Search citation statements
Paper Sections
Citation Types
Year Published
Publication Types
Relationship
Authors
Journals
Age-related changes in the renin-aldosterone system in normal humans are well documented. The most pronounced changes are observed at the extremes of life: plasma renin activity and plasma aldosterone levels are highest in the newborn, and lowest in the elderly population. There is a close temporal and directional relationship between the age-related decrease in plasma renin activity and the age-related decrease in plasma aldosterone. The renin-aldosterone system is also influenced by sex and race. The activation of the renin-aldosterone system in newborns and infants probably represents an important physiological mechanism designed to maintain positive sodium balance. The decreases in plasma renin activity and plasma aldosterone levels observed in elderly persons are usually only modest, and are not associated with clinical alterations in fluid or electrolyte metabolism. The superimposition of a disease process, or the injudicious prescription of a drug, inhibiting renin release or angiotensin II production, could theoretically facilitate sodium wasting in newborns or infants, or precipitate hyporeninaemic hypoaldosteronism in older adults. The primary clinical importance of age-related changes in the renin-aldosterone system relates to its impact on the proper classification of an individual's renin-aldosterone profile when attempting to diagnose a clinical condition (e.g. low, normal or high renin hypertension). This is particularly true for newborns, infants and children to age 4, and for adults entering the sixth decade of life.
Age-related changes in the renin-aldosterone system in normal humans are well documented. The most pronounced changes are observed at the extremes of life: plasma renin activity and plasma aldosterone levels are highest in the newborn, and lowest in the elderly population. There is a close temporal and directional relationship between the age-related decrease in plasma renin activity and the age-related decrease in plasma aldosterone. The renin-aldosterone system is also influenced by sex and race. The activation of the renin-aldosterone system in newborns and infants probably represents an important physiological mechanism designed to maintain positive sodium balance. The decreases in plasma renin activity and plasma aldosterone levels observed in elderly persons are usually only modest, and are not associated with clinical alterations in fluid or electrolyte metabolism. The superimposition of a disease process, or the injudicious prescription of a drug, inhibiting renin release or angiotensin II production, could theoretically facilitate sodium wasting in newborns or infants, or precipitate hyporeninaemic hypoaldosteronism in older adults. The primary clinical importance of age-related changes in the renin-aldosterone system relates to its impact on the proper classification of an individual's renin-aldosterone profile when attempting to diagnose a clinical condition (e.g. low, normal or high renin hypertension). This is particularly true for newborns, infants and children to age 4, and for adults entering the sixth decade of life.
The renin-angiotensin-aldosterone system (RAAS) is one of the main systems involved in the regulation of blood pressure and sodium homeostasis. In animal experiments and in humans, the plasma renin activity and aldosterone levels are reduced with aging. The age-related differences in plasma renin activity and aldosterone are more pronounced in stimulated conditions (when sitting in an upright position, when salt intake is restricted and when plasma volume is depleted) than under basal conditions. Age-related alterations of the kidney (glomerulosclerosis, decreased number of functional nephrons) might account for the age-related differences in the active to inactive plasma renin ratio. In the same way, a diminished synthesis of angiotensinogen by the liver could contribute to the decrease in the activity of the RAAS in aging. This is partially compensated for by increases in the density of angiotensin II receptors reported in elderly patients. Furthermore, aging is associated with a reduced adrenal responsiveness to angiotensin II, contributing to lower production of aldosterone and alterations of sodium homeostasis. Estradiol and progesterone help stimulate the secretion of renin. Reduced levels of these hormones at menopause also lead to reduced plasma renin activity. In relation to these findings, several studies have shown that reductions in blood pressure, induced by short or long term treatment with angiotensin converting enzyme (ACE) inhibitors, were more pronounced in old than young hypertensive patients. An insertion/deletion polymorphism in the ACE gene has been described; the genotype deletion/deletion of this gene has been reported to be closely associated with longevity. This result was unexpected since the same deletion polymorphism was also shown to represent a potent risk factor for myocardial infarction.
High blood pressure (BP) in the elderly must not be ignored as a normal consequence of aging. The criteria for the diagnosis of hypertension and the necessity to treat it are the same in elderly and younger patients. The aim of treatment of elderly hypertensive patients is to decrease BP safely and to reduce risk factors associated with cerebrovascular, cardiovascular and renal morbidity and mortality. The treatment of elderly hypertensive patients should be adjusted according to the needs of the individual, based upon age, race, severity of hypertension, co-existing medical problems, other cardiovascular risk factors, target-organ damage, risk-benefit considerations and costs. In addition to the elevated BP, other cardiovascular risk factors include smoking, glucose intolerance, hyperinsulinaemia, dyslipidaemia, hypercreatininaemia, peripheral vascular disease, left ventricular hypertrophy, and microalbuminuria (or albuminuria). Thus, the choice of initial antihypertensive therapy in elderly hypertensive patients should be based not only on the expected response, but also on the effects of therapy on lipid, potassium, glucose and uric acid levels, and left ventricular anatomy and function. Co-existing medical conditions (such as asthma, diabetes mellitus, heart failure, renal failure, gout, coronary artery disease, hyperlipidaemia and peripheral vascular disease) are major determinants for the selection of antihypertensive medications. With previous therapies (diuretics, beta-blockers, etc.), good BP control in the elderly was associated with clear and statistically significant reductions in stroke-related morbidity and mortality, but the overall effects on cardiovascular and renal complications of hypertension was either more variable or less obvious. Angiotensin converting enzyme (ACE) inhibitors are not only efficacious antihypertensive agents in the elderly, but also appear promising in counteracting some of the cardiovascular and renal consequences of hypertension. They are well tolerated and have a relatively low incidence of adverse effects. ACE inhibitors possess ancillary characteristics that are potentially beneficial for many elderly patients, including reduction of left ventricular mass, lack of metabolic and lipid disturbances, no adverse CNS effects, no risk of induction of heart failure, and a low risk of orthostatic hypotension. Since ACE inhibitors may improve perfusion to the heart, kidney and brain, they are well worth considering for the treatment of elderly patients with hypertensive target organ damage, especially in patients with heart failure, and diabetic patients with early nephropathy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.