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[Mechanism of the radioprotective effect of catecholamine receptor agonists. Inclusion in the radioprotective effect of both subtypes of alpha-adrenoreceptors].

alpha-Adrenoceptor agonists of both main groups, i. e. arylalkylamines and imidazolines, have a pronounced radioprotective effect. Their chemical analogs, which fail to stimulate alpha-adrenoceptors, do not protect mice. The effect of phenylephrine, adrenaline, and noradrenaline comes into play via alpha 1-adrenoceptors and that of clonidine, via alpha 2-adrenoceptors and also via alpha 1-adrenoceptors. Adrenoceptor agonists can probably manifest their radioprotective action via both subtypes of alpha-adrenoceptors. Possible intracellular mechanisms of the radioprotective action are discussed.

Adrenergic Agonists↗
PubMed1987

Catecholamine receptors involved in the inhibitory effects of dopamine on vagally stimulated gastric acid secretion and mucosal blood flow in rats.

The mechanisms of inhibitory effects of dopamine on the vagally stimulated gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of dopamine significantly reduced both gastric acid secretion and MBF. The inhibitory effect of dopamine on the vagally stimulated gastric acid secretion was not attenuated by sulpiride, metoclopramide or domperidone. Haloperidol abolished the inhibitory effect of dopamine on the acid secretion; it also abolished the inhibitory effect of norepinephrine on the vagally stimulated acid secretion. The inhibitory effect of dopamine on the acid secretion was abolished by phentolamine and yohimbine but not by propranolol or prazosin. Dopamine-induced reduction in the vagally stimulated gastric MBF was abolished by haloperidol and was partially antagonized by sulpiride or metoclopramide. In addition, the dopamine-induced reduction in the MBF was abolished by phentolamine and prazosin and was partially antagonized by yohimbine. These results indicate that the inhibitory effect of dopamine on the vagally stimulated gastric acid secretion is mediated by alpha-2 adrenoceptor mechanisms and that the inhibitory effect of dopamine on the MBF is, at least in part, mediated by alpha-1 adrenoceptor mechanisms. The authors did not obtain evidence for the existence of dopamine receptor-mediated mechanisms.

Animals↗
PubMed1983

[Catecholamine receptors and renal function].

Renal function was assessed through clearance studies in man under initial conditions marked by retention (23 experiments) and hydro-saline depletion (19 experiments). Further evaluations were carried out in depletion combined with treatment with (+/-)-propranolol (9 experiments) or with prazosin (9 experiments). In each study, clearance was checked during and after venous infusion of 0.1 micrograms/kg-1/min-1 DA, in addition to the control clearance. Adrenolytic drugs and renal function in hydro-saline depletion. Combination with propranolol had no significant effect on renal function, whereas prazosin led to a significant increase in both total and afferent renal vascular resistance; the flow rate and filtrate were less despite higher arterial pressure. Both the absolute and the percentage loading value of isosmotic and anisosmotic sodium reabsorption were inhibited. Renal action of DA in depletion with and without adrenolytic drugs. DA failed to produce either vasodilatation or a hydro-natriuretic effect during hydro-saline depletion, by contrast with its effect at the same dose during retention. During its infusion, however, it led to sodium saving dependent on stimulation of distal sodium reabsorption; following suspension, this saving increased still further, and there was a significant decrease in flow rate, filtrate and diuresis. Pretreatment with either drug restored the vasodilatatory and hydrosaluretic capacity of DA. Modalities whereby renal function is controlled in the presence of changes in body water and salt content. 1) During retention and during depletion in association with prazosin, anisosmotic transport of sodium is efficient in inverse proportion to the sodium load reaching the diluting segments. Prazosin depresses reabsorption efficiency in the presence of load values similar to those observed during simple depletion. 2) During retention, urinary sodium naturally depends on plasma osmolarity, whereas blood sodium appears to depend on urinary excretion of sodium. During depletion, renal excretion apparently depends on mean blood pressure. These extra-renal control mechanisms probably result in alteration of one or more of the components of the direct line running from the filtrate to the formation urine. 3) When DA is infused during water-salt retention, renal excretory function can be seen to depend on the glomerular filtrate through direct control of diuresis. During depletion in the early stage of DA infusion, on the other hand, the filtrate depends on excretory function through tubulo glomerular feedback control.

