The pressure exerted by the blood inside the arteries is termed blood pressure. Several factors are accountable for its levels, the heart rate, volume and viscosity of blood pumped per beat, force of the heartbeat, elasticity and resistance of vessel walls, and the resistance of the capillary bed (i.e., the network of capillary vessels that permeates tissues). Capillaries are minute blood vessels connecting the arterioles to either veins or lymphatic vessels. Other factors with a role in blood pressure levels are the balance between potassium and sodium levels, and the action of pressure-controlling hormones.
As the heart contracts and relaxes in a pulsatile rhythm, systole, the contraction of the left ventricle that ejects blood into the aorta, distending its walls, exerts a pressure level of 120 mm Hg, whereas diastole (i.e., momentary heart relaxation) has a level pressure of 80 mm Hg, due to the elastic recoil of arterial walls. As the blood flows along the systemic vessels, the pressure gradually falls to almost 0 mm Hg when the blood reaches the end of the cava vein, as is emptied into the right coronary atrium. In the capillary bed, the average pressure is about 17 mm Hg, varying from about 35 mm Hg in the arteriolar ends to 10 mm Hg near the venous ends.
The normal mean blood pressure is about 100 mm Hg. If for some reason the pressure level falls significantly below the mean level, it triggers a cascade of nervous reflexes that promotes contraction in the large venous reservoirs, and increases both the rate and force of cardiac contractions as well as induces a general constriction of small arteries (arterioles) throughout the body. Therefore, more blood is made available in the arterial tree. The substance released by the nervous system in the smooth muscle cells of the blood vessel walls is norepinephrine, a vasoconstrictor (vessel-constricting chemical).
However, if the causes leading to such low blood pressure persist and are no longer beneficial, other regulatory systems are activated, such as the secretion of pressure-controlling hormones. For instance, the kidneys control arterial pressure inducing changes in the volume of extra cellular fluids through the renin-angiotensin system. Renin is an enzyme released by the kidneys when the blood pressure is dangerously low. Renin helps to increase blood pressure through several ways. It promotes the release of angiotensin I, a mild vasoconstrictor, by entering the blood circulation. Angiotensin I is then enzymatically processed to become angiotensin II, a powerful vasoconstrictor that acts mainly on the small arterioles, and in a lesser way on veins. Arteriolar constriction increases the total vascular peripheral resistance, what elevates blood pressure in the arteries and the mild venal constriction helps the return of the blood to the heart. Angiotensin II also inhibits the elimination of sodium and water by the kidneys, thus augmenting the volume of extra cellular fluid. Even small elevations in the volume of extra cellular fluid can induce a blood pressure increase. Whereas the vasoconstriction by angiotensin II lasts for just a few minutes, the elevation of extra cellular fluid volume lasts for several hours or days, and is, therefore, the major effect in pressure elevation by the renin-angiotensin system. A smaller quantity of renin remains in the renal system where it elicits other regulatory functions.
Another pressure-controlling hormone, vasopressin, is secreted by the posterior pituitary gland, and also increases water reabsorption by the kidneys, and in turn, causes constriction of the blood vessels, thus elevating blood pressure. ADH (antidiuretic hormone), also secreted by the posterior pituitary, promotes the renal water reabsorption and vasoconstriction, increasing blood pressure. Aldosterone, secreted by the cortex of adrenal glands, is a hormone activated by angiotensin II that also increases sodium reabsorption and the elimination of potassium, which increases blood pressure as well. It also increases extra cellular fluid volume.
Arterial pressure is also regulated by vasodilator substances, such as bradykinin, acetylcholine, mineral ions, and endogenous nitric oxide, carbon dioxide and hydrogen gases. Bradykinin promotes arteriolar dilatation and increased capillary permeability. Mineral ions that induce vasodilatation are potassium and magnesium.
High intake of salt in the diet causes an increase in the volume of extra cellular fluid that ultimately leads to an increase in blood pressure above normal levels (i.e., hypertension). Although some cases of chronic high blood pressure are due to hereditary traits, a sodium-rich diet through childhood and young adulthood may also lead to chronic hypertension during later life. Hypertension, in turn, may lead to blood vessel ruptures in the brain, or strokes (cerebral infarct). Hypertension causes progressive destruction of the kidneys through successive ruptures of vessels in this organ, which leads to renal failure, an increased level of urea in the blood (uremia), and ultimately death.
Blood pressure measurements are usually done in millimeters of mercury (mm Hg) with a mercury manometer used for this purpose. The mercury manometer measures the force of blood against any unit area of the vessel wall. However, it is only useful for measuring stable pressures. When it is necessary to monitor unstable blood pressure, oscillating rapidly, electronic pressure transducers are utilized. These instruments convert pressure into electrical signals that are recorded at high speed.
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