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PubMed1989

Beta-adrenergic agents stimulate tissue plasminogen activator activity and messenger ribonucleic acid levels in cultured rat granulosa cells.

Expression of tissue plasminogen activator (tPA) gene is stimulated by gonadotropins in granulosa cells. Because adrenergic agents interact with specific granulosa cell receptors to increase progesterone biosynthesis, the effects of these pounds on tPA activity and mRNA levels were also investigated. Cells obtained from immature estrogen-treated rats were initially cultured with FSH or medium alone for 2 days. They were then reincubated with various adrenergic agents before measurement of medium tPA activity using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, followed by a fibrin overlay technique. In addition, cellular RNA was extracted, and tPA mRNA levels were analyzed using a specific rat cRNA probe. Isoproterenol, a beta-adrenergic agonist, stimulated the secretion of tPA activity in a dose-dependent manner, with FSH-pretreated cells secreting higher levels of the enzyme than cells without FSH priming. Northern blot hybridization of total RNA showed the accumulation of a 22S species tPA message in cells treated with isoproterenol, suggesting increased expression of the tPA gene. Furthermore, slot blot hybridization of RNA from these cells indicated a time-dependent increase in tPA mRNA, with maximal induction between 1-3 h of incubation. A selective beta 2-adrenergic agonist, terbutaline, but not the beta 1-agonist dobutamine, stimulated tPA activity. Also, the stimulatory effect of isoproterenol was blocked by a beta 2-antagonist (ICI-118,551) but not by a beta 1-antagonist (practolol), suggesting the involvement of a beta 2-receptor. Like FSH and LH, isoproterenol increased extra- and intracellular cAMP levels. Cotreatment of a saturating dose of isoproterenol with FSH or LH did not further stimulate tPA activity. Similar to that in cells treated with FSH, inhibition of protein synthesis by cycloheximide resulted in the superinduction of tPA mRNA in isoproterenol-treated cells. Thus, activation of beta 2-adrenergic receptors in granulosa cells induces tPA mRNA and activity, presumably through the protein kinase-A pathway shared by gonadotropins. Adrenergic neurotransmitters may be potential intraovarian regulators of this important protease.

Actins↗
PubMed1980

Study on the pharmacological actions of beta-adrenoceptor blockers with reference to their physico-chemical properties.

The relationship between the membrane stabilizing action of beta-adrenoceptor blockers and their physico-chemical properties was investigated. Their depressing effects on the action potential amplitude of isolated Rana sciatic nerve were examined. The orde of their depressing potencies was propranolol (PROP) greater than dichloroisoproterenol (DCI) greater than alprenolol (ALP) greater than methoxamine (MEX) greater than practolol (PRAC) = sotalol (SOTA). The order of the negative chronotropic potency on the isolated rabbit atrial rate was PROP greater than ALP greater than DCI greater than MEX greater than PRAC greater than SOTA. The order of beta-blocking activity in isolated guinea-pig tracheal chain or in isolated rabbit atrial rate was ALP greater than PROP greater than SOTA greater than DCI greater than MEX greater than PRAC or PROP greater than ALP greater than PRAC greater than DCI greater than SOTA greater than MEX respectively. A high correlation was observed between membrane stabilizing actions (depressing effect on sciatic nerve action potential and negative chronotropic effect on atrial rate) and physico-chemical properties (the apparent partition coefficient and pKb). No relation was observed between beta-blocking effect on tracheal chain or right atrial rate and physico-chemical properties. It is suggested that the active sites for beta-blocking action and membrane stabilizing action might be different.

Adrenergic beta-Antagonists↗
PubMed1988

The partial agonist activity of xamoterol (ICI 118,587) studied by heart rate response in pithed rats.

