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PubMed2002

The regulation of human vascular smooth muscle extracellular matrix protein production by alpha- and beta-adrenoceptor stimulation.

OBJECTIVE: The sympathetic nervous system (SNS) is commonly activated in hypertension; however, the role of SNS activation in the pathogenesis of cardiovascular structural changes remains poorly defined. In particular, the effect of adrenergic stimulation on extracellular matrix (ECM) protein production by human cardiovascular cells is unknown. The present study thus investigated the direct effect of adrenergic stimulation on ECM protein production by cultured human vascular smooth muscle (VSM) cells. METHODS AND RESULTS: Exposing human VSM cells to norepinephrine increased collagen protein production by 42%, P < 0.01, when compared to control (unstimulated) cells. This effect was mediated by the alpha1-adrenoceptor, since it was inhibited by the selective alpha1-adrenoceptor antagonist; prazosin (2 micromol/l) and reproduced by the selective alpha1-adrenoceptor agonist; phenylephrine (10 micromol/l). In contrast, beta-adrenoceptor stimulation - isoprenaline (1 micromol/l) or norepinephrine (10 micromol/l) + prazosin (2 micromol/l) - inhibited collagen production by 12%, P < 0.01. This inhibitory effect was mediated via the beta1-adrenoceptor, since it was blocked by atenolol (beta1-adrenoceptor antagonist) but not butoxamine (beta2-adrenoceptor antagonist). Fibronectin, another ECM protein, was similarly regulated by alpha- and beta-adrenoceptor stimulation. Transforming growth factor beta1 (TGFbeta1) mRNA expression by human VSM cells was also significantly influenced by adrenergic stimulation, being increased by phenylephrine (alpha-agonist) and inhibited by isoprenaline (beta-agonist). CONCLUSIONS: These results uniquely demonstrate the capacity for adrenergic stimulation to directly modulate TGFbeta1 expression and ECM protein synthesis by the human cardiovascular system.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

The pharmacology of a beta 2-selective adrenoceptor antagonist (ICI 118,551).

While specific antagonists of the beta 1-adrenoceptor, such as atenolol and betaxolol, are widely available, a potent specific antagonist selective for the beta 2-adrenoceptor has yet to be described. Previously described beta 2-selective antagonists such as butoxamine, H 35/25, and IPS 339 are lacking in potency, specificity, or appropriate beta 2-selectivity. ICI 118,551 [erythro-dl-1-(7-methylindan-4-yloxy)-3-isopropylaminobutan-2-ol] possesses a high degree of selectivity and specificity for the beta 2-adrenoceptor. The affinity of propranolol and ICI 118,551 for beta-adrenoceptors has been determined by comparing their antagonist potencies, expressed as pA2 values, against the actions of isoproterenol on the guinea pig atrium and uterus. ICI 118,551 had a higher affinity for the uterine beta 2-receptor than did propranolol (pA2 9.26 and 8.64, respectively) but a lower affinity for the atrial beta 1-receptor (pA2 7.17 and 8.30, respectively). Thus, the beta 2/ beta 1-selectivity ratios, in vitro, were 123 for ICI 118,551 and 2.2 for propranolol. The potency and selectivity of ICI 118,551 and atenolol on the chronotropic and vasodilator actions of isoproterenol were compared in anaesthetised dogs. The apparent K' B values at the vascular beta-adrenoceptor were 2.1 micrograms/kg for ICI 118,551 and 253 micrograms/kg for atenolol, and the potency ratio for antagonism of vascular versus atrial actions of isoproterenol was greater than 250:1. In regard to ancillary pharmacological properties, ICI 118,551 has no partial agonist activity but has a membrane-stabilising action similar to that of propranolol.

Adrenergic beta-Antagonists↗
PubMed2003

Involvement of the beta3 adrenoceptor in nebivolol-induced vasorelaxation in the rat aorta.

