Indomethacin-Induced Rises in Blood Pressure

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Abstract
The role of prostaglandins in the control of blood pressure is not well understood. Prostaglandins of the 2 series are ubiquitous local hormones derived from the unsaturated fatty acid, arachidonic acid. Prostaglandins are produced by most mammalian cells. Locally produced prostaglandins may modulate blood pressure by opposing the vasoconstrictor effect of norepinephrine and angiotensin II, as well as by limiting the extent of sympathetic neurotransmission. In addition, renally generated prostaglandins are involved in the release of renin, inhibition of antidiuretic hormone action, and excretion of sodium chloride. Because prostaglandins have multiple effects in the kidney, vasculature, and sympathetic neurotransmission, the use of nonsteroidal antiinflammatory drugs (which inhibit prostaglandin synthesis) has not resulted in a consistent effect on blood pressure in humans. Clinical studies using indomethacin have reported an increase, no change, or a decrease in blood pressure after drug administration. Because of this unpredictability in response, the addition of a nonsteroidal antiinflammatory drug to an already hypertensive patient should be followed by more frequent blood pressure measurements.