The partial agonist activity of xamoterol was evaluated by measuring changes in heart rate (HR) in pithed rats. Xamoterol showed dose-dependent positive chronotropic effects in catecholamine-depleted pithed rats (HR: 199 +/- 6 beats/min) and dose-dependent negative chronotropic effects in sympathetic nerve-stimulated pithed rats (HR: 325 +/- 16 beats/min). In contrast, isoproterenol exerted dose-dependent positive chronotropic effects in either condition (HR: 189 +/- 7 and 332 +/- 5 beats/min) and propranolol exerted dose-dependent negative chronotropic effects in either condition (HR: 209 +/- 5 and 344 +/- 19 beats/min). When exogenous noradrenaline was continuously infused into catecholamine-depleted pithed rats, xamoterol showed dose-related positive chronotropic effects with noradrenaline at 0.5 micrograms/(kg min) (HR: 235 +/- 4 beats/min), virtually no effects at 1.5 micrograms/(kg min) (HR: 297 +/- 11 beats/min) and dose-related negative chronotropic effects at 5 micrograms/(kg min) (HR: 330 +/- 5 beats/min). During continuous infusion of xamoterol [100 ng/(kg min)] into pithed rats, the control HR before stimulation was increased and the maximum increase produced by the sympathetic nerve stimuli at 0.25 to 4 Hz decreased. The maximum increase in HR brought about by xamoterol was about 71% of that induced by isoproterenol, and those by pindolol and practolol were about 40% and 21% respectively. It is concluded that xamoterol is a partial agonist with a strong agonist action.

Adrenergic beta-Agonists↗
PubMed1979

Effects of palytoxin on mechanical and electrical activities of guinea pig papillary muscle.

Effects of palytoxin (PTX) on isolated papillary muscles of guinea pigs were studied in an attempt to elucidate the mechanical and electrical activities. Inotropic effects of PTX above 3 x 10(-9) g/ml; an early positive inotropic effect, slowly developing contracture accompanied by decline in phasic tension, appearance of aftercontractions and arrhythmias at high doses. The positive inotropic effect of PTX was enhanced in high Ca2+ medium but was not modified by propranolol. PTX induced a sustained depolarization and decrease in the amplitude, upstroke velocity and duration of action potential. During development of depolarization, arrhythmias occurred, which lasted for 5--10 min and reappeared 30--60 min after. Oscillatory afterpotential often appeared. Neither reserpine nor practolol prevented the PTX-induced arrhythmia while propranolol prevented it. Tetrodotoxin slowed the development of depolarization due to PTX and inhibited PTX-arrhythmias. In low Na+ medium, PTX exerted fewer effects on resting and action potentials and produced no arrhythmia. The results suggest that PTX-induced depolarization is responsible for the generation of contracture and arrhythmia and that the depolarization is due to the change in membrane Na permeability.

Acrylamides↗
PubMed1983

Characterization of propranolol-induced relaxation of coronary artery.

Effects of propranolol on coronary artery were investigated in isolated dog coronary arteries and in isolated hearts of rats and guinea-pigs. Cumulative administration of dl-propranolol produced concentration-dependent relaxation of coronary arterial strips under potassium-contracture. There was no difference in relaxant potency between the optical isomers of propranolol. Lidocaine produced less relaxation than dl-propranolol, while atenolol and practolol scarcely affected the contraction. dl-Propranolol-induced relaxation was significantly restored by additional calcium or prevented by prior administration of calcium. In isolated hearts of rats and guinea-pigs which were perfused at a constant coronary inflow and paced at a constant rate, bolus administration of dl-propranolol produced dose-dependent falls in coronary perfusion pressure without significant changes in myocardial contractile force. Results indicate that propranolol may have relaxant activities on coronary arteries through inhibition of calcium influx in the cell membrane of coronary arterial smooth muscle.

Animals↗
PubMed1983

Binding characteristics of 3H-dihydroalprenolol to beta-adrenoceptors of rat heart treated with neuraminidase.

Binding characteristics of the beta-blockers and beta-agonists with the beta-adrenoceptors were investigated in 3H-dihydroalprenolol (3H-DHA) binding to rat heart membranes treated with neuraminidase. When 60% of the total sialic acid content in the membranes was removed, reproducibility of the binding assay became much better than was attainable without neuraminidase treatment, and the maximum density of beta-adrenoceptors was increased. These data suggest that the binding of the test compounds with the beta-adrenergic receptors in cardiac muscle was under the influence of the sialic acid of the glycocalyx of the membrane. The 3H-DHA binding sites in membranes treated with neuraminidase showed a strict stereo-specificity when tested with propranolol. The ranking order of inhibition of beta-antagonists or agonists is: dl-propranolol greater than oxprenolol greater than alprenolol greater than pindolol greater than YM-09538 greater than labetalol greater than acebutolol greater than atenolol greater than metoprolol greater than sotalol greater than butoxamine greater than practolol as antagonists or l-isoproterenol greater than l-epinephrine greater than l-norepinephrine as agonists. A good correlation (r = 0.91, P less than 0.001) was observed between the Ki values observed by the present binding assay and the pA2 observed in the guinea-pig atria relative to the positive inotropic effect by Bieth et al. (Br. J. Pharmacol. 68, 563-569, 1980), indicating that the present method will be useful for screening new beta-adrenergic receptor antagonists or agonists.