Nebivolol is a highly selective beta(1) adrenoceptor blocker with additional vasodilating properties. Although it has been shown that the nebivolol-induced vasorelaxation is nitric oxide (NO) and cGMP dependent, the receptor that mediates these actions remains controversial, and serotonergic as well as beta-adrenergic pathways may be involved. Therefore, functional experiments investigating the receptor involved in nebivolol-induced vasorelaxation were performed in the rat aorta. Isolated aortic rings were exposed to cumulative concentrations of nebivolol. Nebivolol concentrations of 3 micromol/L and higher caused vasorelaxation, which was inhibited by the presence of the NO synthase inhibitor l-NNA (100 micromol/L), or by mechanical removal of the endothelium. Exposure of the vessel rings to the selective 5-HT(1A) antagonist NAN-190 (1 micromol/L) or the 5-HT(1/2) antagonist methysergide (1 micromol/L) did not influence nebivolol-induced vasorelaxation. Similarly, the incubation with the beta(2)-adrenoceptor antagonist butoxamine (50 micromol/L) did not prevent vasorelaxation. The selective beta(3)-adrenoceptor antagonist S-(-)-cyanopindolol (1 micromol/L), however, significantly counteracted the nebivolol-induced vasorelaxation. Furthermore, exposure of the aortic rings to cumulative concentrations of the beta(3) selective adrenoceptor agonist BRL37344 caused, like nebivolol, NO-dependent vasorelaxation that was antagonized by S-(-)-cyanopindolol. The results suggest that nebivolol-induced NO-dependent vasorelaxation is, at least in part, caused by a beta(3)-adrenoceptor agonistic effect.

Animals↗
PubMed1983

Characterization of alpha- and beta-adrenergic agonist stimulation of adenylate cyclase activity in human epidermal keratinocytes in vitro.

Adrenergic receptors are responsible for selective recognition and binding of catecholamines and may in turn have an effect on epidermal cell growth and maturation via adenosine-3',5'-monophosphate (cAMP). Using endogenous catecholamines and drugs specific for alpha- and beta-receptor subtypes, we have characterized the adrenergic receptor coupled to adenylate cyclase in cultured human epidermal keratinocytes. The relative potency order of stimulation of adenylate cyclase was: isoproterenol greater than epinephrine much greater than norepinephrine. The predominant adrenergic receptor is of the beta 2-subtype, as also confirmed by use of the selective antagonists propranolol, butoxamine, and atenolol. No evidence of alpha-adrenergic receptor mediation of adenylate cyclase was noted with the alpha 2-specific agonist, clonidine. Phenylephrine, the alpha 1-specific agonist, affected cAMP formation but this response could not be totally inhibited with prazosin, suggesting an unknown mechanism of action. Human keratinocytes retained the same beta-adrenergic receptor potency order properties throughout growth and maturation.

Adenylyl Cyclases↗
PubMed1995

Regulation of IgE production from human mononuclear cells by beta 2-adrenoceptor agonists.

The present study examined the effect of beta 2-adrenoceptor agonists on the interleukin-4 (IL-4)-driven IgE production and on the possible mechanisms of action of these compounds. We present evidence that salbutamol and fenoterol potentiated the IL-4-induced IgE production by human peripheral blood mononuclear cells (PBMC). No significant effect of incubation in the presence of beta 2-adrenoceptor agonists on IgG, IgA and IgM production was observed. Salbutamol and fenoterol inhibited interferon-(IFN)-gamma production by PHA-activated human PBMC suggesting that the blockade of the production of this cytokine could possibly explain the enhancement of IgE production. Salbutamol and fenoterol potentiated the IL-4-induced production of sCD23 whereas no effect on CD23 expression was observed. The potentiating effect of salbutamol on IgE production was blocked by two antagonists of beta 2-adrenoceptor, namely butoxamine and D,L-propranolol, suggesting a beta-adrenoceptor-mediated event. These results demonstrate that beta 2-adrenoceptor stimulation results in an increase in IgE production by human B lymphocytes.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Beta-adrenoreceptors in denervated skeletal muscles of the cat.

