Causal and homoeostatic factors in hypertension

It is an honour and privilege to give this lecture to commemorate the great contributions made by Franz Volhard to hypertension research. Through outstanding clinical and pathological studies, Volhard and his collaborators separated what we now know as essential hypertension from the hypertension associated with nephritis and other types of parenchymal renal disease, and described malignant hypertension. Up till then these disorders had all been lumped together as complications of Bright’s disease. Volhard’s great monograph Die Doppelseitigen Haematogenen Nierenerkrankungen (Bright’sche Krankheit) [ll was published in 1918 and contains a wealth of material and hypotheses about the causes of hypertension. He speculated that the pale, sickly looking patient with renal disease, the ‘blasse Hochdruckkranke’, had a humoral factor constricting his arteries, and showed that this was not a catecholamine. In addition, he considered that primary arteriosclerotic changes of the renal arteries might be responsible for the hypertension in the well looking patient with essential hypertension, the ‘rote Hochdruckkranke’. The modern classification of hypertension into primary or essential hypertension, and secondary hypertension with known pathological causes [2], grew directly from the famous classification of Volhard & Fahr [31. All types of established hypertension have, however, many features in common; for example, the adaptive hypertrophy of the heart and resistance vessels which Bjorn Folkow discussed in the Fourth Volhard Lecture [41. Unfortunately we still know too little about the full sequence of steps in the pathogenesis of almost every type of secondary hypertension, even when we produce it ourselves in the laboratory. Such knowledge is important if we