Question
I have seen a case in the forum: a 45-year-old female patient. She had a history of hypertension for 3 years, with a maximum blood pressure of 170/100 mmHg. She had been taking Captopril 50 mg orally for a long Time to control her blood pressure, which was controlled at 130/80 mmHg.
Three days ago, he was given oral ibuprofen extended-release capsules 300 mg bid as an anti-inflammatory and analgesic treatment for rheumatoid arthritis and joint pain. After taking the drug, the pain was significantly reduced, but the blood pressure spiked to 180/110 mmHg.
Three days later, the patient returned to the clinic with stable blood pressure and relief of joint pain.
Such a case raises many questions: Why did the combination of NSAIDs and the antihypertensive drug captopril raise blood pressure? Does the combination of aspirin, an NSAID, and captopril also have an effect on blood pressure? What should be done in such a clinical situation? Let’s run through it today.
1
NSAIDs can cause an increase in blood pressure
In fact, NSAIDs can cause an increase in blood pressure whether or not they are combined with antihypertensive drugs.
NSAIDs are anti-inflammatory and pain relievers that work by inhibiting cyclooxygenase (COX) and reducing prostaglandin (PGs) production. The mechanism by which they cause an increase in blood pressure is related to PGs.
COX can be divided into various subtypes, the most common of which are COX-1 and COX-2. They have different cardiovascular roles, with COX-1 mediating the formation of thromboxane (TXA2) and COX-2 mediating the formation of prostacyclin (PGI2).
TXA2 promotes thrombus formation, platelet aggregation and vasoconstriction [1], while PGI2 has vasodilatory, smooth muscle cell proliferation and platelet aggregation inhibiting effects [2].
(▲▼ Scroll up and down to see the whole content)
When COX is inhibited, prostaglandin E2 (PGE2) synthesis is reduced, resulting in increased sodium and chloride ion uptake by the renal tubules [3]; also in the collecting duct, PGs act as antidiuretic hormone antagonists, reducing water reabsorption, and with reduced PGs synthesis, water reabsorption by the kidney is increased [4].
When selective COX-2 is inhibited, PGI2 synthesis is reduced, vascular smooth muscle contracts, renal vasoconstriction, decreased blood flow to the renal medulla, and decreased urinary sodium excretion, which causes water and sodium retention, which in turn leads to increased blood pressure [5-6]. In addition, there are other mechanisms of action that lead to increased blood pressure.
In general, the mechanisms by which NSAIDs increase blood pressure are mainly vasoconstriction and sodium retention.
2
The combination of NSAIDs with captopril
Can cause an increase in blood pressure
Why does the combination of NSAIDs and captopril cause an increase in blood pressure? The reason is that it weakens the antihypertensive effect of ACEI/ARB drugs.
When combined, NSAIDs inhibit the synthesis of PGs, leading to water and sodium retention, which induces constriction of small renal arteries and a decrease in renal blood flow. This decrease in renal blood flow activates the renin-angiotensin system, thereby antagonizing the antihypertensive effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers [7].
In addition, NSAIDs can reduce the antihypertensive effects of diuretics and β-blockers.
In combination with diuretics, NSAIDs diminish the diuretic effect by blocking PGs and promoting water and sodium retention, especially in elderly patients [8].
When combined with β-blockers, they may render β-blockers ineffective by downregulating basal plasma renin activity [9], and their mechanism of elevating blood pressure is thought to be related to PGs.
When combined with these three antihypertensive agents, the effect on blood pressure is greater.
3
Low-dose aspirin has no effect on blood pressure
Aspirin, an NSAID, is also commonly used in combination with antihypertensive drugs in clinical practice, so does it have any effect on blood pressure?
In fact, most of the aspirin used in clinical practice is in small doses (100 mg/d). Small doses of aspirin are COX-1 inhibitors, which act as antiplatelet aggregators by inhibiting TXA2 and have little effect on COX-2.
Ana Catarina Costa et al [10] also concluded that low doses of aspirin do not negatively affect the control of blood pressure by antihypertensive drugs and appear to enhance cardioprotection when used in combination with ARB.
However, when aspirin is used for anti-inflammatory and analgesic purposes, higher doses are required. Higher doses of aspirin inhibit PGI2 synthesis by blocking COX-2, which may have a negative impact on blood pressure.
In conclusion, low doses of aspirin do not affect blood pressure and do not increase blood pressure when combined with antihypertensive drugs.
4
What should I do in this clinical situation?
When two drugs are used together, especially in different departments for different diseases, it is common for interactions to occur. How should this be handled?
In this case of rheumatoid arthritis combined with hypertension alone, try changing the NSAIDs or changing the antihypertensive medication.
If changing the antihypertensive medication, a calcium channel blocker can be used. Because the antihypertensive effect of calcium channel blockers is independent of the renal PGs system, NSAIDs have little effect on blood pressure when combined with them [11].
If changing NSAIDs, consult rheumatology or orthopedics for advice on replacing oral NSAIDs with topical NSAIDs.
As mentioned in the Chinese clinical practice guidelines for osteoarthritis pain management (2020 edition), topical NSAIDs can be the first choice for the treatment of osteoarthritis pain in the knee, especially for patients with comorbid gastrointestinal disease, cardiovascular disease, or frailty.
As to whether to change NSAIDs or antihypertensive drugs, a comprehensive consideration is needed, which disease has a greater potential risk, and changing the medication for that disease needs to be more cautious, and changing the medication for the disease with less risk should be the key factor in the comprehensive consideration.
Recent Comments