1. A number of sympathomimetic amines have been compared with (-)-isoprenaline for their ability to produce contractions in chronically denervated soleus and tibialis anterior muscles and to increase heart rate in bilaterally vagotomized anaesthetized cats. 2. The mean dose-ratios ((-)-isoprenaline equals 1) for adrenaline, orciprenaline and salbutamol were 2.9, 29.7 and 11.5 respectively in the tibialis anterior muscle and 3.5, 24.1 and 14.3 in the soleus muscle. The dose-ratios for noradrenaline were 21.1 in the tibialis anterior and 57.6 in the soleus muscle. 3. The dose-ratios ((-)-isoprenaline equals 1) obtained for the positive chronotropic effects of the drugs in bilaterally vagotomized cats were 14.5, 14.6, 29.6 and 24.2 for adrenaline, noradrenaline, orciprenaline and salbutamol respectively. 4. The beta2-receptor antagonists butoxamine and H35/25 antagonized the vasodepressor and skeletal muscle responses to (-)-isoprenaline to a greater extent than the cardiac responses, whereas the beta1-receptor selective antagonists practolol and H93/26 antagonized cardiac to a greater extent than vascular and skeletal muscle responses. 5. The results obtained suggest that the contractions of denervated skeletal muscle to sympathomimetic drugs result from stimulation of beta2-adrenoreceptors.

Adrenergic beta-Agonists↗
PubMed1993

Epinephrine reduces the severity of catheter-induced urethral inflammation by action at the alpha 2-adrenoceptors.

We have studied the contribution of epinephrine to experimentally induced urethral inflammation in the rat. Inflammation was induced by inserting latex strips into the urethra. The effects of various experimental procedures were assessed according to a 4-point scale based on histological findings. The results showed that 0.5 mg/kg epinephrine decreased the severity of catheter-induced urethral inflammation. This effect was blocked by the alpha 2-adrenergic agonist, yohimbine, but not by alpha 1 (prazosin), beta 1 (M32 MTC), or beta 2 (butoxamine) antagonists. The results suggest that the suppressive effect of epinephrine is mediated by action at the alpha 2 adrenergic receptor.

Animals↗
PubMed1981

Adrenoreceptors in the human penis.

1. Adrenaline, noradrenaline and phenylephrine caused contraction of the corpus cavernosum muscle of the human penis. These sympathomimetic amines did not product inhibitory effects even in the presence of the alpha-adrenoreceptor blocker, phentolamine. The effect of dopamine was similar to that produced by these three sympathomimetic amines. Higher doses of isoprenaline and salbutamol also contracted this preparation. 2. Cocaine and guanethidine enhanced the motor response to adrenaline, noradrenaline and phenylephrine while the action of dopamine was blocked by these two drugs. 3. The motor response to adrenaline, noradrenaline and phenylephrine was antagonized by phentolamine and often potentiated by the beta-adrenoreceptors blocking drug, propranolol. The contractions produced by high doses of salbutamol and isoprenaline were also abolished by phentolamine. These findings indicate that the motor response to sympathomimetic amines is the result of activation of alpha-adrenoreceptors in the corpus cavernosum muscle. 4. At low doses, isoprenaline and salbutamol relaxed the corpus cavernosum muscle strip. The inhibitory action was blocked by low concentrations of the beta-adrenoreceptor antagonist, propranolol but not by practolol (beta 1-adrenoreceptor antagonist) and butoxamine (beta 2-adrenoreceptor antagonist). beta-adrenoreceptors are present in the corpus cavernosum muscle but these are unlikely to be either of the beta 1 or beta 2 type. The possible existence of a third type of beta-adrenoreceptor is suggested.

Catecholamines↗
PubMed1995

The mechanistic pathway of gastric adaptive cytoprotection: a study on different components of the autonomic nervous system.

