Related Experiment Video

Updated: May 1, 2026

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography
07:51

Mesenteric Artery Contraction and Relaxation Studies Using Automated Wire Myography

Published on: September 22, 2011

28.4K

Mechanistic view of renal protective action of calcium channel blockade

Naoki Sugano, Koichi Hayashi, Tatsuo Hosoya

  • 1Division of Kidney and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, 3-19-18 Nishi-Shinbashi, Minato-ku, Tokyo 105-8471, Japan. n-sugano@jikei.ac.jp.

Current Hypertension Reviews
|April 23, 2014
PubMed

Insights

Calcium channel blockers lower blood pressure effectively. Blocking T-type and N-type calcium channels may offer kidney protection beyond blood pressure control, but clinical evidence is needed.

Area of Science:

  • Pharmacology
  • Nephrology
  • Cardiovascular Medicine

Background:

  • Calcium channel blockers are primary antihypertensive agents.
  • Their main effect is lowering blood pressure via L-type calcium channel blockade.
  • Emerging research suggests other calcium channel subtypes have distinct actions.

Purpose of the Study:

  • To explore the potential renal protective effects of blocking T-type and N-type calcium channels.
  • To understand the mechanisms underlying these potential renal benefits.
  • To assess the clinical relevance of these findings.

Main Methods:

  • Review of recent studies on calcium channel blocker subtypes.
  • Analysis of effects on glomerular capillary pressure.
  • Examination of impacts on renal fibrosis, sympathetic activity, and aldosterone.

Main Results:

  • L-type calcium channel blockade is key for blood pressure reduction.
  • T-type and N-type calcium channel blockade show promise for renal protection.
  • Potential benefits include reduced glomerular pressure and fibrosis, and modulated sympathetic/aldosterone pathways.

Conclusions:

  • While L-type calcium channel blockers are established antihypertensives, T-type and N-type blockade warrant further investigation for renal benefits.
  • The mechanisms involve direct effects on the kidney, sympathetic nervous system, and hormone regulation.
  • Extensive clinical studies are necessary to confirm the therapeutic utility of these actions in patients.

More Related Videos

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis08:21

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Published on: October 26, 2020

4.9K
Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli12:19

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

10.6K

Related Concept Videos

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,...
2.4K
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...
2.9K
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
1.9K
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
2.6K
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...
1.9K
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,...
2.2K