(Hypertension. 1997;30:157-162.)
© 1997 American Heart Association, Inc.
Articles |
From the Departments of Pharmacology and Medicine, Vanderbilt University School of Medicine, Nashville, Tenn.
Abstract Enhanced sympathetic reactivity may predispose
blacks to the development of hypertension and may occur because of
increased sympathetic stimulation and/or attenuated sympathoinhibition.
A potential site for such attenuated sympathetic inhibition may be at
the level of central
2-adrenergic receptors, which play
an important role in the feedback inhibition of
norepinephrine release. We used cumulative doses (1, 2, and
3 µg/kg IV) of the centrally acting
2-adrenergic
agonist clonidine to measure the sensitivity of
2-adrenoceptormediated sympathoinhibition and the
resultant hypotensive response in 8 normotensive blacks and 10
normotensive whites. Sympathetic activity was determined by
radioisotope dilution methodology. Basal norepinephrine
spillover was similar in blacks (0.80±0.14 µg/min) and whites
(0.73±0.19 µg/min, P=NS) and after clonidine decreased
significantly in both blacks (0.21±0.07 µg/min, P<.0001)
and whites (0.24±0.06 µg/min, P<.0001), with no
difference between the groups (P=NS). Despite this similar
degree of sympathoinhibition, the hypotensive response to clonidine was
markedly blunted in blacks, such that mean arterial
pressure decreased by only 10% in blacks but by 21% in whites
(P<.0001). The smaller blood pressure decrement after
clonidine in normotensive blacks, in the face of an equal degree of
sympathoinhibition, suggests that even when sympathetic tone is
decreased to the same level in blacks and whites, normotensive blacks
have less reduction in blood pressure than whites, implying that
nonadrenergic mechanisms contribute more to blood
pressure maintenance in blacks than whites. Whether a similar
interethnic difference in response to sympathoinhibition occurs in
hypertensive patients is as yet unknown.
Key Words: receptors, adrenergic, alpha blacks clonidine norepinephrine
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