1. The involvement of different components of the autonomic nervous system in the pathogenesis of ethanol-induced damage and the adaptive cytoprotection of mild irritants were studied in the gastric mucosa of male rats. 2. Capsaicin, yohimbine, and domperidone aggravated the 100% ethanol-induced gastric mucosal damage and attenuated the cytoprotective action of 20% ethanol, but not of 5% NaCl and 0.3 M HCl. Butoxamine and prazosin blocked the adverse actions of yohimbine and domperidone respectively. 3. Atropine, pirenzepine, and lidocaine lessened the severity of 100% ethanol-induced mucosal injury and further increased the cytoprotective action of 5% NaCl and 0.3 M HCl, but not of 20% ethanol. 4. Our results demonstrated that sensory afferent neurones, alpha 2-adrenoceptors and D2-dopaminergic receptors all play a significant role in the defensive mechanism of the gastric mucosa and the adaptive cytoprotection of 20% ethanol, while the M1- and M2-muscarinic receptors and sensory chemoreceptors on the gastric mucosa contribute only to the former action. The adverse effect of yohimbine and domperidone on lesion formation is probably mediated through the release of catecholamines, which subsequently act on the beta 2- and alpha 1-adrenoceptors respectively.

Adaptation, Physiological↗
PubMed1970

Actions of some sympathomimetic bronchodilator and beta-adrenoceptor blocking drugs on contractions of the cat soleus muscle.

1. (-)-Isoprenaline, salbutamol, orciprenaline and quinterenol injected intravenously decreased the tension and degree of fusion of incomplete tetanic contractions of the soleus muscle of the anaesthetized cat.2. Under the most sensitive conditions, the smallest effective dose of (-)-isoprenaline was of the order of 0.01 mug/kg intravenously. Salbutamol was usually 6-10 times, orciprenaline 20-30 times and quinterenol about 35 times less potent than isoprenaline. The effects of salbutamol were about 1.6 times, of orciprenaline about 1.8 times and of quinterenol more than 20 times as long lasting as those of (-)-isoprenaline.3. The effects of the sympathomimetic amines were blocked by propranolol, H56/28, H35/25 and butoxamine but not by ICI 50172. The combined results with agonists and antagonists indicate that the receptors involved can be classified as of the beta(2) type.4. The effect of the amines on the cat soleus muscle appears to be analogous to that causing enhancement of physiological tremor in man, which suggests that skeletal muscle tremor may be an occasional unwanted side effect of the use of these bronchodilators.

Acetanilides↗
PubMed1972

The presence of -adrenoceptors in the guinea-pig seminal vesicle.

1. The preparation of longitudinal smooth muscle strips from guinea-pig seminal vesicles is described.2. Isoprenaline and salbutamol inhibited contractions produced by parasympathomimetic agents.3. The inhibitory action of isoprenaline was blocked by low concentrations of propranolol and butoxamine. It was concluded that beta(2)-adrenoceptors were present in the tissue.4. The inhibitory action of isoprenaline was not apparent when adrenaline, noradrenaline, hypogastric nerve or transmural stimulation were used to contract the tissue.

Acetylcholine↗
PubMed1978

Characterization of the adrenoceptor in the isolated cremaster muscle of the guinea-pig.

1 Contractions of the isolated cremaster muscle of the guinea-pig obtained in response to direct electrical stimulation were augmented by salbutamol, isoprenaline, adrenaline, noradrenaline and orciprenaline (in that order of potency), and by potassium chloride. Phenylephrine and xylometazoline had no effect. 2 The augmenting effect of isoprenaline on the twitch response was not altered by yohimbine or tolazoline, but was totally prevented by butoxamine, (--)-1-(4-nitrophenyl)-2-isopropylamino-ethanol (INPEA), (+/-)-INPEA, sotalol, metalol and practolol; (+)-INPEA was much less effective. The augmenting effect of potassium was not altered by beta-adrenoceptor blockade. 3 The results are consistent with the view that the augmenting effect of the sympathomimetic agents is mediated through beta2-type of adrenoceptor in the skeletal muscle fibres.

