Abstract

Renal blood flow, which is lower in the immature than in the mature animal, achieves adult values in human subjects by 1-2 years of age. The age-related increase in renal blood flow cannot be completely explained by increases in kidney size, since nephrogenesis is complete by 36 weeks' gestation in humans. Thus, other factors, especially changes in renal hemodynamics, are likely to be responsible for the increase in renal blood flow. The increase in renal blood flow appears to be directly related to the decrease in renal vascular resistance during the postnatal period. Decreases in the effect of renal vasoconstrictors, increases in the effect of renal vasodilators, or a combination of the two, may be responsible. Many mediators of vasoconstriction have been studied, including adenosine, catecholamines, endothelin, endogenous digitalis-like peptide, and the renin-angiotensin system. Mediators of vasodilation include endothelium-derived relaxing factor (e.g., nitric oxide), prostaglandins, atrial natriuretic peptide, dopamine, and kinins. However, the decrease in renal vascular resistance with age is most likely related to decreases in activity of the renin-angiotensin system and responsiveness to catecholamines; these effects are modulated by nitric oxide. Other mediators may also be important in determining the age-related decrease in renal vascular resistance, but their exact roles remain to be defined.

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