Alprenolol↗
PubMed1984

Cardiovascular effects of a new positive inotropic agent, (-)-(R)-1-(p-hydroxyphenyl)-2-[(3,4-dimethoxyphenethyl)amino]-ethanol (TA-064) in the anesthetized dog and isolated guinea pig heart.

The positive inotropic effect of TA-064, (-)-(R)-1-(p-hydroxyphenyl)-2-[(3,4-dimethoxyphenethyl)amino]ethanol, was studied in the anesthetized dog and isolated guinea pig heart. An intravenous administration of TA-064 dose-dependently increased the cardiac contractile force with little effect on blood pressure in dogs. The positive inotropic activity of TA-064 was 1/100 that of isoproterenol and similar to that of dobutamine. This effect of TA-064 was stereospecific, and it was blocked by practolol. Thus TA-064 has beta 1-adrenoceptor agonistic action. The positive inotropic effect of TA-064 was more pronounced than the positive chronotropic effect, compared with those of isoproterenol. Similar effect of TA-064 was observed in the reserpinized dog and in the isolated perfused heart of the guinea pig as well. TA-064 administered intraduodenally at a dose of 0.1 mg/kg increased contractile force by 120% of the control, and the effect lasted for more than 150 min. TA-064 given in the femoral artery demonstrated a very weak vasodilating effect on the artery. TA-064 is an orally active, positive inotropic agent. The selective positive inotropic action of TA-064 may result from its beta 1-adrenoceptor agonistic property.

Adrenergic beta-Agonists↗
PubMed1984

Pharmacological properties of presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries.

Pharmacological properties of the facilitatory presynaptic beta-adrenoceptor mechanism were studied in superfused spiral preparations of guinea-pig pulmonary arteries preloaded with 3H-norepinephrine. (-)-Isoproterenol (0.3 microM)-induced increases in total 3H efflux per pulse evoked by transmural field stimulation (1, 5, 10 and 20 Hz, 10 V, 2 msec pulse width, 100 pulses and 30 min intervals) were neither dependent on impulse-frequencies nor selective at lower frequencies. Isoproterenol increased 3H efflux at 5 Hz in a concentration-dependent manner (1 nM to 1 microM): pD2 was 7.7. Salbutamol increased 3H efflux in a similar manner to isoproterenol: pD2 was 7.4. Prenalterol at 3 microM only slightly increased 3H efflux. Tazolol (10 nM to 3 microM) produced no increases. Atenolol (3 microM) and practolol (3 microM) did not antagonize isoproterenol (0.3 microM)-induced increases in 3H efflux. Butoxamine (3 microM) and H 35/25 (3 microM) did antagonize this parameter. (-)-Epinephrine (1 nM to 0.1 microM) decreased 3H efflux at 5 Hz and concentration-dependently increased this parameter in the presence of 10 microM phentolamine. (-)-Norepinephrine (10 nM to 1 microM) concentration-dependently inhibited evoked 3H efflux and did not increase the parameter in the presence of 10 microM phentolamine, 10 microM cocaine and 10 microM normetanephrine. Thus, there exist presynaptic beta 2-subtype receptors on noradrenergic nerve endings innervating guinea-pig pulmonary arteries.

Adrenergic beta-Agonists↗
PubMed1985

Studies on the affinity and selectivity of denopamine (TA-064), a new cardiotonic agent, for beta-adrenergic receptors.

