Endothelium-dependent control of vascular tone during early postnatal and juvenile growth.
Endothelial dysfunction can develop at an early age in children with risk factors for cardiovascular disease. A clear understanding of the nature of this dysfunction and how it can worsen over time requires detailed information on the normal growth-related changes in endothelial function on which the pathological changes are superimposed. This review summarizes our current understanding of these normal changes, as derived from studies in four different mammalian species. Although the endothelium plays an important role in controlling vascular tone from birth onward, the vasoactive molecules that mediate this control often change during postnatal or juvenile growth. The specifics of this transition to an adult endothelial cell phenotype can vary depending on the vascular bed. During growth, the contribution of nitric oxide to endothelium-dependent dilation generally increases in the lung, cerebral cortex, and skeletal muscle, but decreases in the intestine. Endothelial capacity for release of other vasoactive factors (e.g., cyclooxygenase products, hydrogen peroxide, carbon monoxide) can also increase or decrease during growth. Although these changes have been well documented, there is less information on their underlying cellular or molecular events. Further research is required to clarify these mechanisms, and to evaluate the functional significance of such shifts in endothelial phenotype.
Boegehold
Matthew A
MA
Department of Physiology and Pharmacology and Center for Cardiovascular and Respiratory Sciences, Robert C. Byrd Health Sciences Center, West Virginia University School of Medicine, Morgantown, WV 26505-9105, USA. mboegehold@hsc.wvu.edu
D000818:Animals; D000831:Animals, Newborn; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D004730:Endothelium, Vascular / Q000254:growth & development* / Q000502:physiology*; D020345:Enterocolitis, Necrotizing / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D007231:Infant, Newborn; D007422:Intestines / Q000098:blood supply; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000098:blood supply; D009131:Muscle, Smooth, Vascular / Q000254:growth & development / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D010547:Persistent Fetal Circulation Syndrome / Q000209:etiology / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology; D051381:Rats; D012307:Risk Factors; D012756:Sheep; D013552:Swine; D014655:Vascular Resistance / Q000502:physiology
D009569:Nitric Oxide