Adult↗
PubMed1989

Catecholamine receptors regulating serotonin N-acetyltransferase activity and melatonin content of chicken retina and pineal gland: D2-dopamine receptors in retina and alpha-2 adrenergic receptors in pineal gland.

The type of catecholamine receptor involved in the regulation of serotonin N-acetyltransferase (NAT) activity and melatonin (N-acetyl-5-methoxytryptamine) level in chicken retina was compared to that regulating these parameters in the pineal gland. Systemic administration of apomorphine, a dopamine receptor agonist, resulted in marked inhibition of the nocturnal increase of retinal NAT activity and melatonin content. Apomorphine did not affect NAT activity or melatonin content of the pineal gland. In contrast, clonidine, an alpha-2 adrenergic receptor agonist, inhibited the nocturnal rise in pineal NAT activity and melatonin content although being without effect on these parameters in retina. Apomorphine-induced inhibition of retinal NAT activity was blocked by spiperone, a D2-dopamine receptor antagonist, but not by antagonists of D1-dopamine, alpha-1, alpha-2 and beta adrenergic receptors. Systemic or intraocular injection of quinpirole, a D2-dopamine receptor agonist, in the middle of the dark phase of the light-dark cycle markedly reduced retinal NAT activity and melatonin level, whereas injections of SKF 38393-A, a D1-dopaminergic agonist, had no effect. The inhibitory effect of clonidine on pineal NAT activity was blocked by yohimbine, an alpha-2 adrenergic receptor antagonist. The results presented in this paper demonstrate that NAT activity and melatonin content in chicken retina and pineal gland are differentially modulated in vivo by D2-dopamine and alpha-2 adrenergic receptors, respectively. Despite the different types of receptors involved, both tissues may share a common pathway for catecholamine-mediated inhibition of melatonin biosynthesis, i.e., inhibition of adenylate cyclase activity.

Acetyltransferases↗
PubMed1985

Effects of bromocriptine on catecholamine receptors mediating cardiovascular responses in the pithed rat.

The interaction of bromocriptine with several catecholamine receptors that control the sympathetic responses at cardiac and vascular level has been studied in pithed adrenalectomized and vagotomized normotensive rats. Bromocriptine (30 and 100 micrograms/kg) inhibited the stimulation-induced pressor responses in the pithed rat without modifying the pressor responses induced by noradrenaline. Sulpiride (0.3 mg/kg) abolished the effects of bromocriptine (30 micrograms/kg) but only partially prevented the effects of bromocriptine (100 micrograms/kg) on the stimulation-induced pressor responses. Yohimbine (0.3 mg/kg) partially antagonised the inhibitory effect of bromocriptine on stimulation-induced pressor responses. Combination of yohimbine and sulpiride abolished attenuation of the stimulation-induced pressor responses by bromocriptine (100 micrograms/kg). Bromocriptine (0.3 and 1 mg/kg) shifted to the right the frequency-response curve of increases in heart rate. This effect was prevented by yohimbine (0.3 mg/kg) but not by sulpiride (0.3 mg/kg). The same doses of bromocriptine were ineffective on heart rate increases induced by noradrenaline. Bromocriptine (0.3 and 1 mg/kg) shifted to the right the increases in diastolic blood pressure induced by methoxamine without modifying those induced by xylazine and noradrenaline. These results suggest that bromocriptine acts on the peripheral sympathetic nervous system of the pithed rat as an agonist of presynaptic dopamine receptors and alpha 2-adrenoreceptors and as an antagonist of postsynaptic alpha 1-adrenoreceptors.

Animals↗
PubMed1996

The energetics of ligand binding at catecholamine receptors.