Animals↗
PubMed1978

beta-Adrenoceptor antagonists inhibit the behavioural responses of rats to increased brain 5-hydroxytryptamine.

1 The effect of various beta-adrenoceptor blocking agents on the 5-hydroxytryptamine (5-HT)-induced hyperactivity response produced in rats by administration of tranylcypromine (10 mg/kg i.p.) followed by L-tryptophan (50 mg/kg i.p.) has been investigated. 2 (+/-)-Alprenolol, (+/-)-timolol, (+/-)-sotalol, (+/-)-pindolol (all at 40 mg/kg) all inhibited the hyperactivity response to some degree when given 45 min before the tranylcypromine, as did (+/-)-oxprenolol when given after the L-tryptophan. 3 beta-Adrenoceptor antagonists that are not found in the brain appreciable amount after peripheral injection, (+/-)-atenolol, (+/-)-practolol, (+/-)-labetalol and (+/-)-acebutalol, did not inhibit the 5-HT-mediated behaviour. 4 Neither the beta1-selective drug (+/-)-metoprolol, nor the beta2-selective drug (+/-)-butoxamine inhibited the behavioral response. 5 The drugs that blocked the 5-HT-mediated behaviour did not alter brain 5-HT concentrations, synthesis rate or the accumulation of 5-HT following tranylcypromine/L-tryptophan. However, they did inhibit the hyperactivity produced by the suggested 5-HT agonist, 5-methoxy N,N-dimethyltryptamine, indicating that the beta-adrenoceptor blocking drugs were inhibiting the post-synaptic 5-HT-mediated response. 6 Circling produced by methamphetamine (3 mg/kg) in unilateral nigro-striatal lesioned rats was not altered by alprenolol, sotalol, pindolol or metaprolol, indicating that these drugs do not alter dopamine-mediated behaviour. 7 It is concluded that non-selective (beta1 and beta2) adrenoceptor antagonists which have a high brain/blood ratio following their peripheral injection, block 5-HT-mediated behavioural responses in the rat.

Adrenergic beta-Antagonists↗
PubMed1980

Relationship between the (--)-[3H]-dihydroalprenolol binding to beta-adrenoceptors and transmembrane 86Rb efflux of the BC3H1 nonfusing muscle cell line.

1 We have studied the binding properties of the beta-adrenoceptor antagonist [3H]-dihydroalprenolol ([3H]-DHA) on a membrane preparation of the non-fusing muscle cells BC3H1. 2 [3H]-DHA appears to bind to two classes of sites. The first site has a high affinity (KD = 0.53 nM) and a low capcity (Bmax = 58 fmol/mg of protein). The second site has a low affinity (KD = 110 nM) and a high capacity (Bmax = 1100 fmol/mg of protein). 3 The pharmacological properties of the high affinity low capacity site correspond to the known properties of the beta 2-adrenoceptors since the agonists inhibit [3H]-DHA binding following the series isoprenaline greater than adrenaline greater than noradrenaline greater than phenylephrine and the antagonists following the series alprenolol congruent to propranolol greater than butoxamine greater than practolol greater than phentolamine. 4 The binding properties of the beta-adrenoceptors were correlated with the effect of beta-adrenoceptor agonists and antagonists on 86Rb efflux rate from BC3H1 Cells. 5 There is very good correlation between the dissociation constants obtained by inhibition of [3H]-DHA binding by the antagonists alprenolol and propranolol, and the inhibition constants calculated from their antagonism of the 86Rb efflux rate stimulation by adrenaline. The ratio of the dissociation constants obtained by inhibition of [3H]-DHA binding by agonists and their EC50, calculated from 86Rb efflux curves, is higher than 1. This high KD/EC50 ratio indicates a high coupling efficiency between receptor occupancy by agonists and the biological effect measured.

