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Figure 1 Hourly ambulatory blood pressure (BP) measurements in a 58-year-old man with borderline hypertension. Solid circles, systolic pressure; open circles, diastolic pressure.

150/90 mmHg at 09:00 h and be classified as hypertensive, while at 14:00 h it might be 137/85 mmHg and would be classified as normotensive. Thus in a normal person blood pressure may vary markedly during a day associated with reactive events, but in some people the baseline blood pressure eventually rises to a level that is defined as 'hypertension.' In this person with hypertension there will be fluctuations in blood pressure associated with the same controls as in normal people, but the fluctuations may be exaggerated, leading to high blood pressure levels.

At different times of the day blood pressure is regulated by different systems. Thus, during the day the cardiovascular sympathetics activated by the barorecep-tors are important controls of blood pressure. When asleep the cardiovascular sympathetics turn off and blood pressure then appears to be maintained more by the renin angiotensin system. The variability in the activity of systems controlling blood pressure means that in hypertensive patients the response to drugs that act on these systems may have a circadian variation.

The etiology of essential hypertension is unknown; however, the condition is believed to result from an interaction of environmental and genetic factors. Environmental factors are undoubtedly of major importance, because in certain communities hypertension is virtually nonexistent; however, when such a community alters its life style, hypertension becomes common and may exist in 30% of the population. Not all people develop hypertension, and the ones who do are determined by their genetic composition (Figure 2). Investigations are under way to attempt to determine which individuals are more likely to develop hypertension and its complications, so that life style and environmental alterations can be initiated to prevent the disease occurring in such people. Certain specific genetic abnormalities have been identified and these cases are then removed from the classification of essential hypertension. It is of interest that the disorders that have been found in general alter sodium handling by the body. These have been either abnormalities in channels or transporters in the nephron that alter sodium excretion, or alternatively defects in circulating hormones that regulate the activity of the renal transporters. Hypertension is not seen in hunter-gatherer communities where sodium intake is low and potassium intake is high, and thus the genetic abnormality is not expressed phenotypically even though the genotype is probably present.

In established hypertension the defect is an increased peripheral resistance rather than an increased cardiac output. However, in people with minor blood pressure elevations and prehypertensive people cardiac output is increased, and it has been postulated that increased cardiac output in response to the retention of sodium

Figure 2 The interrelationships between sodium intake, renal function, hormonal control systems, and genetic inheritance in the etiology of hypertension and cardiac hypertrophy. BP, blood pressure.

is the initial hemodynamic change that leads to hypertension (Figure 2). However, experimentally hypertension can be produced without a stage of increased cardiac output, and increased peripheral resistance can result without an antecedent high cardiac output. It is likely that there is heterogeneity in the way people respond. The concept of an increased cardiac output leading to hypertension has been extensively developed by Guyton in a variety of computer and experimental models. However, in carefully conducted studies in which blood volume was measured in hypertensive patients, blood volume was decreased rather than increased, making this theory probably not applicable to all people. The relationship with sodium is also complicated. In young hypertensive subjects there is a better inverse correlation with total body potassium rather than a direct correlation with total body sodium content. In older people the correlation with body sodium content becomes more pronounced. The lack of a direct correlation between body sodium and hypertension in the young casts doubt on the absoluteness of the link between sodium and hypertension, and clearly potassium has an important effect modulating the response.

It has been suggested that the prime defect leading to increased peripheral resistance is the presence of a circulating factor that inhibits (Na+-K+)-ATPase

High sodium intake or impaired excretion

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