Drugs online research references
J Pharmacol Exp Ther. 1984 Sep;230(3):607-13.
Effects of metal cations and calmodulin antagonists on [3H] nitrendipine binding in smooth and cardiac muscle.
Luchowski EM, Yousif F, Triggle DJ, Maurer SC, Sarmiento JG, Janis RA.
It was previously reported that [3H]nitrendipine binding to a microsomal fraction from intestinal smooth muscle was dependent upon the presence of divalent metal cations (Bolger et al., J. Pharmacol. Exp. Ther. 225: 291-309, 1983). The effects of cations and calmodulin antagonists on [3H]nitrendipine binding in smooth and cardiac muscle have been studied further. Treatment of ileal and aortic smooth muscle and cardiac muscle with EDTA reduced specific [3H]nitrendipine binding by 70 to 95%. Microsomes from rabbit ventricle were more resistant to EDTA treatment than were those from ileal smooth muscle, but low concentrations of Ca++ (less than 10(-5) M) produced half-maximal restoration of binding in both tissues. The ability of cations at a concentration of 10(-3) M to restore binding to membranes from guinea-pig ileum was in the sequence, Ca++ = Sr++ greater than Mg++ = Mn++ = Co++ greater than Ba++ = Ni++ greater than Zn++ = Cd++ greater than La = Sm = Tm . In contrast to the activation of calmodulin-dependent processes, the ability of these cations to restore [3H]nitrendipine binding did not correlate linearly with ionic radius. However, calmodulin antagonists were found to inhibit [3H]nitrendipine binding with the order of potency: pimozide greater than less than calmidazolium (R 24571) greater than trifluoperazine greater than chlorpromazine greater than promethazine greater than chlorpromazine sulfoxide, that correlates quite well with the potency of these drugs as inhibitors of calmodulin-dependent processes. The results suggest that calmodulin antagonists bind to a protein associated with the [3H]nitrendipine binding site that has a hydrophobic domain similar to that exposed on calmodulin by Ca++, but that this protein is not calmodulin itself.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6433001&dopt=Abstract
Res Commun Chem Pathol Pharmacol. 1978 Feb;19(2):361-4.
In vitro and in vivo effects of promethazine (Phenergan) on drug metabolism.
Fernandez G, Castro JA.
Prolongation effects of promethazine on the pentobarbital sleeping time are not due to interactions of this drug with cytochrome P-450 or cytochrome c reductase or inhibition of drug metabolism because pentobarbital plasma levels in promethazine treated animals before awakening are not different than in controls. Results suggest additive effects of both drugs on the central nervous system. Those interactions do however play a role during in vitro studies.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=644127&dopt=Abstract
Brain Res. 1992 Jan 8;569(1):100-5.
Effect of histamine and antagonists on electrical resistance across the blood-brain barrier in rat brain-surface microvessels.
Butt AM, Jones HC.
Biomedical Sciences Division, King's College, London, U.K.
The effect of histamine on blood-brain barrier permeability was investigated using in situ measurement of transendothelial electrical resistance in brain-surface microvessels of anaesthetized rats. Mean resistance of vessels superfused with artificial cerebrospinal fluid was 1500 omega.cm2, indicating a tight barrier with low ion permeability. The addition of 10(-4) M histamine resulted in a 75% decrease in resistance, in both arterial and venous vessels, indicating a marked increase in barrier permeability. To determine the nature of the response to histamine, rats were given presurgical intraperitoneal injections of promethazine (H1 receptor antagonist), cimetidine (H2 receptor antagonist) or indomethacin (cyclo-oxygenase inhibitor), singularly and in combinations. Cimetidine completely blocked the histamine-mediated increase in barrier permeability whereas promethazine only had a small effect and indomethacin was ineffective. In addition, cimetidine treatment resulted in a 100% increase in basal resistance in both arterial and venous vessels, suggesting endogenous histamine was acting to increase blood-brain barrier permeability. It is concluded that histamine causes an increase in blood-brain barrier permeability which is mediated via endothelial H2 receptors, and that the electrical resistance in cimetidine-treated rats most closely represents the true permeability of the blood-brain barrier.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1611469&dopt=Abstract
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