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Towards understanding the aetiology and pathophysiology of human hypertension: where are we now?

Journal of Human Hypertension volume 20, pages 833–836 (2006)Cite this article

As one of the earliest recorded medical conditions, hypertension and its consequences contribute significantly to worldwide morbidity and mortality. In spite of its widespread prevalence and intense research into its pathophysiology, only 5% of hypertensive patients have an identifiable cause. While our understanding of the ‘cause’ of hypertension is ever increasing, we now know that hypertension is the product of dynamic interaction between various diverse genetic, physiological, environmental and psychosocial factors. Of considerable interest is the fact that we have not yet fully determined the extent to which each of these factors contributes to the hypertensive status of an individual. While traditional teaching has associated hypertension with ‘tangible’ risk factors, such as obesity and smoking, our understanding of the underlying pathophysiology of human hypertension has grown tremendously in the past few years.

Where shall we start? The original ‘foetal origins hypothesis’ of hypertension (the so-called ‘Barker hypothesis’) generated considerable interest and controversy in assessing the significance of low birth weight and other prenatal antecedents of adult cardiovascular diseases, including hypertension. Indeed, initial nutritional experiments in animals using low-protein diets in gestation to produce hypertensive offspring appeared to validate the above hypothesis. More recently, further evidence has extended this hypothesis in human populations. For example, Pearce and Sullivan1 found a significant inverse association of birth weight and pulse pressure of schoolchildren in a cross-sectional analysis. A longitudinal analysis by Li et al.2 also showed a strong prepubertal association between low birth weight and systolic blood pressure. However, Koupil et al.3 could not find any significant association between birth weight and high blood pressure (as measured by 24 h ambulatory readings). Clearly, the debates and uncertainties will remain over the foetal origins hypothesis, and its applicability to diverse populations worldwide.

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  1. University Department of Medicine, Haemostasis, Thrombosis and Vascular Biology Unit, City Hospital, Birmingham, UK

    P Kakar & G Y H Lip

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  1. P Kakar
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Correspondence to G Y H Lip.

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Kakar, P., Lip, G. Towards understanding the aetiology and pathophysiology of human hypertension: where are we now?. J Hum Hypertens 20, 833–836 (2006). https://doi.org/10.1038/sj.jhh.1002082

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