| Literature DB >> 7969508 |
L J Bryan-Lluka1, H E Vuocolo.
Abstract
There is evidence that hyperpolarization of cells by various mechanisms results in stimulation of uptake2 of catecholamines and, conversely, that depolarization causes inhibition of uptake2. The aim of this study was to examine whether changes that have been shown to occur in the resting membrane potential of the trachealis muscle of guinea pigs that have been sensitized to albumin (hyperpolarization) or albumin-sensitized followed by inhalational albumin challenge (depolarization) are reflected in changes in uptake2 in the smooth muscle. Uptake2 of isoprenaline (as measured by the steady-state rate of specific 3H-O-methylisoprenaline formation normalized for the isoprenaline concentration) was determined in isolated segments of trachealis muscle that were incubated in 3H-(+/-)-isoprenaline and were from guinea pigs from three treatment groups: (i) controls, (ii) albumin-sensitized and (iii) albumin-sensitized and challenged. At an isoprenaline concentration that does not hyperpolarize the trachealis muscle (1 nmol/l), uptake2 was significantly greater in the muscle from sensitized guinea pigs than that from control or sensitized and challenged guinea pigs. When a drug that hyperpolarized the trachealis muscle was present (25 nmol/l isoprenaline or 10 mumol/l (-)-cromakalim), there were no differences in uptake2 between the three groups. Propranolol prevented the stimulation of uptake2 by isoprenaline and glibenclamide prevented stimulation of uptake2 by (-)-cromakalim. In the presence of propranolol or glibenclamide, there were no differences in uptake2 between the three treatment groups of guinea pigs.(ABSTRACT TRUNCATED AT 250 WORDS)Entities:
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Year: 1994 PMID: 7969508 DOI: 10.1007/BF01258462
Source DB: PubMed Journal: Naunyn Schmiedebergs Arch Pharmacol ISSN: 0028-1298 Impact factor: 3.000