Denopamine is a new orally active cardiotonic agent. The present experiment was carried out to characterize the binding affinity and selectivity of this drug for beta-adrenergic receptor subtypes. Binding studies were performed using 3H-dihydroalprenolol as the radioligand. Binding affinities of denopamine and some beta-agonists for rat heart membranes (KiH), which contain predominantly the beta 1-subtype, were in the order of isoproterenol (Iso, 14.1 nM) greater than prenalterol (158) greater than norepinephrine (Nor, 227) greater than or equal to epinephrine (Epi, 248) greater than denopamine (545) greater than or equal to dobutamine (645) greater than procaterol (1440) greater than terbutaline (6420). In rat lung membranes (predominantly beta 2-subtype), the order of potency (KiL) was Iso (20.6 nM) greater than procaterol (70.2) greater than Epi (136) greater than prenalterol (412) greater than dobutamine (735) greater than or equal to Nor (744) greater than denopamine (2205) greater than terbutaline (2500). The beta 1/beta 2-selectivity as judged from the KiL/KiH values was in the order of denopamine (4.1) greater than Nor (3.3) greater than prenalterol (2.6) greater than Iso (1.5) greater than dobutamine (1.1) greater than Epi (0.55) greater than terbutaline (0.39) greater than procaterol (0.05). Practolol, a beta 1-antagonist, showed a high beta 1-selectivity (KiL/KiH = 15.3). In the presence of guanine nucleotide (GTP), the denopamine radioligand competition curve showed a rightward shift, and its Hill coefficient increased like other agonists, although the degree of the shift was less than that observed with full agonists such as Iso. These results essentially correspond with the pharmacological and biochemical properties of denopamine and confirm the beta 1-selectivity and the agonist property of this compound.

Animals↗
PubMed1990

Characteristics of 125I-iodocyanopindolol binding to beta-adrenergic and serotonin-1B receptors of rat brain: selectivity of beta-adrenergic agents.

The present study was designed to examine the specificity of beta-adrenergic antagonists for beta 1-, beta 2-adrenergic and 5HT1B-serotonergic receptors by the competitive interaction with 125I-iodocyanopindolol (125I-ICYP) as a radioligand. The beta 1-adrenoceptors were preferred by acebutolol, atenolol, betaxolol, practolol, and l-, dl- and d-metoprolol, while butoxamine and lCl-118,551 preferred beta 2-adrenoceptors. The selectivities of these beta 1- and beta 2-antagonists are well-known, but alprenolol which is known as a non-selective antagonist was 7.2-fold more selective for the beta 2-adrenoceptors in the present study. All beta-antagonists used were more selective towards beta-adrenoceptors as compared with 5HT1B-receptors. Good correlations were observed between the potencies of beta-adrenoceptor antagonists for inhibition of 125I-ICYP binding to beta 1- and beta 2-adrenoceptor sites and their potencies for inhibiting the binding of the same radioligand to 5HT1B-serotonergic receptor sites. These results suggest that beta-adrenoceptor antagonists can bind to beta-adrenoceptors and 5HT1B-receptors.

Adrenergic beta-Agonists↗
PubMed1994

Positive chronotropic and inotropic effects of higenamine and its enhancing action on the aconitine-induced tachyarrhythmia in isolated murine atria.

Aconitine and higenamine are the components of aconite root. We investigated the cardiac effects of these compounds on murine right and left atria and the interaction of higenamine with aconitine on the rate of spontaneously beating right atria. Higenamine increased the rate (EC50 = 38 nM) and the force of contraction (EC50 = 97 nM), the maximal responses being comparable with those of isoproterenol. The positive chronotropic effect of higenamine was antagonized by propranolol (30-300 nM) and practolol (10 nM-3 microM), but not by butoxamine (1 microM), indicating that it was a beta 1-adrenoceptor-mediated action. The positive chronotropic effect of higenamine was not changed by pretreatment with reserpine (4 mg/kg, i.p., 4 hr). Aconitine (0.16-0.25 microM) induced tachyarrhythmia in right atria was attenuated by quinidine (1 microM), atropine (8.6 microM) and AF-DX 116 (8.6 microM), suggesting that aconitine activates sodium channels and muscarinic receptors. Higenamine (2.5 nM) and dobutamine (1 nM) did not cause chronotropic effects by themselves, but enhanced the aconitine-induced tachyarrhythmia. These results indicate that higenamine is a beta 1-adrenoceptor full agonist in murine atria and that the aconitine-induced tachyarrhythmia is augmented by the beta 1-adrenergic action of higenamine.

