ABSTRACT
The effects of Arecoline (Are) on calcium mobilization were investigated. In isolated single ventricular myocyte of guinea pig, patch clamp whole cell recording techniques were used to record the current of L-type calcium channel and cytosolic Ca2+ level ([Ca2+]i) labeled with fluorescence probe Fluo-3/AM was measured under a laser scanning confocal microscope. Results revealed that Are (3-100 mumol/L) could inhibit L-type calcium current in a concentration-dependent manner and the value of IC50 was 33.73 mumol/L (n = 5). In the absence of extracellular calcium, the resting levels of [Ca2+]i was not affected by Are (n = 6, P > 0.05), but pretreatment with Are (30 mumol/L) could significantly inhibit the [Ca2+]i elevation induced by caffeine (10 mmol/L, n = 6, P < 0.01). It was concluded that Are could inhibit not only calcium influx through L-type calcium channel but also calcium release from sarcoplasmic reticulum.
Subject(s)
Animals , Arecoline , Pharmacology , Biological Transport, Active , Caffeine , Pharmacology , Calcium , Metabolism , Calcium Channels, L-Type , Metabolism , Cell Separation , Cholinergic Agonists , Pharmacology , Guinea Pigs , Heart Ventricles , Cell Biology , Myocytes, Cardiac , Cell Biology , Metabolism , Patch-Clamp Techniques , Sarcoplasmic Reticulum , MetabolismABSTRACT
AIM To investigate the effect of 4-aminopyridine (4-AP) on ion channels of myocytes. METHODS L-type calcium channel and sodium channel currents were recorded in guinea pig single ventricular myocyte using whole-cell patch-clamp techniques. RESULTS 4-AP, 0.1, 0.5 and 1.0 mmol*L-1 were shown to inhibit L-type calcium channel currents (ICa,L) and sodium channel currents (INa) concentration-dependently. The percentage of inhibition were (11.6±1.7)%, (37.5±8.3)% and (54.5±6.9)% (P<0.01) respectively for ICa,L, and (22.1±14.3)% (P<0.05), (39.4±8.8)% and (62.3±6.8)% (P<0.01) respectively for INa. 4-AP 0.5 mmol*L-1 shifted the I-V curves of ICa,L and INa upwardly. CONCLUSION 4-AP blocked L-type calcium channel and sodium channels in guinea-pig ventricular myocytes concentration-dependently.
ABSTRACT
The action of BTHP on a-adrenoceptor was studied in anococcy-geus muscles, vas deferens and cell membrane of cerebral cortex of rats and aortic strips, saphenous vein of rabbit. BTHP produced parallel shifts to the right of dose-response curves for phenylephrine in rat anococcygeus muscle and rabbit aortic strips without change in the maximal responses. Their pA2 values were 5.8 and 5.86 respectively. BTHP was also a competitive antagonist for presynaptic and postsynaptic ?2-adrenoceptors on prostatic portion of rat vas deferens( pA2 against clonidine=5.2 ) and on rabbit saphenous vein ( pA2 against B-HT920=5.3 ) . BTHP decreased in dose-dependent manner 〔8H〕 prazosin and 〔3H〕 clonidine specific binding to ?1- and ?2- adrenoceptors on cell membrane of cerebral cortex in rats with IC50 of4 and 9.5 ?mol/L and with Ki ( apparent dissociation constant ) of 3.5 and 8.1?mol/L respectively, suggeating that BTHP has affinity for both ?1 and ?2- adrenoceptors of rat cerebrance.
ABSTRACT
I sopropylmine vanillinate (IV) given iv 5 , 10 mg/kg in anesthe tized rats produced a dose-dependent decrease in mean arterial pressure and a concomitant decrease in heart rate.In pithed rats IV was unable to shift the phenylephrine doserespon-se curve to the right, but prazosine caused 53-fold shift.No direct effect of vasodilation was shown by IV on rabbit aorta strips .The concentration-response curve of isoprenaline in isolated rat right atrium was competitively inhibited by IV and propranolol. pA2 value was 4.0 for IV and 8.2 for propranolol. In addition, 'IV depressed contractility & heart rate of isolated rat atria.These results suggest that the hypotensive action of IV may be related to the decrease of HR, inhibition of contractility and slight blocking of B-adrenergic receptor. However the mechanism underlying the hypotensive effect of IV is to be further studied.
ABSTRACT
IQ86034 (5.3).In addition, the blocking action of 4 isoquinoline derivatives on ?1 and ?2 adrenoceptors was similar to that of benzoquinolizine derivatives.
ABSTRACT
Benzyltetrahydropalmatine ( BTHP ) which is a derivative of tet-rahydropalmatine, induced concentration-dependent decreases of the APA & dV/dt max and prolongation of conduction delay (CD) in toad sciatic neural action potential while it has little effect on APD.Bloocking action of Na+ -channel was measured with the dose required to produce 50% diminution of the value of APA, ie,EC50. EC50 of BTHP was 2.8 folds less than that of lidocaine and 11.9 folds more than that of quinidine, reflecting blocking action of Na+ -channel by BTHP, lidocaine, quinidine respectively.