The effects of nitrendipine and bepridil were studied in isolated rings of human crural veins contracted by noradrenaline (NA) or potassium (K). Both drugs had a concentration dependent inhibitory effect on active tone and shifted the NA and K concentration-response curves to the right in a non-parallel manner and reduced the maximum contractile response. Both drugs had a more potent inhibitory effect on K than on NA-induced contractions. Nitrendipine was far more potent in inhibiting the K-induced contractions than bepridil while the drugs were equipotent in inhibiting NA-induced contractions. Human veins were less sensitive than rat aorta to the inhibitory effect of nitrendipine. In contrast to nitrendipine the effect of bepridil was gradual and slow in onset. The inhibitory effect of both drugs was strong and long-lasting and resistant to washout procedures. Both drugs effectively eliminated spontaneous mechanical activity and reduced K-induced contractions in rat portal veins. The results support that nitrendipine and bepridil are effective vasodilators in arteries as well as in veins. The main action of both nitrendipine and bepridil seems to be attributed to an inhibitory effect on cellular Ca-entry.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1600-0773.1984.tb01927.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Extracorporeal treatment for calcium channel blocker poisoning: systematic review and recommendations from the EXTRIP workgroup.
Clin Toxicol (Phila)
May 2021
Research Center, CIUSSS du Nord-de-l'île-de-Montréal, Hôpital du Sacré-Coeur de Montréal, University of Montreal, Montreal, QC, Canada.
Background: Calcium channel blockers (CCBs) are commonly used to treat conditions such as arterial hypertension and supraventricular dysrhythmias. Poisoning from these drugs can lead to severe morbidity and mortality. We aimed to determine the utility of extracorporeal treatments (ECTRs) in the management of CCB poisoning.
View Article and Find Full Text PDFTreatment for calcium channel blocker poisoning: a systematic review.
Clin Toxicol (Phila)
November 2014
Ontario and Manitoba Poison Centre, Toronto, ON , Canada.
Context: Calcium channel blocker poisoning is a common and sometimes life-threatening ingestion.
Objective: To evaluate the reported effects of treatments for calcium channel blocker poisoning. The primary outcomes of interest were mortality and hemodynamic parameters.
Neuronal injury in chronic CNS inflammation.
Best Pract Res Clin Anaesthesiol
December 2010
Universitätsmedizin der Johannes Gutenberg Universität, Klinik und Poliklinik für Neurologie, Langenbeckstr. 1, 55131 Mainz, Germany.
Introduction: Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system which is characterized by inflammatory demyelination and neurodegeneration. Neurological symptoms include sensory disturbances, optic neuritis, limb weakness, ataxia, bladder dysfunction, cognitive deficits and fatigue.
Pathophysiology: The inflammation process with MS is promoted by several inflammatory cytokines produced by the immune cells themselves and local resident cells like activated microglia.
BCRP transports dipyridamole and is inhibited by calcium channel blockers.
Pharm Res
December 2005
Department of Pharmaceutics, School of Pharmacy, University of Washington, Box 357610, Seattle, Washington 98195-7610, USA.
Purpose: We investigated whether dipyridamole and various calcium channel blockers are inhibitors and/or substrates of breast cancer resistance protein (BCRP).
Methods: The effect of dipyridamole and the calcium channel blockers on mitoxantrone efflux by BCRP-overexpressing human embryonic kidney (HEK) cells was determined by flow cytometry. The ability of some of these compounds to reverse BCRP-mediated mitoxantrone resistance was measured by cytotoxicity assays.
Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis.
Exp Neurol
September 2004
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, are inflammatory demyelinating diseases of the central nervous system. The inflammatory attacks lead to glial dysfunction and death, axonal damage, and neurological deficits. Numerous studies in rat suggest that extracellular calcium influx, via voltage-gated calcium channels (VGCC), contributes to white matter damage in acute spinal cord injury and stroke.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!