Drugs online research references
Int J Clin Pharmacol Biopharm. 1979 Jul;17(7):290-3.
The cardiac electrophysiological effects of nifedipine.
Padeletti L, Franchi F, Brat A, Dabizzi RP, Michelucci A.
A study was carried out on the electrophysiological effects of a sublingually administered antianginal drug: nifedipine (20 mg). The results show a significant shortening of sinus cycle length from 925 +/- 249 msec to 810 +/- 245 msec, (p less than 0.005) and the disappearance of some interpolation and echo zones. There are no significant effects on the other evaluated parameters of sino-atrial and AV-node function. In one case, during atrial pacing, a second-degree, Wenckebach type, A-V block was present only before nifedipine. The following conclusions were reached: 1. nifedipine has no significant electrophysiological effect on the human heart; 2. the electrophysiological effects observed are probably indirect and related to the vasodilating effect of the drug; 3. the absence of direct cardiac electrophysiological actions may be useful in patients suffering from coronary artery disease and presenting disturbances in the formation and/or conduction of the cardiac impulse.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=489193&dopt=Abstract
Int J Clin Pharmacol Ther Toxicol. 1987 Dec;25(12):670-2.
Non-invasive electrophysiological evaluation of calcium antagonist long-term therapy.
Adinolfi L, Golia B, Montano A, Marino M, Napolano S, Mazza F.
1st Medical Clinic, 2nd School of Medicine, University of Naples, Italy.
The evaluated effects of oral administration of verapamil, diltiazem, and nifedipine in patients with first degree A-V block by using a new noninvasive technique: signal averaged ECG. The study group consists of 5 females and 3 males ranging from 52 to 70 years old. All patients showed a first degree A-V block at surface ECG and an abnormal A-V time (suprahisian lengthening) during signal averaged ECG (SAECG). Verapamil 240 mg/daily, diltiazem 180 mg/day and nifedipine 30 mg/day were given separately for a week followed by a wash out period of 5 days before giving next drugs. An ECG and SAECG were performed before and after every administration. PR, A-H and H-V interval were evaluated in every recording. Verapamil and diltiazem induced a significant lengthening of A-V conduction (PR increase was 15.4% and 15.1%, respectively). No significant modification appeared after nifedipine. Our data, using a noninvasive technique, agreed with values of previous invasive evaluations. We suggest precaution in using verapamil and diltiazem in patients with BAV 1 degree and advise a selective use of calcium antagonist therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3436687&dopt=Abstract
Br J Pharmacol. 2002 Jan;135(1):197-205.
Mechanical and electrophysiological effects of endothelin-1 on guinea-pig isolated lower oesophageal sphincter circular smooth muscle.
Imaeda K, Trout SJ, Cunnane TC.
Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT.
1. The effects of endothelin-1 (ET-1) on guinea-pig lower oesophageal sphincter (LOS) circular smooth muscle were investigated by using intracellular microelectrodes and isometric tension recording techniques. 2. ET-1 produced biphasic mechanical responses; an initial transient relaxation followed by a sustained contraction. The initial relaxation was not inhibited by either tetrodotoxin (TTX, 1 microM) or L-N(G)-nitroarginine (L-NOARG, 100 microM). The sustained contraction was greatly attenuated by nifedipine (1 microM). 3. ET-1 (1 - 30 nM) induced a concentration-dependent hyperpolarisation that was unaffected by TTX or L-NOARG. The ET(A) receptor antagonist, BQ123 (0.3 microM) abolished the ET-1-induced hyperpolarisation, whereas the ET(B) receptor antagonist, BQ788 (0.3 microM) had no detectable effect. Sarafotoxin S6c (10 nM) did not change the membrane potential. 4. The ET-1-induced hyperpolarisation was abolished by apamin (0.1 microM). Interestingly, apamin abolished the ET-1-induced transient relaxation but potentiated the sustained contraction. 5. In Ca(2+)-free Krebs solution, the ET-1-induced hyperpolarisation was greatly attenuated and returned to the control value when the tissue was reperfused with Krebs solution containing Ca(2+). The ET-1-induced hyperpolarisation was insensitive to nifedipine but was attenuated by SK&F 96365 (1 - [beta-[3-(4 - methoxy - phenyl)propoxy] - 4 - methoxyphenethyl] - 1H-imidazole hydrochloride, 50 microM), an inhibitor of receptor-mediated Ca(2+) entry. The residual component of the ET-1-induced hyperpolarisation was sensitive to thapsigargin (1 microM). 6. These results demonstrate that, in guinea-pig LOS circular smooth muscle, ET-1 hyperpolarizes the membrane by activating apamin-sensitive K(+) channels, mainly as a result of receptor-mediated Ca(2+) entry and partly by Ca(2+) release from intracellular stores. The hyperpolarisation triggers the initial transient relaxation, which acts to oppose the sustained contraction.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11786495&dopt=Abstract
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