Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of several drugs on the automaticity of blood-perfused canine sino-atrial node preparation were examined by injecting drugs into the sinus node artery. All drugs produced a dose-dependent decrease in sino-atrial rate, although dl-alprenolol in low doses produced a slight increase, and their relative potencies determined on the basis of the molar doses producing a decrease by 15 beats/min (ED 15) were in the descending order: SK&F24260 greater than or equal to nifedipine greater than or equal to adenosine greater than quinidine greater than dl-propranolol greater than or equal to dl-alprenolol greater than procaine, and 1:1/1.2:1/2.0:1/28.8:1/114.2:1/123.8:1/704.2. Potencies of dl- and d-alprenolol and propranolol in causing a negative chronotropic action were almost equal. In higher doses, SK&F24260 and nifedipine (3-10 microgram), quinidine (0.3-1 mg), dl-propranolol and alprenolol (0.3-1 mg), and procaine (1-3 mg) caused a sino-atrial arrest. The order of potency in causing arrest was approximately similar to that in causing arrest was approximately similar to that in causing a negative chronotropic action (ED 15). Adenosine showed a profound negative chronotropic effect but did not cause a sino-atrial arrest. The negative chronotropic action and sino-atrial arrest caused by dl- and d-alprenolol and propranolol, quinidine and procaine maybe due mainly to their calcium antagonistic properties, but it is considered that their action sites are individually different. Furthermore, we suggest that in conscious dogs the tachycardia produced by the systemic administration of dl-alprenolol is not entirely due to its intrinsic sympathomimetic effect.
 ...
PMID:Change in automaticity of excised, sino-atrial node by alprenolol and its dextro isomer and several drugs injected into the sinus node artery of the dog. 60 19

We showed previously that circulating adenosine potentiates pressor responses to nicotine in rats, apparently by enhancing the effects of nicotine in sympathetic ganglia. In the present studies, we examined the effects of adenosine (or synthetic adenosine receptor agonists) on a variety of sympathomimetic responses to nicotine (or other nicotinic cholinergic agonists). Indices of sympathetic activity examined were: blood pressure; heart rate; eyelid tension; and vas deferens perfusion pressure. Elevation of arterial plasma adenosine from its basal level (approximately 1.5 microM) to 2 to 3 microM (by i.v. adenosine infusion) had no effect on the basal value of any of these indices, but increased by 2.5 to 4-fold their peak responses to nicotine (40 microgram/kg i.v.). Adenosine also strongly enhanced sympathomimetic responses to inhaled cigarette smoke. The adenosine receptor antagonist caffeine (10 mg/kg) suppressed the ability of adenosine to potentiate these responses to nicotine. Pressor responses to the nicotinic cholinergic receptor agonists dimethylphenylpiperazinium iodide, tetramethylammonium, lobeline and cytisin were also potentiated by adenosine. Low doses (0.25-5 mu/kg) of synthetic adenosine receptor agonists potentiated all four of the tested sympathomimetic responses to nicotine, exhibiting the rank order of potency: N-Cyclopropylcarboxamidoadenosine greater than 2-Chloroadenosine greater than N6-R-Phenylisopropyl adenosine greater than N6-S-Phenylisopropyladenosine. The nonpurinergic vasodilator sodium nitroprusside failed to potentiate responses to nicotine, suggesting that the influence of adenosine on responses to nicotine is not secondary to its direct circulatory effects.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Adenosine potentiates sympathomimetic effects of nicotinic agonists in vivo. 300 40

1. Adenosine 5'triphosphate (ATP) as well as [3H]-noradrenaline ([3H]-NA) is released by perfusion of the vas deferens with the indirect sympathomimetic tyramine (100 microM); this result is consistent with the concept of sympathetic cotransmission. 2. While tyramine produced a strong contraction in the vas deferens of the rat, it had little mechanical action in the guinea-pig vas deferens. This appears to be largely because tyramine induces considerably lower levels of release of both ATP and NA from the guinea-pig vas deferens compared to that of the rat. Furthermore, NA released by tyramine appears to release ATP from a secondary pool in the rat vans deferens, but not that of the guinea-pig, since prazosin reduced the tyramine-induced release of ATP in the rat vas deferens. 3. alpha,beta-Methylene ATP (alpha,beta-meATP) increased both the spontaneous release of ATP and the tyramine-evoked efflux of ATP and [3H]-NA. The basal and tyramine-induced efflux of [3H]-NA was also enhanced by the alpha 1-adrenoceptor antagonist, prazosin, suggesting that prejunctional alpha 1-adrenoceptors may modulate neurotransmitter release.
 ...
PMID:Release of endogenous ATP from the vasa deferentia of the rat and guinea-pig by the indirect sympathomimetic tyramine. 782 37