Effects of low-dose aspirin on endothelial function in hypertensive patients

H Monobe1, H Yamanari, K Nakamura

  • 1Department of Cardiovascular Medicine, Okayama University Medical School, Japan.

Clinical Cardiology
|November 21, 2001
PubMed

Insights

Low-dose aspirin improved blood vessel function in hypertensive patients by restoring endothelium-dependent vasodilation. This suggests aspirin enhances nitric oxide production, benefiting cardiovascular health.

Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Low-dose aspirin is known to reduce cardiovascular events in hypertensive and coronary artery disease patients.
  • Its preventative effects are attributed to inhibiting platelet aggregation.

Purpose of the Study:

  • To investigate if low-dose aspirin administration restores endothelium-dependent vasodilation in hypertensive patients.

Main Methods:

  • Assessed flow-mediated endothelium-dependent dilatation and glyceryl trinitrate-induced endothelium-independent dilatation in 18 hypertensive patients and 10 controls.
  • Measured plasma cyclic guanosine monophosphate (cGMP) before and after 8 weeks of 162 mg daily aspirin in hypertensive patients.

Main Results:

  • Hypertensive patients had significantly reduced flow-mediated dilatation compared to controls (6.4% vs. 11.3%).
  • Aspirin administration improved flow-mediated dilatation in hypertensive patients (from 6.4% to 10.4%).
  • Plasma cGMP levels were significantly higher after aspirin treatment.

Conclusions:

  • Low-dose aspirin may restore endothelium-dependent vasodilation in hypertension.
  • Increased nitric oxide production likely contributes to aspirin's beneficial effects on endothelial function.
Abstract

Related Concept Videos

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...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
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...
Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...
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...