Although it is now possible to bring most high blood pressure under control, the muses of essential hypertension remain elusive. Understanding how hypertension begins is at least partly a problem of understanding when in life it begins, and this may be very early--perhaps within the first few months of life. Since the beginning of the century, physicians have been aware that hypertension may run in families, but before the 1970s, studies of the familial aggregation of blood pressure treated only populations 15 years of age or older. Few studies were attempted in younger persons because of a prevailing notion that blood pressures in this age group were difficult to measure and unreliable and because essential hypertension was widely regarded as a disease of adults.
In 1971, a study of 700 children, ages 2 to 14, used a special blood pressure recorder which minimizes observer error and allows for standardization of blood pressure readings. Before then, it had been well established that the blood pressure of adults aggregates familially, that is, the similarities between the blood pressure of an individual and his siblings are generally too great to be explained by chance. The 1971 study showed that familial clustering was measurable in children as well, suggesting that factors responsible for essential hypertension are acquired in childhood. Additional epidemiological studies demonstrated a clear tendency for the children to retain the same blood pressure patterns, relative to their peers, four years later. Thus, a child with blood pressure higher or lower than the norm would tend to remain higher or lower with increasing age.
Meanwhile, other investigators uncovered a complex of physiologic roles--including blood pressure--for a vasoactive (作用于血管的)system called the kallikrein-kinin(血管舒缓酶－激酞原)system. Kallikreins are enzymes in the kidney and blood plasma which act on precursors (先兆) called kininogens to produce vasoactive peptides(酞)called kinins. Several different kinins are produced, at least three of which are powerful blood vessel dilators. Apparently, the kallikrein-kinin system normally tends to offset the elevations in arterial pressure that result from the secretion of salt-conserving hormones such as aldosterone(醛固酮) on the one hand and from activation of the sympathetic nervous system (which tends to constrict blood vessels) on the other hand.
It is also known that urinary kallikrein excretion is abnormally low in subjects with essential hypertension. Levels of urinary kallikrein in children are inversely related to the diastolic blood pressures of both children and their mothers. Children with the lowest kallikrein levels are found in the families with the highest blood pressure. In addition, black children tend to show somewhat lower urinary kallikrein levels than white children, and blacks are more likely to have high blood pressure. There is a great deal to be learned about the biochemistry and physiologic roles of the kallikrein-kinin system. But there is the possibility
that essential hypertension will prove to have biochemical precursors.
The argument in the passage leads most naturally to which of the following conclusions().
A. A low output of urinary kallikrein is a likely cause of high blood pressure in children.
B. The kallikrein-kinin system plays an important role in the regulation of blood pressure.
C. Essential hypertension may have biochemical precursors which may be useful predictors in children.
D. The failure of the body to produce sufficient amounts of kinins is the cause of essential hypertension.