One of the key events in the actions of agonists and antagonists is their binding to receptors. Understanding this event is of interest in terms of understanding receptor function but it also has immense practical relevance for the design of drugs. If the ligand-binding process could be understood in detail, including the nature of the interactions made between ligand and receptor, then this could help in the design of more-selective drugs. The interaction of a ligand with its receptor is clearly of importance in determining the specificity of ligand action but ligand-receptor interaction also initiates the processes of signalling that are exhibited in the efficacy of ligand action. Here Philip Strange considers these events for catecholamine receptors, concentrating mostly on dopamine receptors; where necessary the discussion is widened to include other receptor systems.

Drug Design↗
PubMed1998

Influence of catecholamine receptor agonists and antagonists on the ultradian rhythm of the EEG in the posterior hypothalamus.

The power of delta and theta frequency bands of the EEG in the posterior hypothalamus of the rat fluctuates according to an ultradian rhythm. To investigate, whether catecholamine receptor ligands influence the ultradian EEG rhythm, drugs were applied intracerebroventricularly into the lateral ventricle of anaesthetized rats. Injection of the alpha1-adrenoceptor agonist (+/-)-methoxamine (150 nmol) abolished, while 25 nmol of the compound prolonged the cycle duration of the rhythmic changes in the delta and theta frequency bands. Injected into the lateral ventricle, the alpha2-adrenoceptor agonists 6-ethyl-5,6,7,8-tetrahydro-4H-oxazol[4,5-d] azepin-2-amine (B-HT 933) or clonidine (150 nmol each) prolonged the duration of the cycles of both frequency bands. The beta1/2-receptor agonists (+/-)-orciprenaline (300 nmol) and (R)-(-)-isoprenaline (150 nmol) slowed down the cycle durations of both frequency bands. The beta1-receptor agonist (+/-)-xamoterol (300 nmol) also prolonged the cycle durations of the delta and theta frequency bands. The beta1-receptor antagonist (S)-(-)-atenolol was ineffective (150 and 300 nmol). The beta2-receptor agonist (+/-)-salbutamol (300 nmol) shortened the duration of the ultradian rhythm in the two frequency bands, while the beta2-receptor antagonist (+/-)-1-[2,3-(dihydro-7-methyl-1 H-inden-4-yl) oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551) (300 nmol) exerted the opposite effect. On the other hand, the D1 receptor agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-1H)-3-benzazepine-7,8-diol (SKF 38393) and the D2 agonist (4aR,8aR)-(-)-quinpirole (150 nmol each) slowed down the frequency of the ultradian rhythm. The powers of alpha and beta frequency bands were not significantly influenced by the catecholamine receptor ligands used in this study. The findings suggest that, in the posterior hypothalamus, the ultradian rhythm of the delta and theta frequency bands are prolonged when beta1-receptors are stimulated and shortened on stimulation of beta2-adrenoceptors. Endogenous catecholamines released from their neurons seem to shorten the duration of the rhythmic fluctuations by stimulating beta2-receptors and to slow down the frequency of the cyclic fluctuations by stimulating alpha2-adrenoceptors. The ultradian rhythm is also slowed down on stimulation of D1 and D2 receptors by endogenous dopamine. Together with previous observations, the results indicate that the ultradian EEG rhythm is susceptible to modulatory mechanisms mediated by catecholaminergic neurons.

Activity Cycles↗
PubMed1982

Competition by estrogens for catecholamine receptor binding in vitro.

