular histological observations in patients with Bright's disease. We note the striking physiological measurements in hypertensives by Gómez and Bolomey in the 1950s, moving on to the mathematical modelling of the circulation from the 1960s up to the ∼100-parameter computer models of the present day. Confusion has been generated by the fact that peripheral resistance is raised in hypertension in close proportion to MAP whilst cardiac output often stays normal, an apparent autoregulation, the mechanism of which is poorly understood. All models allowing for the circulation to be an open system show that isolated changes in peripheral resistance cannot lead to long-term hypertension, but models fail so frequently to account for results from experiments such as salt loading that their credibility with regard to this key finding is compromised. Laboratory animal models of adrenergic renal actions resonate with a contemporary emphasis on the sympathetic nerve supply to the kidney as contributing to the characteristically markedly elevated renal afferent resistance that appears to be the most common cause of hypertension. Remarkably, there remains no account of the way in which the fixed structural changes in vessels observed by Johnson relate to this sympathetic overactivity, which can itself be modified by drugs in the medium term. In this account, we seek to locate the crime scene and identify a smoking gun.