Drugs online research references
Eur J Pharmacol. 1981 Oct 15;75(1):7-10.
Limitation of myocardial infarct size by atenolol, nadolol and propranolol in dogs.
Burmeister WE, Reynolds RD, Lee RJ.
The importance of cardioselectivity and membrane depressant activity in the ability of beta-adrenergic antagonists to limit myocardial infarct size was assessed in the dog. Infarction was produced by a 60 min occlusion of the left circumflex coronary artery followed by reperfusion into a critical stenosis. Infarct size was significantly reduced by atenolol, nadolol and propranolol. Thus, limitations of infarct size by beta-adrenergic antagonists occur with agents which possess or lack cardiac selectivity or membrane depressant activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6119212&dopt=Abstract
Clin Exp Hypertens A. 1985;7(2-3):159-66.
Adrenergic and vagal influences on blood pressure variability.
Clement DL, De Pue N, Jordaens LJ, Packet L.
The present paper reviews our recent studies set up to define the role of sympathetic and vagal nervous influences on blood pressure variability. Blood pressure and its variability was measured in men by Arteriosonde or by Portometer (the latter recording 12 hours ambulatory blood pressure) and in the dog by intraarterial recordings. It was shown that sympathetic nerves do not influence variability as no change was seen with drugs acting on either beta (atenolol, metoprolol, propranolol) or alpha adrenergic receptors (prazosin, phentolamine, guanfacine). Also no correlation was found with plasma catecholamines or sympathetic function tests. By contrast, clear inhibition was demonstrated with atropine indicating an important role of vagal nerves on variability. However, in men, inhibition was not complete with atropine; thus, also other mechanisms play a role but these are, at present, largely unknown.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2860986&dopt=Abstract
Am J Physiol. 1984 Apr;246(4 Pt 2):R578-86.
Genetic and environmental influences on developing autonomic control of heart rate.
Tucker DC, Bhatnagar RK, Johnson AK.
Individual differences in cardiovascular regulation result from a dynamic interaction between genetically programmed developmental processes and extrinsic (environmental) conditions. The alterations in autonomic functioning previously identified among pups of the spontaneously hypertensive rat (SHR) strain suggest a genetic influence on autonomic development. In the present studies, an early stimulation procedure previously shown to reduce the behavioral and endocrine responsiveness of rodents in adulthood was demonstrated to alter both neural control of heart rate and regional brain catecholamine levels during the preweaning period. Pups from litters of SHR and Wistar-Kyoto (WKY) rats were handled daily during the first postnatal week. Selective pharmacological blockade with atenolol and atropine methylnitrate was used to identify autonomic controls of heart rate at 16 and 28 days of age. Combined blockade was used to estimate intrinsic heart rate. In both SHR and WKY, early handling was associated with elevated basal heart rate, elevated intrinsic heart rate, and decreased sympathetic tone. Parasympathetic influence on heart rate was elevated by early handling in WKY and decreased by handling in SHR. In addition, an increase in dorsal cortical norepinephrine concentration was produced by early handling in both strains. These data suggest that early environmental conditions can interact with the genetic predisposition for elevated blood pressure and may play a potentially important role in organizing the neural controls of cardiovascular regulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6144274&dopt=Abstract
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