We have examined the ability of various steroids to compete for high-affinity binding of 3H-labeled ligands to catecholamine receptors in membranes prepared from rat cerebral cortex, striatum, and anterior pituitary. Ligands employed were: [3H]WB4101, [3H]prazosin, [3H]yohimbine, and [3H]clonidine (alpha-noradrenergic); [3H]dihydroalprenolol (beta-noradrenergic); [3H]spiperone and [3H]ADTN (dopaminergic). Only the 17 beta estrogens were effective and only binding of [3H]spiperone and [3H]ADTN in striatum and [3H]WB4101 and [3H]prazosin in cerebral cortex was reduced. Thus putative dopaminergic and alpha 1-noradrenergic sites alone appear to recognize estrogens. A slight competitive effect on [3H]spiperone binding to anterior pituitary membranes was also observed. Among the 17 beta estrogens tested, the most effective in all cases was the catechol estrogen 2-hydroxyestradiol (2-OHE2). The ability of 2-OHE2 (IC50 = 20-30 micro M) to inhibit ligand binding to alpha 1 receptors was comparable to that of norepinephrine (IC50 = 10-20 micro M), whereas for dopamine receptors in striatum and pituitary 2-OHE2 was an order of magnitude less effective than dopamine (IC50 = 12 micro M) in reducing binding of 3H ligands. Estradiol-17 beta and 2-hydroxyestrone were also able to inhibit binding, but the order of steroid potency was different for alpha 1 and dopaminergic receptors. Progesterone, testosterone, and corticosterone were without effect in all cases. These results show that there is specificity of steroid interactions with catecholamine receptors in the brain, both in terms of steroid structure and receptor type. The possible relevance of these interactions to neuroendocrine function is discussed.

Animals↗
PubMed1978

[New aspects of catecholamin-receptor interactions. Pathophysiological and clinical implications (author's transl)].

The molecular aspects of catecholamine-receptor interactions are reviewed with respect to their clinical implications. Beta- and in some tissues alpha-adrenergic receptors are coupled to the membrane-bound adenylate cyclase. The adrenergic receptor sites are distinct membrane constituents. Their number and the ratio alpha-to beta-receptor site depend on the plasma concentration of catecholamines and are affected by diet and endocrinological factors. Recent clinical studies suggest that long-term treatment with beta-adrenergic agonists may induces desensitization of target tissues due to changes in the adrenergic receptor moieties.

Adenylyl Cyclases↗
PubMed1988

Effects of retinoic acid on alkaline phosphatase messenger ribonucleic acid, catecholamine receptors, and G proteins in ROS 17/2.8 cells.

Retinoic acid (RA) inhibits the increases in alkaline phosphatase (AP) and hormone-stimulated adenylate cyclase that accompany the growth of ROS 17/2.8 osteosarcoma cells in culture. The RA effects were first detected 2 days after initiation of treatment and were dose dependent, with an EC50 of 100 nM. The reduction in the hormone-responsive adenylate cyclase activity was associated with lower levels of beta-catecholamine receptors, without a change in apparent receptor affinity and with lower levels of the GTP-binding proteins Gs and Gi, visualized by NAD-dependent [32P]ADP ribosylation. The reduction in AP was correlated with a decrease in the steady state level of AP mRNA. RA had no effect on cell proliferation or saturation density. Retinoids thus inhibit the same features that are promoted by glucocorticoids in ROS 17/2.8 cells. These features seem to be subject to coordinate regulation, probably at the pretranslational level.

Adenylyl Cyclases↗
PubMed1976

Catecholamine receptor sensitivity and the regulation of lipolysis in adult diabetes.

The sensitivity of alpha- and beta-adrenergic receptors, and the antilipolytic actions of prostaglandin E1 or insulin on adipose tissue of obese diabetic and non-diabetic subjects have been studied. Accumulation of cyclic AMP in adipose tissue and release of glycerol in response to several catecholamines (adrenaline, noradrenaline and isoprenaline) in the presence or absence of an alpha-adrenergic blocker (phentolamine) have been used to assess catecholamine receptor sensitivity. No differences in beta-receptor activity were observed between diabetics and non-diabetics, either on glycerol release or accumulation of cyclic AMP; alpha-receptor activity was also similar, except for significantly less accumulation of cyclic AMP in diabetic tissue incubated with noradrenaline and phentolamine (p less than 0.01). The antilipolytic action of prostaglandin E1 (at concentrations of 30 fM to 30 pM) on lipolysis (stimulated submaximally with isoprenaline, 10(-7) M) was similar in diabetic and control groups. The antilipolytic action of insulin (from 10(-10) to 10(-6) M) on lipolysis was also similar between the groups. It is concluded that neither disorders of the catecholamine receptor nor of the antiliolytic actions of prostaglandin E1 or insulin are responsible for the abnormalities of fatty acid metabolism in adult diabetes.

