Porth's Essentials of Pathophysiology, 4e

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Disorders of Blood Flow and Blood Pressure

C h a p t e r 1 8

Blood Pressure

Peripheral resistance

3

Aorta

Diastolic Pressure. The diastolic blood pressure reflects the closure of the aortic valve, the energy that has been stored in the elastic fibers of the large arteries during systole, and the resis- tance to flow through arterioles into the capillaries. Closure of the aortic valve at the onset of diastole and recoil of the elastic fibers in the aorta and large arter- ies continue to drive the blood forward, even though the heart is not pumping. These effects, largely restricted to the elastic vessels, convert the discontinu- ous systolic flow in the ascending aorta into a continuous flow in the peripheral arteries.

Diastolic

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Left atrium

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90

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Left ventricle

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with cardiovascular centers in the brain stem and can induce widespread vasoconstriction. Whenever the arterial pressure drops below a critical level, the chemoreceptors are stimulated because of diminished oxygen supply and a buildup of carbon dioxide and hydrogen ions. In persons with chronic lung disease, systemic and pulmonary hypertension may develop because of hypoxemia (see Chapter 23). Persons with sleep apnea may also experience an increase in blood pressure because of the hypoxemia that occurs during the apneic periods. Humoral Mechanisms. The humoral control of blood pressure relies on a number of mechanisms, including the renin-angiotensin-aldosterone system and vasopres- sin. 26 Other humoral substances, such as epinephrine, a sympathetic neurotransmitter released from the adrenal gland, have the effect of directly producing an increase in heart rate, cardiac contractility, and vascular tone. The renin-angiotensin-aldosterone system plays a central role in blood pressure regulation. Renin is an enzyme that synthesized and stored by the juxtaglo- merular cells of the kidney and released in response to an increase in sympathetic nervous system activity or a decrease in blood pressure, extracellular fluid vol-

ume, or extracellular sodium concentration. 26 Most of the renin that is released leaves the kidney and enters the bloodstream, where it acts enzymatically to convert an inactive circulating plasma protein called angioten- sinogen to angiotensin I (Fig. 18-15). Angiotensin I is then converted to angiotensin II. This conversion occurs almost entirely in the small vessels of the lung, catalyzed by an enzyme called the angiotensin-converting enzyme that is present in the endothelium of the lung vessels. Although angiotensin II has a half-life of only several minutes, renin persists in the circulation for 30 minutes to 1 hour and continues to cause production of angio- tensin II during this time. Angiotensin II functions in both the short- and long- term regulation of blood pressure. It is a strong vasocon- strictor, particularly of arterioles and, to a lesser extent, of veins. Constriction of the arterioles increases the peripheral vascular resistance, thereby contributing to the short-term regulation of blood pressure. Angiotensin II also reduces sodium excretion by increasing sodium reabsorption by the proximal tubules of the kidney. A second major function of angiotensin II, stimulation of aldosterone secretion from the adrenal gland, contrib- utes to the long-term regulation of blood pressure by increasing salt and water retention by the kidney.