Regression of structural vascular changes in hypertensives after captopril treatment

S Novo1, M G Abrignani, A Pinto

  • 1Chair of Clinical Pathophysiology, University of Catania, Italy.

European Heart Journal
|August 1, 1992
PubMed

Insights

Captopril, an angiotensin-converting enzyme inhibitor, effectively lowers blood pressure in hypertensive patients. This antihypertensive treatment reduces vascular resistance and increases blood flow, indicating its efficacy in managing hypertension.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Essential arterial hypertension is associated with structural vascular changes.
  • Antihypertensive treatments aim to mitigate these vascular effects.

Purpose of the Study:

  • To investigate the influence of antihypertensive treatment on hypertension-related structural vascular changes.
  • To evaluate the effects of captopril on blood pressure and vascular resistance.

Main Methods:

  • 10 patients with essential arterial hypertension received placebo then captopril (75 mg b.i.d.) for 3 months.
  • Evaluated parameters included systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), basal vascular resistance, and minimal vascular resistance.
  • Blood flow was measured using strain gauge plethysmography.

Main Results:

  • Captopril significantly decreased SBP, DBP, and MBP compared to placebo (P < 0.01).
  • Basal vascular resistance decreased significantly (P < 0.01) and minimal vascular resistance decreased (P < 0.025) after captopril treatment.
  • Rest and peak blood flows significantly increased (P < 0.01) with captopril therapy.

Conclusions:

  • Captopril is an effective antihypertensive treatment, significantly reducing blood pressure.
  • The drug's efficacy is linked to reduced basal vascular resistance via vasodilating effects.
  • Captopril also demonstrates an ability to reduce minimal vascular resistance in hypertensive patients.

Related Concept Videos

Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
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: 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...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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...