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Biomedical subjects

W G Anderson

Publications and source records attributed to W G Anderson.

12 recordsLinked to original sources
PubMed1985

Pharmacological activity of ACC-7513, a selective alpha-adrenoceptor and 5-hydroxytryptamine receptor blocking agent.

The pharmacological activity of N-[2-(2,6-dimethoxyphenoxy) ethyl]-2-(2-methoxyphenoxy) ethanaminium chloride (ACC-7513) was determined in isolated smooth and cardiac muscle and its effect on blood pressure and heart rate assessed in the spontaneously hypertensive rat (SHR). ACC-7513 was found to be a potent alpha-adrenoceptor blocking agent (pA2:8.33) and a 5-hydroxytryptamine (5-HT) antagonist (pA2:7.01), both in rabbit aortic strips. The affinity for alpha-adrenoceptors was about 20 times greater than that for 5-HT-receptors. High concentrations of ACC-7513 did not block histamine in rabbit aortic strips, or beta 1- or beta 2-adrenoceptor responses induced by isoprenaline in guinea-pig right atria and trachea, respectively, but did block cholinoceptor responses induced by carbachol in rat uterus, non-competitively. High concentrations of ACC-7513 also produced sino-atrial depression in guinea-pig right atria and direct relaxation of depolarized rabbit aortic strips. ACC-7513 depressed blood pressure of conscious SHRs and produced a reflex increase in heart rate. The reductions in pressure were modest and of short duration. It is concluded that: (a) ACC-7513 is a potent, selective alpha-adrenoceptor and 5-HT receptor antagonist; and (b) ACC-7513 is not likely to be useful in the treatment of hypertension.

Adrenergic alpha-Antagonists↗
PubMed1979

Conformational analogues of dopamine. Synthesis and pharmacological activity of (E)- and (Z)-2-(3,4-dihydroxyphenyl)cyclopropylamine hydrochlorides.

(E)- and (Z)-(+/-)-2-(3,4-dihydroxyphenyl)cyclopropylamine hydrochlorides were synthesized as part of a program to assess the importance of conformational isomerism with respect to the various peripheral biological actions of dopamine. Although neither of the compounds possessed dopaminergic activity in the canine renal blood-flow model, both agents were weak alpha-adrenergic agonists and exhibited cardiostimulatory properties similar to dopamine. The E isomer was apprxoximately 5 times more potent than the Z isomer in its alpha-adrenergic activity and approximately 15 times as potent in its cardiac effects. Possible reasons for the lack of renal dopaminergic activity exhibited by the E isomer are presented.

Adrenergic alpha-Agonists↗
PubMed1976

Ozone exposure modifies prostaglandin biosynthesis in perfused rat lungs.

Exposure of perfused rat lungs to 3.0 ppm of ozone produced a rapid onset of edema and an increased resistance to inflation. Both the Km and Vmax of the enzymic conversion of arachidonic acid to prostaglandins were decreased by ozone exposure suggesting an uncompetitive inhibition of prostaglandin synthetase by O3. Reduced glutathione failed to prevent the inhibition of prostaglandin synthesis by O3.

Air↗
PubMed1975

Kinetic measurements of the release of prostaglandins from perfused rat lungs.

Prostaglandins released from isolated ventilated and perfused rat lungs were measured by a simple modification of the Vane technique using the rat stomach fundus as a continuous bioassay tissue. Exogenously supplied arachidonic acid was converted mainly to PGF2alpha which was determined by bioassay. A novel method for mixing a stream of inhibitors with the perfusate was used to determine PGF2alpha in the presence of substrate amounts of arachidonic acid. Using this system the apparent Km for PGF2alpha production with arachidonic acid as the substrate was found to be 1.90 X 10(-4)M, while the Ki for aspirin was found to 2.47 X 10(-4)M. These kinetic parameters are close to those reported for cell free systems and subcellular fractions suggesting that both substrate and inhibitor have ready access to the site of prostaglandin synthesis. The method appears to be generally useful to determine the effect of drugs and environment factors on the release of prostaglandins by the lung.

Animals↗
PubMed1975

Antagonism of the uterotonic action of oxytocin in vitro.

Cumulative concentration-effect curves of oxytocin alone and with various antagonists were obtained in vitro on uteri from estrogen-treated rats. Graded concentrations of salbutamol, isoproterenol, papaverine, theophylline, thioglycollate, and MgCl2 produced a decrease in the maximal effect of oxytocin and a shift of the concentration-effect curves to the right. Salbutamol and isoproterenol appeared to act as functional antagonists of oxytocin in which agonist and antagonist each interacted with its own specific receptor to produce a decreased combined effect on a common effector. Antagonism by papaverine or theophylline was increased by prior or simultaneous treatment with salbutamol, isoproterenol, epinephrine, or norepinephrine. The potentiation had a rapid onset, was partially blocked by propranolol, persisted for at least 85 minutes following washout of salbutamol, and was not due to a residual effect of salbutamol. This interaction could result from phosphodiesterase inhibition by papaverine and the accumulation of higher levels of cyclic 3',5'-adenosine monophosphate brought about by adenyl cyclase activation with the sympathomimetic amines.

Albuterol↗
PubMed1975

Interaction between halothane and propranolol on oxytocin-induced uterine contractions.

Halothane and other volatile anesthetics were found to relax uteri maximally contracted by oxytocin and to enhance the relaxant effect of propranolol and other agents (tetracaine, quinidine and chlorpromazine) with local anesthetic properties. Concentration-effect curves for inhibition by propranolol or tetracaine were shifted to the left by halothane. Methoxyflurane, chloroform and diethyl ether also increased the effect of propranolol. The tissue/medium ratio for propranolol was increased by halothane. The uptake of propranolol was saturable and was decreased at 2.5 degrees C, suggesting an active transport mechanism. The increased uptake of propranolol in the presence of halothane was probably insufficient to account for the synergism noted. Inhibition by propranolol and tetracaine was inversely related to the concentration of calcium in the medium. The inhibitory effect of propranolol, tetracaine, quinidine and chlorpromazine appeared to be related to their ability to inhibit calcium transport.

Anesthetics↗