Drugs online research references
Am Heart J. 1983 Nov;106(5 Pt 1):1023-8.
Comparative study of the effect of slow channel inhibiting agents on ischemia-induced conduction delay as relevant to the genesis of ventricular fibrillation.
Peter T, Fujimoto T, Hamamoto H, Mandel WJ.
Conduction delay has been shown to be an important factor in the genesis of ventricular fibrillation (VF). We evaluated the relationship between conduction delay and (1) initiation of VF and (2) the effects of Ca++ blockers on conduction delay in 41 dogs: eight control (nontreated, non-VF); nine ischemic VF; eight verapamil-treated (0.15 mg/kg bolus followed by 7.5 micrograms/kg/min); eight diltiazem-treated (20 micrograms/kg/min); and eight nifedipine-treated (0.1 mg/kg bolus). Propagation of electrically-induced premature impulses from the midmyocardial bipole of one transmural electrode was recorded at epicardial and endocardial bipoles of other electrodes before and 5, 15, and 30 minutes after coronary ligation. Conduction delay (i.e., conduction times compared to preligation levels) of VF, verapamil, diltiazem, and nifedipine groups were compared to control group in normal and in the center and border of ischemic zones in both base to apex (anterograde) and apex to base (retrograde) directions. Results showed that there was no change in conduction delay in the normal zone between control and VF groups or the treated groups, but both in the center and border of ischemic zone VF was quantitatively related to conduction delay and Ca++ blockers, except that nifedipine significantly reduced conduction delay. We conclude that our model provides a new approach to the assessment of anti-VF intervention. Further, verapamil and diltiazem appear to be useful agents in reducing the risk of ischemia-induced reentrant ventricular tachyarrhythmias.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6637762&dopt=Abstract
J Pharmacol Exp Ther. 1982 Oct;223(1):263-70.
Diuretic and natriuretic effects of nifedipine on isolated perfused rat kidneys.
Marre M, Misumi J, Raemsch KD, Corvol P, Menard J.
The effects of nifedipine, a vasodilating drug which acts through calcium antagonism, were studied in vitro using isolated perfused rat kidneys. Most of the nifedipine was neither metabolized nor excreted by this preparation. Four doses were tested: 50, 250, 500 and 750 nM. The two higher concentrations enhanced urine flow and sodium (UNaV) and potassium excretion. Tubular reabsorption of sodium was reduced compared to untreated control kidneys. The glomerular filtration rate was not modified but the filtration fraction decreased. The magnitude of urine volume, UNaV, urinary potassium excretion and filtration fraction changes were related to the dose of nifedipine. The decrement of total renal resistance and the increment of UNaV were correlated for 500 and 750 nM nifedipine (n = 13; r = -0.77; P less than .001), suggesting that it acted by dilating the renal vascular bed. Nifedipine at 250, 500 and 750 nM significantly increased the renin secretion rate compared to that of untreated control kidneys. When renin secretion was enhanced by 50 nM isoproterenol, this stimulatory effect was enhanced in kidneys concomitantly treated with 500 and 750 nM nifedipine. Dihydralazine, another vasodilating drug, was tested at a comparable molar dose (500 nM) and induced similar changes in urine volume, UNaV, urinary potassium excretion and Na reabsorption. The variations in total renal resistance and UNaV were also inversely correlated (n = 8; r = -0.68; P less than .05). Dihydralazine did not modify renin secretion rate significantly. These results suggest that: 1) both nifedipine and dihydralazine increase diuresis, natriuresis and kaliuresis in the isolated perfused rat kidney and 2) nifedipine enhances basal renin release from the juxta-glomerular cells and potentiates renin release caused by beta receptor stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6750082&dopt=Abstract
Am Heart J. 1983 Aug;106(2):345-55.
Comparison of the direct effects of nifedipine and verapamil on the electrical activity of the sinoatrial and atrioventricular nodes of the rabbit heart.
Ning W, Wit AL.
We compared the effects of nifedipine and verapamil on the rabbit sinus and atrioventricular nodes. Both drugs slowed the rate of impulse initiation by sinus node cells. Verapamil exerted a greater negative chronotropic effect at low concentrations, but at higher concentrations verapamil and nifedipine were equipotent. Nifedipine also reduced the amplitude of sinus node action potentials and the Vmax of phase O, effects which are identical to those previously described for verapamil. Both drugs slowed AV nodal conduction and prolonged refractory periods, but verapamil was more potent than nifedipine. Nifedipine reduced the amplitude of AV nodal action potentials and Vmax of phase O the same as verapamil. Nifedipine and verapamil, therefore, have nearly identical direct effects on the nodes. The failure of nifedipine to depress AV nodal conduction in situ and abolish reentrant AV nodal tachycardia is probably a result of the decreased sensitivity of the AV node to nifedipine compared to verapamil.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6869216&dopt=Abstract
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