Adrenergic beta-Agonists↗
PubMed1982

beta-Adrenoceptor agonists enhance 5-hydroxytryptamine-mediated behavioural responses.

The beta-adrenoceptor agonists, salbutamol, terbutaline and clenbuterol, were investigated for their effect on 5-hydroxytryptamine-mediated (5-HT) hyperactivity. 2 The lipophilic beta-adrenoceptor agonist, clenbuterol (5 mg/kg) enhanced the behaviours induced by quipazine (25 mg/kg), including headweaving, forepaw treading and hind-limb abduction and thus increased automated activity recording. Clenbuterol (5 mg/kg) also enhanced the hyperactivity syndrome produced by the 5-HT agonist, 5-methoxy N,N-dimethyltryptamine (2 mg/kg) and the combination of tranylcypromine (10 mg/kg) and L-tryptophan (50 mg/kg). Salbutamol and terbutaline potentiated quipazine-induced hyperactivity only when given at the higher dose of 20 mg/kg. 3 The effect of clenbuterol in enhancing quipazine hyperactivity was blocked by the centrally acting beta 1-adrenoceptor antagonist, metoprolol (5 mg/kg), but not by the beta 2-adrenoceptor antagonist, butoxamine (5 mg/kg) or the peripherally acting beta 1-adrenoceptor antagonist, atenolol (5 mg/kg). 4 Clenbuterol (5 mg/kg) did not enhance the circling responses produced by methamphetamine (0.5 mg/kg) in unilateral nigrostriatal-lesioned rats. 5 The results suggest that beta-adrenoceptor agonists in common with some established antidepressant treatments produce enhancement of 5-HT-mediated behavioural responses.

Adrenergic beta-Agonists↗
PubMed1983

The effect of chronic antidepressant administration on beta-adrenoceptor function of the rat pineal.

1 The beta-adrenoceptor agonist, isoprenaline (1.5-3.0 mg kg(-1) intravenously), produced a dose-related increase in rat pineal melatonin content. This increase was prevented by pretreatment with the selective beta(1)-adrenoceptor antagonist, atenolol (2 mg kg(-1)), but not by the beta(2)-adrenoceptor antagonist, butoxamine (2 mg kg(-1)). The beta(2)-adrenoceptor agonist, terbutaline (5.0 mg kg(-1)), produced a moderate increase in pineal melatonin content.2 Repeated daily administration of desmethylimipramine (10 mg kg(-1) for 10 days) and maprotiline (10 mg kg(-1) for 10 days), antidepressants predominantly inhibiting noradrenaline (NA) uptake, reduced the isoprenaline-induced increase in pineal melatonin content. Amitriptyline (20 mg kg(-1) for 14 days), a drug which inhibits both NA and 5-hydroxytryptamine (5-HT) uptake, had a similar effect. The beta-adrenoceptor agonist, clenbuterol (5 mg kg(-1) for 14 days), also attenuated the increase in pineal melatonin produced by isoprenaline.3 In contrast, chronic administration of the selective 5-HT uptake inhibitor, fluoxetine (10 mg kg(-1) for 10 days), or the antidepressants, iprindole and mianserin (both 20 mg kg(-1) for 14 days), which do not inhibit monoamine uptake, failed to reduce the increase in pineal melatonin following isoprenaline. Repeated electroconvulsive shock was similarly without effect.4 Ten hours after the final dose of desmethylimipramine (10 mg kg(-1)) once daily for 10 days there was no change in the usual dark phase increase in pineal melatonin.5 The data suggest that repeated administration of certain antidepressant drugs results in reduced pineal beta-adrenoceptor sensitivity. However the lack of change in the dark phase increase in pineal melatonin following repeated desmethylimipramine, implies that the reduced ss-adrenoceptor sensitivity may be part of an adaptive process which maintains normal pineal function. Therefore the decrease in beta-adrenoceptor number in the brain reported after chronic antidepressant administration may not be associated with a change in overall synaptic function.

