Disturbances of Regulation of
Blood Pressure
The regulatory mechanism for maintaining blood pressure at a constant level was presented in chapter 2. This barostatic mechanism (similar to temperature regulation by thermostats) is capable of regulating resistance to blood flow by opening and closing the arterioles to compensate for variation in cardiac output. This pressure regulatory center is located at the base of the brain, where it
receives and sends out signals via the autonomic nervous system. However, the response of the arterioles to these impulses can be either strengthened or weakened by chemical substances circulating in the blood. Thus disturbances of pressure regulation can be related to one of two mechanisms: either the barostatic center is set too high or too low, so that improper nervous impulses reach the arterioles (neurogenic mechanism ), or normal nervous impulses are improperly modified by the presence of chemical substances (humoral mechanism ). Chemical substances that raise blood pressure by sensitizing arteriolar responses to nervous impulses are called pressor substances; those that desensitize responses and lower blood pressure are called depressor . substances. Such pressor and depressor effects are the properties of many chemical substances—hormones normally produced in the body, hormones produced only under abnormal conditions, and drugs.
Disturbances of either the neurogenic or humoral mechanism may occur temporarily or permanently. For example, blood pressure may rise in healthy persons during periods of stress, anger, and excitement, presumably because of an excess of normal pressor hormones. Conversely, temporary falls in blood pressure may result from prolonged standing (fatigue of regulatory center), causing fainting. Furthermore, regulation of blood pressure may be imperfect, leading to abnormal drops in blood pressure when the person switches from a lying to a standing position (postural hypotension ). Permanent disturbances of blood pressure—hypertension or hypotension—may be caused secondarily by disturbances of other organs; however, only hypertension can be a primary, potentially serious disease. Hypotension is consistent with good health and is most frequently merely a variant of the norm, although occasionally it may be a sign of some systemic disease (long-standing wasting diseases such as cancer, tuberculosis, or Addison's disease).
The kidneys play an important role in the regulation of blood pressure. Special cells in the kidneys secrete renin , a chemical that combines with a protein circulating in the blood to produce angiotensin I . This compound has no significant effect on the circulation but is rapidly changed by an enzyme into angiotensin II , a powerful pressor hormone essential in regulating blood pressure. Furthermore, angiotensin II is the principal factor stimulating the adrenal
cortex to secrete aldosterone , which regulates salt and water content in the body. This reaction is referred to as the renin-angiotensin-aldosterone axis. Excess formation of renin may initiate the process leading to hypertension; furthermore, ingestion of salt (sodium) in the diet facilities the development of hypertension, whereas significant reduction of salt intake lowers blood pressure. The renin mechanism is directly involved in one type of secondary hypertension (renovascular hypertension) and may be implicated in some cases of essential hypertension.
The relationship between the kidneys and hypertension has been known since blood pressure measurements first became available at the turn of the century; in the 1930s high blood pressure was experimentally produced in an animal by interfering with the blood supply to the kidneys, thereby stimulating excessive production of renin. Stenosis of the renal artery (supplying the kidney) was experimentally induced, causing hypertension in the animal; relief of the stenosis brought the blood pressure back to normal.