TY - JOUR
T1 - Drug-induced hypertension
T2 - An unappreciated cause of secondary hypertension
AU - Grossman, Ehud
AU - Messerli, Franz H.
N1 - Funding Information:
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 .
PY - 2012/1
Y1 - 2012/1
N2 - 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.
AB - 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.
KW - Hypertension
UR - http://www.scopus.com/inward/record.url?scp=84455178883&partnerID=8YFLogxK
U2 - 10.1016/j.amjmed.2011.05.024
DO - 10.1016/j.amjmed.2011.05.024
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.systematicreview???
AN - SCOPUS:84455178883
VL - 125
SP - 14
EP - 22
JO - American Journal of Medicine
JF - American Journal of Medicine
SN - 0002-9343
IS - 1
ER -