Vascular reactivity and calcium-entry blockers.
Calcium-entry blockers inhibit contractions of vascular smooth muscle cells in response to potassium and to endogenous and exogenous vasoconstrictor stimuli in both normoxic and hypoxic conditions. In this regard, the protecting effect of flunarizine is of long duration and particularly evident on brain arteries at concentrations not affecting vascular myogenic activity or myocardial contractile force. Some calcium-entry blockers (especially flunarizine) also decrease blood hyperviscosity by improving red blood cell deformability. Both vascular and rheological effects reflect a protection against changes in permeability of the cell membrane to calcium.
D000818:Animals; D001809:Blood Viscosity; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002936:Cinnarizine / Q000031:analogs & derivatives / Q000494:pharmacology; D004285:Dogs; D004912:Erythrocytes / Q000502:physiology; D005444:Flunarizine; D000860:Hypoxia / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009200:Myocardial Contraction / Q000187:drug effects; D009638:Norepinephrine / Q000502:physiology; D011188:Potassium / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D051381:Rats; D012701:Serotonin / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects*
D002121:Calcium Channel Blockers; D011453:Prostaglandins; D012701:Serotonin; D002936:Cinnarizine; D005444:Flunarizine; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine