Search results for "norepinephrine"
showing 10 items of 234 documents
Autoinhibition of noradrenaline release from the rat heart as a function of the biophase concentration. Effects of exogenous alpha-adrenoceptor agoni…
1984
1. Rat isolated perfused hearts with the right sympathetic nerves intact were loaded with 3H-(-)-noradrenaline. The nerves were stimulated with trains of 180 pulses at 3 Hz and at 10 min intervals. The overflow of 3H-noradrenaline and 3H-metabolites was determined by liquid scintillation spectrometry. 2. Clonidine (IC50 17 nM), oxymetazoline (IC50 63 nM), and α-methylnoradrenaline (apparent IC50 35 nM, determined in the presence of cocaine and propranolol) decreased the stimulation-evoked overflow of 3H-noradrenaline by 26, 49, and 78%, respectively, but not methoxamine up to 100 μM (propranolol present). Oxymetazoline and α-methyl-noradrenaline did not cause desensitization of the presynap…
Presynaptic effects of scopolamine, oxotremorine, noradrenaline and morphine on [3H] acetylcholine release from the myenteric plexus at different sti…
1987
The inhibition by three modulators (oxotremorine, noradrenaline, morphine) of acetylcholine release from the myenteric plexus preincubated with [3H]choline was investigated at different stimulation frequencies and calcium concentrations. Moreover, [3H]acetylcholine release evoked by a low (0.1 Hz) or a high (10 Hz) stimulation rate was investigated at different calcium concentrations either in the absence or presence of scopolamine. A reduced calcium concentration (0.6 mmol/l) inhibited acetylcholine release more at 0.1 Hz (74% +/- 3%) than at 10 Hz (44% +/- 8%). Scopolamine enhanced the stimulated acetylcholine release at a calcium concentration of 1.8 mmol/l. At calcium concentrations hig…
The effect of physostigmine on the vagally induced muscarinic inhibition of noradrenaline release from the isolated perfused rabbit atria.
1982
1. Presynaptic cholinergic-adrenergic interactions were studied on isolated perfused rabbit atria with the extrinsic right vagus and sympathetic innervation intact. The transmitter stores were labelled with 14C-choline and 3H-noradrenaline. The radioactive compounds were separated on columns and determined by scintillation spectrometry. The stimulation-evoked overflow of both transmitters was calcium-dependent and abolished by tetrodotoxin. 2. Methacholine caused a concentration-dependent decrease of atrial tension development and 3H-noradrenaline overflow evoked by 3 Hz sympathetic stimulation. Vagus nerve stimulation (1–20Hz), although nearly abolishing tension development at 20Hz, decrea…
The role of choline in the release of acetylcholine in isolated hearts.
1978
1. The concentrations of acetylcholine, choline and noradrenaline were estimated in the perfusate (overflow) of isolated hearts of chickens, cats, rabbits and guinea pigs. Neurotransmitter release was evoked by stimulation of both vagus nerves and by direct stimulation of the heart (field stimulation). 2. In the absence of exogenous choline and physostigmine, field stimulation at 20 Hz for 20 min caused an overflow of acetylcholine from the hearts of the 4 species investigated. During vagal stimulation, however, acetylcholine was detected only in the perfusate of the chicken heart. 3. Field stimulation for 2 min caused an overflow of 193 pmol g−1 min−1 acetylcholine and of 666 pmol g−1 min−…
The use of the de deckere-ten hoor preparation for study of nicotinic and potassium-evoked dopamine ?-hydroxylase release from the rabbit heart
1980
1. Dopamine β-hydroxylase (DBH) and noradrenaline were determined both in the venous effluent (perfusate) and in the transmyocardial fluid (TMF) collected from the apex of the rabbit isolated heart which was prepared according to De Deckere and Ten Hoor (1977) and perfused with Tyrode's solution at 20 ml/min. 2. Perfusion for 2 min with the nicotinic drug, p-aminophenethyl-trimethylammonium (PAPETA), both in the absence of presence of atropine evoked noradrenaline overflow into the perfusate and TMF that was maximal in the 0–2 min sample and declined from maximum with a t1/2 of 0.6 min. DBH was released into TMF with the maximum from 2–4 min and a t1/2 of decline of 5.6 min. 3. High K-low N…
The inhibition by dopamine of cholinergic transmission in the isolated guinea-pig ileum. Mediation through alpha-adrenoceptors.
1982
1. Segments of the guinea-pig ileum were incubated in Tyrode's solution containing 3 μM propranolol. Dopamine, like noradrenaline and clonidine, inhibited the twitch response to field stimulation. The inhibitory action of dopamine remained unchanged in the presence of the dopamine uptake inhibitor nomifensine (1 μM). Tissue from reserpine-pretreated amimals was insensitive to tyramine but the response to dopamine was not affected. It is, therefore, assumed that the effect of dopamine is due to a direct receptor stimulation and not to the release of noradrenaline. 2. The inhibitory action of dopamine was not antagonized by the dopamine receptor antagonists cis-flupenthixol, pimozide or dompe…
Pharmacological analysis of the responsiveness of guinea-pig lung parenchymal strip to dopamine
1984
Abstract Responses to dopamine were examined in the guinea-pig isolated lung parenchymal strip. Complete cumulative concentration-response curves to dopamine exhibited a biphasic pattern with a small initial contraction at concentrations below 10(-5) M followed by a dose-dependent relaxation at higher concentrations. Phentolamine (10(-5) M) completely abolished the contractile component and enhanced sensitivity and maximal relaxation to dopamine. In the presence of phentolamine, propranolol antagonized the dopamine-induced relaxation (pA2 = 8.54 +/- 0.07). In the presence of propranolol (10(-6) M), dopamine produced a dose-related contraction displaced to the right by phentolamine. Incubati…
INTERACTIONS OF ISOPRENALINE AND PROSTAGLANDIN E2 WITH RESPECT TO MYOCARDIAL CONTRACTILE FORCE, CORONARY VASCULAR RESISTANCE AND MYOCARDIAL OXYGEN CO…
1976
Left ventricular pressure (LVP), left ventricular pressure derivative (LV dp/dtmax), coronary vascular resistance (CVR) and myocardial oxygen consumption (Qo2) were measured simultaneously in isolated, electrically driven hearts of guinea-pigs at constant perfusion rate. 2 LVP, LV dp/dtmax, CVR and Qo2 were greatly decreased by either the addition of prostaglandin E2 (50 ng/ml) to the perfusion fluid or pretreatment of the animals with reserpine. 3 Isoprenaline (0.5 nM to 100 nM) induced increases in LVP, LV dp/dtmax and Qo2. In the presence of prostaglandin E2, there was a parallel shift of the isoprenaline concentration-response curve for LVP and LV dp/dtmax. This effect was not seen, aft…
Evidence that depletion of internal calcium stores sensitive to noradrenaline elicits a contractile response dependent on extracellular calcium in ra…
1993
1. Noradrenaline 1 microM induced a contractile response in rat isolated aorta in the presence or in the absence of extracellular Ca2+ with depletion of intracellular Ca2+ stores. Thereafter, during incubation in the presence of Ca2+, an increase in the resting tone was observed. Such a contractile response did not occur after exposure to caffeine or 5-hydroxytryptamine. 2. This increase in tension was inhibited in a concentration-dependent manner by alpha-adrenoceptor antagonists (prazosin, phentolamine and yohimbine), the non-specific relaxing compound, papaverine and by the Ca(2+)-entry blocker, nifedipine. Therefore, this contractile process is related to depletion of Ca2+ stores sensit…
Neurotransmitters adenosine triphosphate and noradrenaline induce nitric oxide release in rat vas deferens.
2000
1. In rat vas deferens, electrical field stimulation (EFS) evoked a muscular biphasic tetrodotoxin (TTX)-sensitive contractile response. 2. The amplitude of this response increased with the frequency of stimulation. 3. After each stimulation, nitric oxide (NO) release was assayed and found to be released in a frequency-dependent manner. 4. NO release also occurred after treatment with exogenous neurotransmitters, adenosine 5'-triphosphate (ATP) and noradrenaline (NA). 5. Prazosin and pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), respective antagonists of alpha1-adrenoceptors and P2x purinoceptors, inhibited NO release induced by NA and ATP. Both prazosin and PPADS inhibited…