Abstract
A myriad variety of therapeutic agents or chemical substances can induce either a
transient or persistent increase in blood pressure, or interfere with the blood pressure-lowering
effects of antihypertensive drugs. Some agents cause either sodium retention or extracellular
volume expansion, or activate directly or indirectly the sympathetic nervous system.
Other substances act directly on arteriolar smooth muscle or do not have a defined
mechanism of action. Some medications that usually lower blood pressure may paradoxically
increase blood pressure, or an increase in pressure may be encountered after their
discontinuation. In general, drug-induced pressure increases are small and transient:
however, severe hypertension involving encephalopathy, stroke, and irreversible renal
failure have been reported. The deleterious effect of therapeutic agents is more pronounced
in patients with preexisting hypertension, in those with renal failure, and in the
elderly. Careful evaluation of a patient's drug regimen may identify chemically induced
hypertension and obviate unnecessary evaluation and facilitate antihypertensive therapy.
Once chemical-induced hypertension has been identified, discontinuation of the causative
agent is recommended, although hypertension can often be managed by specific therapy
and dose adjustment if continued use of the offending agent is mandatory. The present
review summarizes the therapeutic agents or chemical substances that elevate blood
pressure and their mechanisms of action.
Keyword
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Article info
Footnotes
Funding: None.
Conflict of Interest: Ehud Grossman has received ad hoc consultant and speaker fees from Novartis, Sanofi-Aventis, AstraZeneca, Novo Nordik, Dexon Israel, and Teva Israel Intercure, and grant support from Novartis, Bristol-Myers Squibb, Daiichi Sankyo, and Neurim Pharmaceuticals Ltd, Israel. Franz Messerli serves as a consultant to Takeda, Novartis, Bayer, Pfizer, Daiichi Sankyo and received grants from Boehringer Ingelheim, Forest.
Authorship: Both authors had access to the data and played a role in writing the manuscript.
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© 2012 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
