Baa, Baa, black sheep, are your kidneys full?

Abstract

The effect of genetic variance on blood pressure is about 50 %. Thus, environmental influences are major. Recent evidence has suggested that environment very early in life may influence blood pressure decades later. Barker and co-workers first proposed that intrauterine malnutrition, marked by low birth weight, predisposes persons to type 2 diabetes mellitus, hypertension, dyslipidaemia, and cardiovascular disease (Barker & Martyn, 1992; Barker et al. 1993). In this issue of The Journal of Physiology Wintour and colleagues observed that if pregnant sheep receive corticosteroids at days 26–28 during their gestation of 150 days, their offspring develop hypertension as adults (Dodic et al. 2002). Brenner & Chertow (1994) have suggested that reduction in the number of nephrons at birth leads to hyperperfusion of each nephron and resulting glomerular sclerosis, further nephron death, and a cycle of increasing blood pressure and nephron death. Glomerular filtration rate need not be reduced in this model, since the remaining (or the fewer) glomeruli do more filtration work and presumably increase in size. In rats, a decrease in nephron number of about 30 % was reported if the mothers received corticosteroids at days 11–16 of their 3-week pregnancy (Ortiz et al. 2001). A similar phenomenon has been described in rats that were food-restricted during pregnancy (Regina et al. 2001). Wintour et al. (2003) now report that dexamethasone treatment of pregnant ewes results in an increase in blood pressure of about a 10 mmHg in their offspring at 7 years of age and that their glomerular number is reduced about 40 %. The glomeruli in the dexamethasone offspring were larger and the proximal tubules were dilated, perhaps reflecting more filtrate per nephron.