Perinatal development and adult blood pressure

Abstract

A growing body of evidence supports the concept of fetal programming in cardiovascular disease in man, which asserts that an insult experienced in utero exerts a long-term influence on cardiovascular function, leading to disease in adulthood. However, this hypothesis is not universally accepted, hence animal models may be of value in determining potential physiological mechanisms which could explain how fetal undernutrition results in cardiovascular disease in later life. This review describes two major animal models of cardiovascular programming, the in utero protein-restricted rat and the cross-fostered spontaneously hypertensive rat. In the former model, moderate maternal protein restriction during pregnancy induces an increase in offspring blood pressure of 20-30 mmHg. This hypertensive effect is mediated, in part, by fetal exposure to excess maternal glucocorticoids as a result of a deficiency in placental 11-ß hydroxysteroid dehydrogenase type 2. Furthermore, nephrogenesis is impaired in this model which, coupled with increased activity of the renin-angiotensin system, could also contribute to the greater blood pressure displayed by these animals. The second model discussed is the cross-fostered spontaneously hypertensive rat. Spontaneously hypertensive rats develop severe hypertension without external intervention; however, their adult blood pressure may be lowered by 20-30 mmHg by crossfostering pups to a normotensive dam within the first two weeks of lactation. The mechanisms responsible for this antihypertensive effect are less clear, but may also involve altered renal function and downregulation of the renin-angiotensin system. These two models clearly show that adult blood pressure is influenced by exposure to one of a number of stimuli during critical stages of perinatal development. Correspondence

Moderate Zinc Deficiency Influences Arterial Blood Pressure and Vascular Nitric Oxide Pathway in Growing Rats

“…The moderate zinc deficiency induced neither growth retardation nor changes in food intake. There are not enough reports on the cardiovascular effects of moderate zinc deficiency in growing animals, even though there is evidence, from animal studies, that postnatal environment may be of great importance in determining adult BP (31). Our experimental data demonstrated that moderate zinc deficiency during growth induces an increase in SBP from day 30 after initiation of the dietary treatment, reaching values Ͼ140 mm Hg at the end of the experimental period.…”

Impacto da desnutrição e do treinamento aeróbico moderado sobre a estrutura da parede arterial de ratos em processo de envelhecimento

“…which may interfere in the development phases, such as malnutrition, may favor the onset of cardiovascular pathologies in late phases of life. The mechanisms which promote such alterations have not been totally elucidated (3) , although such vascular pathologies have already been related to alterations in the structure of vessels, notably to alterations on the arterial wall (24) . The multi-needy malnutrition used in this study during the lactation period promoted reduction in the area of the tunica media of the horizontal aorta artery of 12-month rats, demonstrating that, although malnutrition has occurred in a very early phase of the animal's life, the alterations caused by it remained, reducing hence the thickness of the arterial wall.…”

“…Disorders occurred during this period may determine permanent or long-term alterations in different organs (3) . Among these disorders, we can stress the nutritional deficiencies which, associated with unfavorable socieconomical conditions (4) , may be related to high risk of development of defects in metabolism, as well as trigger diseases such as type diabetes, obesity (5) , systemic arterial hypertension (SAH), as well as cardiovascular diseases in more advanced ages (6,7) .…”

“…Among these disorders, we can stress the nutritional deficiencies which, associated with unfavorable socieconomical conditions (4) , may be related to high risk of development of defects in metabolism, as well as trigger diseases such as type diabetes, obesity (5) , systemic arterial hypertension (SAH), as well as cardiovascular diseases in more advanced ages (6,7) . The type, duration as well as phase of development at which malnutrition occurs may determine the type of interference on the organic structure (3,5) . Thus, malnutrition has been mentioned as one of the main non-genetic factors which can interfere in the normal development of the organs (2) .…”

Prenatal Undernutrition Changes Renovascular Responses of Nimesulide in Rat Kidneys

“…Experimental undernutrition using a diet mimicking that widely used by human beings in these regions [2] leads to alterations in renal structure and function [3], including those related to angiotensin II-modulated renal fluid handling [4] that could be associated with the onset of hypertension in adulthood. Maternal dietary restriction using different protocols has demonstrated programming of renal lesions in cortex and medulla that could be involved in alterations of renovascular responses [5][6][7], although the role of the kidney in perinatal programming of long-term alterations of arterial blood pressure has had only minor attention until recently [8].…”