Olmesartan, but not amlodipine, improves endothelium-dependent coronary dilation in hypertensive patients

Masanao Naya1, Takahiro Tsukamoto, Koichi Morita

  • 1Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Insights

Olmesartan, an angiotensin II receptor blocker (ARB), improved coronary endothelial function in hypertensive patients more than amlodipine, a calcium channel blocker (CCB). This suggests ARBs may offer superior cardiovascular benefits through antioxidant properties.

Area of Science:

  • Cardiology
  • Pharmacology
  • Hypertension Research

Background:

  • Angiotensin II receptor blockers (ARBs) are hypothesized to improve coronary vasomotion more than calcium channel blockers (CCBs) due to direct angiotensin II blockade.
  • Coronary endothelial dysfunction is a key factor in hypertension-related cardiovascular complications.

Purpose of the Study:

  • To compare the efficacy of olmesartan (ARB) versus amlodipine (CCB) in improving coronary endothelial function in patients with essential hypertension.
  • To investigate the impact of these antihypertensive agents on coronary blood flow and vascular resistance.

Main Methods:

  • A prospective study involving 26 untreated hypertensive patients randomized to 12 weeks of olmesartan or amlodipine.
  • Coronary endothelial function assessed by measuring changes in myocardial blood flow (MBF) and coronary vascular resistance (CVR) using positron emission tomography (PET) with 15O-water.
  • Analysis of various blood biomarkers, including lipids, glucose, and inflammatory markers, alongside superoxide dismutase (SOD) activity.

Main Results:

  • Both olmesartan and amlodipine effectively reduced blood pressure to a similar extent.
  • Olmesartan treatment showed a trend towards increased myocardial blood flow (DeltaMBF) and significantly decreased coronary vascular resistance (DeltaCVR), indicating improved vasodilation.
  • Amlodipine did not significantly alter DeltaMBF or DeltaCVR, and serum SOD activity showed a trend to increase only in the olmesartan group.

Conclusions:

  • Olmesartan demonstrated a significant improvement in endothelium-dependent coronary vasodilation in hypertensive patients, independent of blood pressure reduction.
  • These beneficial effects suggest that ARBs, potentially through antioxidant mechanisms like increased SOD activity, may offer superior cardiovascular protection compared to CCBs.
  • The findings highlight the potential of ARBs in managing endothelial dysfunction in hypertension.
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...
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...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
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,...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...