Adipose Tissue↗
PubMed1993

2-Phenylethylamine-induced changes in catecholamine receptor density: implications for antidepressant drug action.

It is now established that (1) concentrations of 2-phenylethylamine (PEA) are greatly increased in brain following administration of monoamine oxidase inhibitor (MAOI) antidepressants; (2) PEA is a metabolite of the MAOI antidepressant phenelzine; and (3) PEA may be a neuromodulator of catecholamine activity. On the basis of these observations, the effects of long term increases in brain PEA on catecholamine receptors have been assessed. Both PEA and antidepressants induced a reduction in the behavioural response to the beta 2 adrenoceptor agonist salbutamol. Radioligand binding measurements revealed that 28 day administration of PEA in combination with the type B MAOI (-)-deprenyl results in a decrease in the density of beta 1 adrenoceptors but not beta 2 adrenoceptors in rat cerebral cortex and cerebellum. (-)-Deprenyl alone also induced a significant decrease in beta 1-adrenoceptors but when PEA was added to this treatment there was a further decrease in beta 1-adrenoceptor density. Only changes in beta 1 adrenoceptor density were evident following 28 day administration of MAOI antidepressants. PEA also induced a decrease in the density of D1-like dopamine (DA) receptors in the rat striatum. MAOI antidepressants induced a decrease in the density of both D1-like and D2-like DA receptors. These data are discussed in terms of a possible role of PEA-catecholamine interactions in antidepressant drug action.

Animals↗
PubMed1981

A hypothesis of thyroid-catecholamine-receptor interaction. Its relevance to affective illness.

Recent prospective studies suggest that thyroid state plays a role in affective disorders. A lack of thyroid hormones can lower the threshold for depression; an excess can contribute to a state of tense dysphoria. Thyroid function in some persons also appears to influence the course of affective disorders. Adequate mobilization of thyroid hormones favors recovery from depression; excess mobilization increases the risk of mania in vulnerable individuals. Although other mechanisms may be involved, evidence suggests that the modulation by thyroid hormones of the beta-adrenergic receptor response to catecholamines may contribute to these effects. Norepinephrine stimulates such receptors; thyroid hormones increase their ability to receive stimulation. The plausibility of such interactions between catecholamines and thyroid hormones occurring in the CNS is strengthened by their common origin in the amino acid tyrosine and by their synergism in many metabolic processes.

Adenosine Monophosphate↗
PubMed1972

Epinephrine binding to the catecholamine receptor and activation of the adenylate cyclase in erythrocyte membranes (hormone receptor- -adrenergic receptor-cyclic AMP-turkey).

Turkey erythrocyte membranes showed specific binding of [(3)H]epinephrine. The concentration of hormone required for half-maximal binding (30 muM) was the same as that required for half-maximal activation of the adenylate cyclase located in the same membrane preparation. The binding reaction at 37 degrees C reached completion during the first minute of incubation, which agrees well with the known rapidity of the biological response to catecholamines. Specific binding was abolished by heating the membranes 1 min at 100 degrees C. Chromatography of the bound (3)H, after its extraction from the membranes, indicated that the hormone had fully retained its chemical structure. Epinephrine binding was inhibited by the beta-adrenergic blocking agent propranolol, which also inhibited the activation of adenylate cyclase by the hormone. The specificity of phenethylamine derivatives in displacing [(3)H]epinephrine from the binding sites showed that a typical catecholamine receptor was responsible for the binding. Displacement of the bound hormone by analogs lacking the catechol group was more extensive at 37 degrees C than at 0 degrees C. Some of the analogs that displaced epinephrine from the binding site caused only a feeble activation of the adenylate cyclase, but were able to inhibit the activation of the enzyme by epinephrine. Thus, binding to a catecholamine receptor on a membrane preparation is an essential, but insufficient, condition to elicit a response.

