Hypertension, Vol 9, 561-565, Copyright © 1987 by American Heart Association
G Feuerstein and AL Siren
This review is an attempt to highlight evidence that may implicate the
endogenous opioid system in the pathogenesis of hypertension in humans. The
evidence raised includes biochemical, physiological, pharmacological, and
behavioral studies conducted in in vitro and in vivo systems, experimental
models of hypertension, and humans with essential hypertension. While the
compelling biochemical and pharmacological evidence in experimental animals
clearly shows the presence of opioid peptides and their receptors in
strategic sites of cardiovascular control and potent cardiovascular
response to opioid peptides, opioid antagonists show no consistent blockade
or reversal of hypertension in experimental animals or humans. One possible
explanation for this phenomenon could be the vast redundancy in systems
regulating blood pressure (i.e., the blockade of one system still leaves
many other systems fully able to rapidly offset the eliminated system).
Regarding the opioid system, the situation is much more complex, since some
opioid receptors (mu-type) mediate pressor responses, while other receptors
(kappa-type) mediate depressor responses. Therefore, nonselective opioid
receptor antagonists (e.g., naloxone), which block both types of receptors,
can be devoid of any cardiovascular activity, while a selective mu-receptor
antagonist or a selective and potent kappa-receptor agonist may produce the
desired antihypertensive effect. A combination of both actions (i.e., a
drug that is both a mu-antagonist and a kappa-agonist) might be even more
advantageous. Until such compounds are developed, this hypothesis will be
hard to prove.
ARTICLES
The opioid peptides. A role in hypertension?
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