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Selective and non-selective beta-adrenoceptor antagonists were used to block the increases in fluid, protein and amylase secretion caused by sympathomimetic stimulation of the parotid gland of red kangaroos during intracarotid infusion of isoprenaline. ICI118551 at antagonist/agonist ratios up to 300:1 caused increasing but incomplete blockade of fluid secretion, and protein/amylase release. Atenolol at antagonist/agonist ratios up to 300:1 was only marginally more potent than ICI118551 at blocking the fluid, protein and amylase responses. Propranolol at antagonist/agonist ratios of 30:1 was as effective at blocking fluid and protein secretion as the highest ratios of either atenolol or ICI118551. Simultaneous administration of atenolol (30:1) with ICI118551 (30:1) was not as potent as propranolol (30:1). Thus, the beta-adrenoceptor/s in the acini of the kangaroo parotid gland appear to have antagonist-binding affinities atypical of those found for eutherian tissues. The data are consistent with the gland possessing either a single anomalous beta-adrenoceptor or functional beta(2)-receptors in addition to the beta(1)-receptors which are characteristic of eutherian salivary glands.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10825691&dopt=Abstract




Pflugers Arch. 1986 Feb;406(2):144-50.
An effect of noradrenaline on resting potential and Na activity in sheep cardiac Purkinje fibres.

Glitsch HG, Rasch R.

Noradrenaline (NA; 10(-9) to 10(-6) M) depolarizes the cell membrane of quiescent sheep Purkinje fibres at resting potential level. A corresponding inward shift of the holding current occurs in voltage clamped preparations in a potential range between ca. -40 and -100 mV. The depolarizing effect is present in phentolamine (1.5 X 10(-6) M) containing solution, mimicked by isoprenaline, blocked by propranolol (5 X 10(-6) M) and is therefore supposed to be beta-adrenoceptor mediated. The inward shift of the holding current is half maximum at 60 nM noradrenaline. The shift is accompanied with an increase of the intracellular Na activity (aiNa) of the fibres as measured by Na sensitive microelectrodes. Both, the inward shift of the holding current and the accompanying aiNa increased are strongly inhibited by 2 mM CsCl. It is concluded that the depolarizing action of noradrenaline is mainly caused by the known catecholamine induced shift of the steady state activation curve of the pacemaker current (if). The shift increases if in a potential range between -40 and -100 mV and augments thereby aiNa.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3960697&dopt=Abstract




Jpn J Pharmacol. 1978 Aug;28(4):627-31.
Cardiovascular actions of optical isomers of propranolol.

Yamamoto J, Sekiya A, Maekawa H, Kato Y.

Effects of the optical isomers of propranolol on blood pressure in the rat, and in the spinal rat during adrenaline infusion were studied to investigate the mechanism of the pressor action of propranolol. Both isomers of propranolol produced a sustained pressor action in the rat and in the spinal rat infused with adrenaline. The magnitude of the pressor action produced by the d- and 1-propranolol was proportional to their beta-adrenoceptor blocking activities in the heart as was reported by several investigators. It is concluded that the pressor action of propranolol is due to the blockade of the beta-adrenoceptors mediating vasodilation in the skeletal muscle vascular beds.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=32418&dopt=Abstract













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