Adenylyl Cyclases↗
PubMed1981

The effect of catecholamine receptor antagonists on ethanol-induced locomotor stimulation.

The effect of various catecholamine receptor antagonists, which differ in their potency to block central dopamine and noradrenaline receptors, respectively, on ethanol-induced locomotor stimulation was investigated. It was shown that small doses of both specific dopamine (pimozide, haloperidol) and noradrenaline (phenoxybenzamine, yohimbine) receptor blocking agents statistically significantly suppressed the ethanol-induced locomotor stimulation. Of special interest in this study was the observation that remarkably small doses of clozapine completely antagonized the ethanol-induced locomotor stimulation. The possibility that this effect of clozapine is mediated via its interference with the activity of central noradrenaline and/or GABA neurons is discussed.

Adrenergic alpha-Antagonists↗
PubMed1992

Studies on the location of catecholamine receptors in canine sympathetic ganglia.

Receptors mediating catecholamine-induced inhibition were studied in cardiac ganglia of pentobarbital-anesthetized dogs. Using selective agonists and antagonists the presence of three receptor subtypes was verified: alpha 1- and alpha 2-adrenoceptors and dopamine D2 receptors. Activation of alpha 1-adrenoceptors or dopamine D2 receptors reduced the response to preganglionic nerve stimulation but not to direct stimulation of the nicotinic acetylcholine receptors of the principal ganglion cells: response to both types of stimulation were reduced by activation of ganglionic alpha 2-adrenoceptors. These results suggested that two inhibitory systems were present in canine sympathetic ganglia and mediated the effects of exogenous catecholamines. One system involved alpha 1-adrenoceptors and dopamine D2 receptors located proximal to the synapse of the pre- and postganglionic neurons and the other involved alpha 2-adrenoceptors located distal to the intraganglionic synapse.

Adrenergic alpha-Agonists↗
PubMed1982

Temporal characteristics of gonadotropin interaction with rabbit luteal receptors and activation of adenylyl cyclase: comparison to the mode of action of catecholamine receptors.

The temporal characteristics of gonadotropin (LH and hCG) and catecholamine interaction with their luteal receptors and activation of adenylyl cyclase were studied in rabbit luteal membranes. studies on hormone-receptor interaction showed that, once bound, [125I]iodo-hCG dissociated from its receptor very slowly. If excess LH was added 30 min after the initiation of [125I]iodo-hCG binding, 85% of the [125I]iodo-hCG bound at 30 min was still bound to the luteal receptors 4.5 h later. The rate of dissociation of [125I]iodo-hCG from its receptor was not altered by 100 microM GTP, 2 mM MgCl2, or GTP plus MgCl2. The slow rate of [125I]iodo-hCG dissociation observed at 30 min was not due to a time-dependent change in the hormone-receptor complex, as the dissociation of [125I]iodo-hCG was equally slow 5 min after the initiation of the binding reaction. Studies on the activation of luteal adenylyl cyclase by LH showed that stimulation by 1 microgram/ml ovine LH (oLH) could be prevented but, once initiated, could not be reversed by antiserum to oLH. This indicates that once bound to the rabbit luteal LH receptor, oLH causes persistent activation of rabbit luteal adenylyl cyclase. In contrast, the activation of luteal adenylyl cyclase by 1 microM isoproterenol could be completely reversed by the addition of 50 nM propranolol 5 min after the initiation of the reaction. The inhibitory effect of the propranolol could be completely overcome by the addition of excess isoproterenol, indicating that catecholamine binding to its luteal beta-receptor is readily reversible. Thus, there appears to be a basic difference in the mechanism by which the gonadotropins and catecholamines interact with their receptors and activate the rabbit luteal adenylyl cyclase.

Adenylyl Cyclases↗