A．A low output of urinary kallikrein is a likely cause ……
TEXT A
Although it is now possible to bring
most high blood pressure under control, the causes 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.