Aconitine↗
PubMed1986

Serotonin-induced stimulation of progesterone production by cow luteal cells in vitro.

The addition of acetylcholine or histamine (10(-7) to 10(-4) M), gamma-aminobutyric acid, a dopamine agonist, and melatonin (10(-7) to 10(-5) M) did not alter basal or LH-stimulated progesterone production (P greater than 0.05). The addition of the specific beta 2-adrenergic agonist terbutaline and salbutamol did not significantly elevate progesterone production. Treatment of luteal cells with serotonin (5-HT), 10(-6) to 10(-4) M, increased the production of progesterone (P less than 0.05). This stimulated production was inhibited by the addition of mianserin (10(-5) M, a 5-HT antagonist; P less than 0.05). Isoproterenol (10(-7) to 10(-4) M) also resulted in significant increases in progesterone production (P less than 0.05). The combined treatments of 5-HT + LH, isoproterenol + LH, or isoproterenol + 5-HT did not result in a further increase in progesterone above that observed in response to LH or isoproterenol alone (P greater than 0.05). The isoproterenol-induced progesterone production could not be blocked by butoxamine (10(-5) M, a beta 2-antagonist), or practolol (10(-5) M, a beta 1-antagonist), but was inhibited by propranolol (10(-5) M, a general beta-antagonist; P less than 0.05). The response to isoproterenol was unaffected by mianserin (10(-5) M). These results demonstrate a possible role for 5-HT in the regulation of steroidogenesis by the corpus luteum of the cow. Furthermore, these results suggest that serotonin-induced progesterone production is a receptor-mediated event.

Amines↗
PubMed1993

The way towards adverse event monitoring in clinical trials.

Different approaches to the monitoring of adverse reactions to drugs have been used over the years, with the aim of preventing catastrophes like the thalidomide episode and to rationalise drug usage. In the 1960s, the use of national and international adverse event monitoring was first suggested by the British statistician, David Finney. According to Finney, the method was well suited for the postmarketing surveillance of drugs. The idea was rejected by the World Health Organization (WHO) but was later taken up by the Prescription Event Monitoring Event System in the UK. Subsequent to problems with practolol in the 1970s it was suggested that adverse event monitoring could also be useful in clinical trials to detect adverse reactions before a drug is launched. The idea of adverse event monitoring has been tested by Astra Hässle in Sweden in clinical trials with felodipine and omeprazole, and is now the standard method within the company. Adverse event monitoring is an expensive and time-consuming method seen from a short term perspective. However, such monitoring offers an opportunity to optimise the use of clinical trials in safety monitoring, and its ability to predict possible adverse drug reactions is superior to other methods.

Adverse Drug Reaction Reporting Systems↗
PubMed1976

Clinical pharmacokinetics of beta-adrenoreceptors blockers.

beta-blockers are completely and rapidly absorbed from the gastro-intestinal tract. In their first passage through the liver they are metabolised to a varying extent - the so-called first-pass effect. For propranolol and alprenolol this degradation is partly compensated for by the formation of active metabolites, the 4-OH derivatives. The beta-blocking effect is linearly correlated with the log plasma concentration of the drugs. Although there is also a relationship between the antihypertensive effect of the drugs and their log plasma concentration, it seems to be of limited value to determine the plasma levels of the drugs in order to adjust the therapeutic dose. This is due to the great inter-individual differences of the plasma concentration-antihypertensive effect relationship. It is essential to investigate whether pharmacologically active metabolites are formed. These may not only influence the relationship between plasma concentration and therapeutic effect but may also modify the pharmacological profile of the drug. The plasma levels, and thereby the effects of the drugs, can be modified by other drugs and diseases. Thus practolol, which is mainly eliminated via the kidneys, has a longer plasma half-life in patients with renal failure. The plasma of propranolol, which is eliminated from the body by bio-transformation in the liver, is not prolonged in patients with renal failure, but its metabolites are excreted at a lower rate in such patients. Although most beta-blockers have a relatively short plasma half-life (2 to 5 hours), the drugs can be administered twice daily in clinical practice. This due to the fact that the effect declines according to zero-order kinetics while the elimination of the drug follows first-order kinetics. It is desirable that all these factors are clarified before a drug is used in clinical practice as they all will have an influence on its dose regimen. The responsibility for this must be on the drug company, which must be able to inform physicians not only about the standard dosage of the drug but also how other drugs and diseases can change the individual responses to the drug.

