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4.7: Age Changes in Arteries

  • Page ID
    83989

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    There are no important age changes in the endothelial structure, its supporting layer, or the outer layer of arteries. These layers function well regardless of age with one major exception. There is an age-related decline in the ability of the endothelium to regulate blood vessels and blood pressure. The cause is not clear. It may be due to aging of endothelial cells, to free radical damage, or to age-related increases in blood pressure. Nitric oxide reacts with superoxide radicals (*O2-), producing toxic ONOO- (peroxynitrite). This reaction reduces the amount of *NO available to regulate vessels and blood clotting, and the ONOO- can slow *NO production further by injuring endothelial cells. These changes may contribute to high blood pressure and to atherosclerosis.

    Middle Layer: Large Arteries

    Numerous age changes occur in the middle layer of large arteries. Age changes in elastic fibers include breakage, glycation, accumulation of calcium and lipid deposits, and faster breakdown by enzymes. Old damaged elastic fibers accumulate. The increase in many substances, including smooth muscle, collagen, calcium deposits, and cholesterol and other fatty materials, causes thickening and stiffening of the arteries. These changes amplify the decline in elasticity caused by the altered elastic fibers. Since the arteries are less able to be stretched by each pulse of blood, systolic pressure tends to rise.

    Since much elastin in the aorta is produced before birth, children with low birth weights may have less aortic elastin, resulting in less aortic strength and elasticity. This can speed up aortic thickening and stiffening during childhood and adulthood, resulting in a greater risk of high blood pressure and related diseases (e.g., atherosclerosis, congestive heart failure). These effects highlight the importance of events in youth or even before birth to age-related changes and disease later in life.

    At the same time the arteries are stiffening, years of containing blood under high pressure causes them to gradually widen and lengthen. This is especially evident in the aorta. These changes provide more space for blood. At first this compensates for the declining ability of large arteries to be stretched, and consequently it keeps the tendency toward increases in systolic pressure in check. Eventually, however, the elastic fibers are stretched so much that they can yield no further. Then each contraction of the heart produces a rapid and dramatic rise in systolic blood pressure. This can increase cardiac oxygen demand by almost 30 percent. At the same time, the high blood pressure and thickening of the heart reduce the amount of *NO in coronary vessels. This limits the vessel dilation required to increase oxygen supply to the heart muscle.

    Once the arteries no longer stretch much with each heartbeat, sensory nerve cells that detect vessel stretching are not activated as much. Age changes in the endothelium that reduce prostacyclin and increase reactive oxygen species (ROS) also reduce the nerve cell activation. The reflex to prevent abnormal increases in blood pressure is suppressed, and the pressure remains high. In most cases sensory nerve cells are fooled and respond as though blood pressure were too low. Age changes in the brain's blood pressure control center amplify this effect. The final result is the release of norepinephrine, which augments the high pressure but also stimulates the heart. In this way, the extra norepinephrine seems to be compensatory because it helps the aging heart maintain cardiac output.

    As with all age changes, there is much variation among individuals with respect to the rise in systolic pressure. While the elevations are modest in most people, about 40 percent of the elderly have systolic pressures above the safe maximum for those of advanced age (140 mmHg). Recall that elevated blood pressure increases the heart’s workload and oxygen needs and the risk of developing atherosclerosis. Therefore, it is important for the elderly to have their blood pressure checked and, when necessary, receive therapy to keep it within safe limits. However, elevated blood pressure in older individuals must not be lowered too quickly or too far, since the result can be weakness, fainting, or more serious damage to the heart, the brain, and other parts of the body.

    In addition to restricting stretching, stiffening of the arteries diminishes their elastic recoil. The slow decline in recoil does not cause a substantial change until about age 60, after which diastolic pressure declines slightly. The result is a slowing of blood flow through coronary arteries and other small arteries between heart beats. Normally, this decline is not large enough to cause significant effects, though it brings a person closer to having inadequate blood flow during each diastole.

    In a large longitudinal study of people with no diseases of the circulatory system, systolic BP does not change until approximately age 40 in women and age 50 in men. Then BP increases approximately 5-8 mmHg per decade. In women, the systolic BP may stop rising and may even begin to decrease after age 70, while in men the systolic BP continues to rise throughout life. The overall increase in systolic pressure averages 21 mmHg in women and 15 mmHg in men. Diastolic pressure in women increases from ages 40 to 60, but then levels off or declines. Diastolic pressure in men increases 1 mmHg per decade. Overall, diastolic pressures increase 5 mmHg in women and 3.5 mmHg in men. Studies that include people with diseases or who take medications show greater changes in BP, and the women may not have the leveling and decline in BP after age 70.

    Middle Layer: Smaller Arteries

    Aging causes little if any change in the overall resistance provided by the smaller arteries. Their thickening seems to help prevent overstretching as systolic blood pressure increases with age. Older arteries do not respond quite as well when conditions such as chemical levels begin to change. This seems to be due in part to decreased functioning of the nervous system and altered levels of the hormones that control the vessels. The vessels also seem to have reduced sensitivity or a reduced ability to respond to control signals. Therefore, the arteries do not dilate as well when the areas they supply need more oxygen. This decrease in supply tends to reduce the maximum rate of work that certain organs (e.g., muscles) can perform.

    The decreased ability of the arteries to respond to rising or falling body temperature is an even greater problem, leaving older people less able to prevent themselves from overheating or becoming chilled. For example, inadequate dilation of dermal vessels prevents the extra heat produced during exercise from leaving the body quickly. This can lead to excessively high body temperature, damage to body molecules and cell parts, malfunctioning of organs such as the brain, illness, or even death. Poor constriction by dermal vessels when a person is in a cold environment can cause excessive loss of body heat and a drop in body temperature. Not only will such an individual feel uncomfortably cold, but because of slowing cell activities and malfunctioning of organs such as the muscles and the heart, he or she may also become ill.

    The declining ability to maintain normal body temperature as age increases is due not only to age changes in the middle layer of smaller arteries but also to age changes in the integumentary system (e.g., sweat glands, fat tissue), the nervous system (e.g., sensory neurons), and the muscle system (e.g., muscle mass).

    Because of reduced thermal adaptability, older individuals should avoid environments and activities that tend to cause significant elevation or depression of body temperature. Hot weather or very warm indoor areas, hot baths or showers, the use of numerous blankets or electric blankets, and strenuous physical activity tend to cause overheating. Cold weather or cool rooms, cool water for swimming or bathing, exposure of the skin, inadequate clothing, and restricted physical activity increase the risk of developing hypothermia.

    Number of Arteries

    The number of larger arteries remains the same throughout life. The number of smaller arteries remains about the same or increases slightly in some areas of the body (e.g., heart and brain). This slight increase helps sustain normal blood flow by compensating for the development of somewhat irregular arteries. Other areas (e.g., skin, kidneys) have decreasing numbers of smaller arteries with age.

    Fortunately, the adverse effects on blood flow caused by the aging of arteries can be largely overcome through steps such as receiving proper medical care, pacing activities, and avoiding situations that place a person in danger of overheating or chilling. Unfortunately, for most individuals, aging arteries are affected not only by age changes but also by arterial diseases.


    This page titled 4.7: Age Changes in Arteries is shared under a CC BY-NC-SA 4.0 license and was authored, remixed, and/or curated by Augustine G. DiGiovanna via source content that was edited to the style and standards of the LibreTexts platform.