Drugs online research references
Gen Physiol Biophys. 1986 Dec;5(6):581-91.
Effects of caffeine on the electrical and mechanical activity of guinea-pig ureter smooth muscle.
Burdyga TV, Magura IS.
The effects of caffeine on the electrical and mechanical activity of the guinea-pig ureter smooth muscle were studied. Under untreated conditions caffeine mainly showed inhibitory action on the ureter, inhibiting the evoked action potentials and phasic contractions as well as potassium contracture. Caffeine was also found to suppress the low-Na contracture of Na-loaded ureter muscle. It is established that Na-loaded tissue is able to generate transient contracture in response to caffeine application at 37 degrees C. These caffeine contractures could be evoked under completely removed [Ca2+]0 and in the presence of high doses of Ca-channel blockers (nifedipine, diltiazem, Mn ions) and could be reversibly blocked by tetracaine, procaine and benzocaine. Caffeine contractures could also be produced by the ureter muscle placed in isotonic K-solution. Cooling significantly potentiated low-Na, potassium and caffeine contractures of the ureter muscle. Filling of the store is totally dependent on the entry of Ca ions from the extracellular Ca2+ store sites which sequester Ca ions entering the cell on either Na-Ca exchange or via voltage operated Ca channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2435612&dopt=Abstract
J Mol Cell Cardiol. 1987 Sep;19(9):853-63.
Comparison of simultaneous electrophysiologic and mechanical effects of verapamil and nifedipine in cultured chick embryo ventricular cells.
Hasin Y, Barry WH.
Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
In order to examine possible differences in mechanisms of action of nifedipine and verapamil, simultaneous recordings of membrane potential and cell motion were made during exposure of cultured chick embryo ventricular cells to these drugs. Both verapamil and nifedipine produced a rapid negative inotropic effect and excitation-contraction coupling delay presumably related to the ability of both agents to inhibit Ca2+ influx via the slow Ca channel, and thus decrease the [Ca2+]i transient. However, for an equivalent negative inotropic effect, verapamil produced relatively more membrane diastolic depolarization and slowing of repolarization than did nifedipine. Verapamil also produced a more marked decrease in +dV/dtmax. In ion flux studies, it was demonstrated that verapamil produced a significant inhibition of 24Na influx, relative to control, whereas nifedipine did not. Verapamil also produced a slight decrease in 42K efflux, of borderline significance. These findings support previous results which indicate there are differences in the mechanisms of action of these Ca2+-channel blocking drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3430638&dopt=Abstract
J Hypertens Suppl. 1988 Dec;6(4):S154-6.
The effects of vasoactive agents on the proliferation of vascular smooth muscle cells grown in vitro.
Kuriyama S, Nakamura K, Kaguchi Y, Kimura M, Tamura H, Tamai K, Hashimoto T, Miyahara T.
2nd Department of Medicine, Jikei University School of Medicine, Tokyo, Japan.
The present study was designed to investigate the effect of vasoactive agents on cellular proliferation in serially passed cultured vascular smooth muscle cells (VSMC). A substantial reduction in the number of vascular smooth muscle cells was observed with the addition of nifedipine, nicorandil, bunazocine and labetalol compared with that in a control sample. Furthermore, noradrenaline significantly increased the number of vascular smooth muscle cells. In contrast, neither propranolol nor captopril had any effect on number of vascular smooth muscle cells. The cell size, measured as water volume of vascular smooth muscle cells based on the equilibrium distribution of 3-O-(14C-methyl)-D-glucose, did not differ between treatments with the above-mentioned agents. It is suggested that in addition to a known calcium-mediated mechanism, an alpha-receptor-mediated property could be involved in the proliferation of vascular smooth muscle cells and that clinical use of a calcium antagonist or an alpha-blocker might be useful to prevent the hyperproliferation of vascular smooth muscle cells commonly seen in the vascular walls of patients with hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2977159&dopt=Abstract
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