Adrenergic beta-Agonists↗
PubMed1983

Cyclic adenosine 3',5'-monophosphate and beta-effects in rat isolated superior cervical ganglia.

Isoprenaline (0.01-1 microM) increased the amount of cyclic adenosine 3',5'-monophosphate (cyclic AMP) in rat isolated superior cervical ganglia by up to 10 times after 10 min application. Cyclic AMP levels returned to control values after 20 min washing. Salbutamol, in concentrations (1-100 microM) that depolarized the ganglion and facilitated submaximal transmission, did not significantly raise ganglionic cyclic AMP levels. The action of isoprenaline was antagonized by butoxamine (apparent KI approximately equal to 0.14 microM) and weakly by practolol (apparent KI approximately equal to 9.1 microM). The effect of 0.1 microM isoprenaline was also inhibited 94% by 100 microM of the adenylate cyclase inhibitor, 9-(tetrahydro-2-furyl)adenine (SQ 22,536). Exogenous dibutyryl cyclic AMP did not replicate the effects of isoprenaline on ganglionic d.c. potentials or submaximal transmission. The phosphodiesterase inhibitors theophylline, isobutylmethylxanthine or 4-(3,4-dibutoxybenzyl)-2-imidazolidinone (Ro 20-1724) did not potentiate these electrical responses to isoprenaline. The adenylate cyclase inhibitor, SQ 22,536, did not inhibit the electrical responses to isoprenaline. It is concluded that available evidence does not support the view that the ganglion depolarization or facilitation of submaximal transmission in rat isolated ganglia produced by isoprenaline are likely to be mediated by cyclic AMP.

Action Potentials↗
PubMed1992

Noradrenaline modulates smooth muscle activity of the isolated intravesical ureter of the pig through different types of adrenoceptors.

1. We have studied the effects of alpha- and beta-adrenoceptor agonists and antagonists on both phasic peristaltic activity and basal tone of the isolated intravesical ureter of the pig by means of isometric techniques in vitro. 2. Spontaneous phasic activity was exhibited by 21% of pig intravesical ureter preparations manifested as rhythmic contractions with average frequency and amplitude of 2.54 +/- 0.18 min-1 and 1.48 +/- 0.16 g (n = 31), respectively. 3. Adrenaline, noradrenaline and phenylephrine induced concentration-dependent increases in both phasic activity and basal tone of ureteral preparations, all three agonists being more potent in modifying ureteral phasic activity than baseline tone. B-HT 920, B-HT 933 and clonidine had no significant effect. 4. Phentolamine (10(-9)-10(-7) M) and prazosin (3 x 10(-11)-3 x 10(-8) M) significantly inhibited increases in both frequency of phasic activity and baseline tone induced by a submaximal dose of noradrenaline. Rauwolscine (10(-9)-10(-7) M) affected only the tone evoked by noradrenaline and higher concentrations of this antagonist were needed to block phasic activity. 5. Pretreatment of ureteral strips with the beta-adrenoceptor antagonist, propranolol (10(-6) M), significantly increased the maximum contraction evoked by noradrenaline. After incubation with phentolamine (10(-6) M), noradrenaline (10(-7)-10(-6) M) decreased phasic activity induced by prostaglandin F2 alpha (10(-5) M). Isoprenaline and salbutamol also abolished PGF2 alpha-induced phasic activity. Pafenolol (10(-6) M) and butoxamine (10(-6) M) blocked the inhibitory effect of noradrenaline, isoprenaline, and salbutamol on PGF2 alpha-induced phasic activity. 6. These results suggest that noradrenaline may modulate both phasic peristaltic activity and basal tone of pig intravesical ureter through both alpha- and beta-adrenoceptors.

Adrenergic alpha-Agonists↗