Adrenergic beta-Antagonists↗
PubMed1980

Antinuclear antibodies and cardiovascular drugs.

Antinuclear antibodies (ANA) can be induced by some drugs used in the treatment of cardiovascular disease. The reported frequency with which these antibodies are detected in patients varies widely. This variation results from a number of factors. The sensitivity of the ANA assay is influenced by the selection of substrates, the concentration of antisera and characteristics of the detection systems such as ultraviolet microscopes or electrophoretic apparatus. The incidence of ANA also varies with age and sex of the patient, being more common in older people and in females. Identification of a drug suspected of producing ANA demands a careful evaluation of the data with precisely standardised laboratory procedures and comparison of data with appropriate control groups of untreated and treated patients. Cardiovascular drugs associated with increased ANA incidence can be considered in two categories: A) A few drugs induce ANA in most patients if therapy is continued for long enough at high enough dosage. Many of these patients develop systemic lupus erythematosus like-syndromes. This group includes procainamide, hydrallazine at high doses and practolol. B) A further group of drugs produces ANA in 20 to 30% of patients, few if any, of whom develop SLE. Methyldopa and acebutolol are clearly in this category, while there is some evidence that labetolol, guanethidine and hydrallazine at low doses may also be implicated. Some very preliminary evidence suggests those patients on the beta-adrenoceptor blocking drugs atenolol, metoprolol and exprenolol exhibit a mildly increased incidence of ANA, but there is no evidence to suggest associated SLE. Only patients who develop ANA while on treatment with category A drugs require careful monitoring for SLE.

Adrenergic beta-Antagonists↗
PubMed1994

The role of beta-blockers in the treatment of cardiomyopathy and ischaemic heart failure.

As first reported by our group in 1975, severe heart failure due to idiopathic dilated cardiomyopathy could be improved in patients receiving beta-blocker therapy starting at a very low dose and followed by a stepwise increase. Since then, these results have been confirmed by our own group and by others, and similar results were also obtained in patients with other forms of cardiomyopathy, including ischaemic cardiomyopathy. In 13 separate studies involving a total of 651 patients with idiopathic dilated cardiomyopathy, beta-blockade for 2 to 19 months (in addition to conventional treatment of heart failure, including angiotensin converting enzyme inhibitor therapy), significantly improved cardiac function. These studies were performed using metoprolol, bucindolol, labetalol and practolol. Eight studies investigated the effects of long term beta-blocker treatment in patients with heart failure and cardiomyopathy due to coronary artery disease, valvular heart disease, diabetes and doxorubicin therapy. A total of 128 patients were treated with metoprolol, carvedilol or bucindolol for periods of 2 to 12 months. All studies reported a significant improvement in cardiac function. Three studies reported results on survival and the need for cardiac transplantation. The first study published by our group reported improved survival in patients with idiopathic dilated cardiomyopathy treated with metoprolol plus digitalis and diuretics compared with a matched control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1982

Effect of dopamine on pentagastrin-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula by using miniature strain-gauge transducers. Infusion of pentagastrin changed the contractile activity to a digestive state. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade or adrenergic and dopaminergic receptors. The stimulated antral motility was inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone and by cis-flupenthixol, which blocks both peripheral and central dopaminergic receptors. The effect of dopamine was not significantly altered by the beta 1-adrenoceptor blocker practolol, the alpha-adrenoceptor blocker phentolamine, or the alpha + beta-adrenoceptor blocker labetalol. Consequently, this study indicates that dopamine acts on gastric antral motility through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, seem not to be involved in the motility response.

Adrenergic alpha-Antagonists↗
PubMed1982

Effect of dopamine on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The alpha-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the beta 1-adrenoceptor blocker practolol or the beta 1 + beta 2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

Adrenergic alpha-Antagonists↗