The effect of angiotensin II receptor blockers on hyperuricemia

Marissa L Wolff1, Jennifer L Cruz2, Adam J Vanderman2

  • 1Geriatric Research, Education, and Clinical Center, Durham VA Medical Center, 508 Fulton Street (182), Durham, NC 27705, USA.

Insights

Losartan is the only angiotensin II receptor blocker (ARB) proven effective in lowering serum uric acid levels for gout and hyperuricemia patients. Further research is needed to confirm its impact on clinical outcomes.

Area of Science:

  • Nephrology
  • Pharmacology
  • Rheumatology

Background:

  • Hyperuricemia, defined as serum uric acid levels ≥7 mg/dl, is a key factor in gout development.
  • Angiotensin II receptor blockers (ARBs) are commonly used antihypertensive medications.
  • The uricosuric effects of ARBs warrant investigation for managing hyperuricemia.

Purpose of the Study:

  • To review the efficacy of angiotensin II receptor blockers (ARBs) in treating hyperuricemia in patients with gout or hyperuricemia.
  • To identify specific ARBs that demonstrate significant uricosuric effects.

Main Methods:

  • A comprehensive literature search was conducted in MEDLINE and EMBASE databases (up to June 2015).
  • Search terms included 'uric acid', 'gout', 'hyperuricemia', and specific ARB names.
  • Included studies focused on serum uric acid or fractional excretion of uric acid as endpoints in patients with gout or hyperuricemia.

Main Results:

  • Eight studies met the inclusion criteria; six examined ARB monotherapy, and two explored ARBs as adjunct therapy.
  • Losartan consistently showed statistically significant reductions in serum uric acid levels or increased uric acid excretion.
  • No other ARB demonstrated statistically significant uricosuric benefits in the reviewed studies.

Conclusions:

  • Losartan is the only ARB that has consistently demonstrated significant efficacy in lowering serum uric acid levels.
  • While safe and effective for reducing uric acid, the impact of losartan on clinical outcomes like gout attacks remains undetermined.
  • Further investigation is required to ascertain the clinical significance of ARB-induced uricosuria in managing gout and hyperuricemia.

Related Concept Videos

Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
3.0K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.8K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.8K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.4K
Antihypertensive Drugs: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various...
2.8K
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this,...
2.2K