Related Experiment Videos

Effects of valsartan and indapamide on plasma cytokines in essential hypertension

Qi-ying Xie1, Yong-jin Wang, Ze-lin Sun

  • 1Department of Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.

Insights

Valsartan significantly reduced inflammatory cytokines like MCP-1 and MIP-1alpha in hypertensive patients, while indapamide showed no significant effect. Both drugs effectively lowered blood pressure, but valsartan demonstrated a superior impact on inflammatory markers.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology
  • Immunology

Background:

  • Hypertension is associated with elevated levels of inflammatory cytokines, including monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-1 alpha (MIP-1alpha).
  • Asymmetric dimethylarginine (ADMA) and soluble P-selectin (sP-selectin) are also implicated in the pathophysiology of hypertension and vascular inflammation.

Purpose of the Study:

  • To investigate and compare the effects of valsartan and indapamide on key inflammatory cytokines in patients with mild to moderate hypertension.
  • To assess the impact of these antihypertensive agents on markers of endothelial dysfunction and inflammation.

Main Methods:

  • A study involving 41 untreated hypertensive patients and 20 normotensive controls.
  • Hypertensive patients were randomized to receive either indapamide (1.5 mg/d) or valsartan (80 mg/d) for 4 weeks.
  • Blood samples were analyzed for MCP-1, MIP-1alpha, sP-selectin, ADMA, angiotensin II (Ang II), and 6-keto-PGF1alpha before and after treatment.

Main Results:

  • Hypertensive patients exhibited higher baseline levels of MCP-1, MIP-1alpha, sP-selectin, and ADMA compared to normotensives.
  • Both valsartan and indapamide significantly reduced systolic and diastolic blood pressure.
  • Valsartan treatment led to significant reductions in MCP-1, MIP-1alpha, and sP-selectin, whereas indapamide showed only non-significant trends towards decrease. Both drugs increased 6-keto-PGF1alpha and decreased ADMA.

Conclusions:

  • Elevated levels of MCP-1, MIP-1alpha, sP-selectin, and ADMA are present in patients with mild to moderate hypertension.
  • Valsartan and indapamide exhibit comparable blood pressure-lowering efficacy.
  • Valsartan demonstrates a more pronounced effect on reducing inflammatory cytokines compared to indapamide.
Abstract

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...
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,...
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...
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...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
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 tubules...