The influence of a direct renin inhibitor on the central blood pressure

Yoshiaki Kubota1, Hiroshi Takahashi, Kuniya Asai

  • 1Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan. ykubota@nms.ac.jp

Insights

Direct renin inhibitors (DRIs) lower central blood pressure (CBP) and augmentation index (AI). High-dose DRI therapy further reduces CBP and AI in hypertensive patients.

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Central blood pressure (CBP) is a superior cardiovascular risk predictor in hypertension compared to brachial blood pressure.
  • The selective effect of direct renin inhibitors (DRIs) on CBP remains unclear.

Purpose of the Study:

  • To investigate the effect of standard and high-dose direct renin inhibitor (DRI) therapy on central blood pressure (CBP) and augmentation index (AI) in patients with essential hypertension.

Main Methods:

  • Thirty essential hypertension patients with elevated CBP were randomized into two groups: high-dose DRI (300 mg) or standard-dose DRI plus hydrochlorothiazide.
  • Systolic blood pressure (SBP), CBP, and AI were measured at baseline, 12, and 24 weeks.

Main Results:

  • Standard-dose DRI significantly reduced SBP, CBP, and AI after 12 weeks.
  • Both high-dose DRI and combination therapy further decreased SBP and CBP from 12 to 24 weeks.
  • High-dose DRI showed a greater CBP reduction and AI decrease compared to the combination group.

Conclusions:

  • Direct renin inhibitor (DRI) treatment effectively lowers CBP and AI.
  • High-dose DRI therapy offers additional benefits in reducing CBP and AI in hypertensive patients.
Abstract

Related Concept Videos

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: 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...
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, β1-blockers...
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...