Drugs online research references
Tohoku J Exp Med. 1986 Aug;149(4):389-95.
Characterization of functional beta-adrenoceptor subtypes in rabbit urinary bladder smooth muscle.
Morita T, Kondo S, Tsuchida S, Weiss RM.
Spontaneous contractile force of muscle strips isolated from male rabbit urinary bladder dome (detrusor) and base (trigonal muscle) was significantly inhibited by isoproterenol (10(-7)-10(-5) M), a non-specific beta-adrenoceptor agonist or by terbutaline (10(-8)-10(-5) M), a selective beta 2-adrenoceptor agonist. The EC50 values for isoproterenol and terbutaline in detrusor were the same as those in trigonal muscle but the maximum relaxant response to isoproterenol or terbutaline was significantly greater in detrusor than in trigonal muscle. Dobutamine (10(-5)-10(-4) M), a relatively specific beta 1-adrenoceptor agonist caused a small but significant relaxant response in trigonal muscle but no change in detrusor. In trigonal muscle the relaxant response to dobutamine was less than that to terbutaline. The relaxant response to 10(-6) M isoproterenol in detrusor was completely blocked by butoxamine (10(-4) M), a selective beta 2-antagonist or by propranolol (10(-6) M), a non-specific beta-antagonist but not by metoprolol (10(-6)-10(-4) M), a selective beta 1-antagonist. Relaxation of trigonal muscle induced by 10(-6) M isoproterenol was inhibited by 10(-5) M metoprolol by 30%, by 10(-4) M butoxamine by 70%, or completely by 10(-6) M propranolol. These findings are consistent with the view that the density of beta-adrenoceptors is higher in the detrusor than in trigonal muscle, and that the relaxant response to beta-adrenoceptor stimulation is mediated by beta 2-subtype in the detrusor and by both of beta 1- and beta 2-subtypes in trigonal muscle of the male rabbit.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3022421&dopt=Abstract
J Hypertens. 1994 Jun;12(6):681-90.
On the existence of functional beta-adrenoceptors on vascular sympathetic nerve endings in the human forearm.
Chang PC, Grossman E, Kopin IJ, Goldstein DS.
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.
OBJECTIVE: To examine the existence of presynaptic beta-adrenoceptors modulating forearm norepinephrine release in 31 healthy volunteers. METHODS: The spillover rate of norepinephrine in forearm venous plasma and the total plasma appearance rate of norepinephrine in the forearm were estimated using intra-arterial infusion of [3H]-norepinephrine. Isoprenaline was infused intra-arterially to stimulate beta-adrenoceptors, terbutaline to stimulate beta 2-adrenoceptors, propranolol to block beta-adrenoceptors, metoprolol to block beta 1-adrenoceptors, isoprenaline combined with metoprolol to stimulate beta 2-adrenoceptors, epinephrine to stimulate alpha- and beta-adrenoceptors, yohimbine to block alpha 2-adrenoceptors and sodium nitroprusside to increase forearm blood flow directly. RESULTS: No systemic hemodynamic effects or changes in arterial plasma norepinephrine level were noted during the intra-arterial infusions. Metoprolol and propranolol decreased norepinephrine spillover and its rate of appearance in the forearm without affecting forearm blood flow. Isoprenaline and sodium nitroprusside increased and epinephrine decreased forearm norepinephrine spillover. Terbutaline increased forearm norepinephrine spillover and its rate of appearance in the forearm. Terbutaline increased the forearm rate of appearance and spillover of norepinephrine more than did sodium nitroprusside or isoprenaline at the same level of forearm blood flow. Infusion of isoprenaline failed to increase norepinephrine spillover or its forearm appearance rate more than would be expected from the increase in forearm blood flow. Administration of epinephrine increased spillover and forearm appearance rate of norepinephrine during intra-arterial infusion of yohimbine. CONCLUSIONS: The terbutaline, propranolol, metoprolol and yohimbine plus epinephrine results suggest that beta-adrenoceptors enhance release of norepinephrine from vascular sympathetic nerve endings in humans.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7963493&dopt=Abstract
Clin Neurol Neurosurg. 1989;91(4):311-6.
Paired stimulation and functional change of the sural nerve during beta blocker therapy.
Husstedt IW, Grotemeyer KH, Schlake HP, Brune G.
Department of Neurology, University of Munster.
29 patients were examined during a therapy with beta blockers. The medication was applied over 12 weeks, 16 patients received propranolol 120 mg/day, 13 patients metoprolol 200 mg/day. Two patients showed side-effects. Neurophysiological examinations, i.e. sural nerve conduction velocity and paired stimulation of the sural nerve, revealed a slight decrease of nerve conduction velocity and a significant increase of the latency prolongation of the second nerve action potential when the medication was finished. These functional changes in the sural nerve may result from the interaction of metoprolol and propranolol with beta-receptors of the peripheral nerve.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2573441&dopt=Abstract
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