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PubMed1975

The effect of alpha and beta adrenergic receptor stimulation on the adenylate cyclase activity of human adipocytes.

The effects of the mixed agonist epinephrine and the beta agonist isoproterenol, each alone and in combination with the alpha adrenergic blocker phentolamine and the beta blocker propranolol on the adenylate cyclase activity of human adipocyte membrane fragments were determined in a calcium free buffer. Neither phentolamine (10 muM) nor propranolol (32 muM) affected basal adenylate cyclase activity. Epinephrine (10 muM) stimulated adenylate cyclase activity and this effect was slightly enhanced by phentolamine. The combination of epinephrine plus propranolol depressed adenylate cyclase below the basal level. Isoproterenol (10 muM) markedly stimulated adenylate cyclase; the addition of phentolamine caused an equivocal further increase while the addition of propranolol depressed adenylate cyclase activity to, but not below, the basal level. These findings are consistent with the hypothesis that human adipocytes have both alpha and beta adrenergic receptors and that these receptors are associated with the cell membrane adenylate cyclase system.

Adenylyl Cyclases↗
PubMedDate not supplied

Protective effect of morphine on ethanol-induced gastric lesions in rats: are ATP-dependent potassium channels involved?

Morphine has a significant protective effect on ethanol-induced gastric lesions. This effect is antagonized by naloxone, suggesting the involvement of opioid receptors. The ATP-dependent potassium channel blockers glibenclamide and phentolamine have different effects on this action of morphine. While glibenclamide potentiates the gastroprotective effect of morphine, phentolamine antagonizes it. However, both prazosin and yohimbine do not affect the gastroprotective action of morphine, suggesting that the influence of phentolamine is not mediated by alpha-adrenoceptors. As phentolamine also prevented the gastroprotective effect of the ATP-dependent K+ channel opener diazoxide, our results suggest that ATP-dependent K+ channels may be involved in the gastro-protective action of morphine.

Adenosine Triphosphate↗
PubMedDate not supplied

Catecholamine modulation of magnesium plasma levels in the rat.

Epinephrine (0.3 microgram/min) or isoproterenol (0.2 microgram/min) were infused for 40 min in rats to determine the role of catecholamines in the short-term control of plasma magnesium levels. Phentolamine (0.2 and 1 mg/kg) or propranolol (5 mg/kg), injected i.p. 10 min following the beginning of the infusion with catecholamines, were used to block alpha- or beta-adrenoceptors. Epinephrine alone elevated the systolic while decreasing the diastolic blood pressure and initially increased heart rate by 8% to 455 +/- 25 beats/min. Plasma potassium declined by 24% but magnesium levels remained constant. Following 0.2 mg/kg of phentolamine, systolic and diastolic blood pressure decreased by 40% and 55% to 95 +/- 11 and 39 +/- 3 mmHg, respectively. Potassium levels were further reduced by 8%. Administration of this dose of phentolamine increased magnesium levels by 8%. Magnesium levels were elevated by 19% to 2.38 +/- 0.20 mEq/l after 1 mg/kg of phentolamine, possibly due to excessive hemodynamic derangements. Propranolol reversed the hypokalemic and hemodynamic effects of the epinephrine infusion without altering plasma magnesium. Similarly, propranolol abolished the tachycardia and hypokalemia elicited by isoproterenol without affecting magnesium levels. These results suggest that catecholamines play no major role in the short-term control of plasma magnesium in the rat.

Adrenergic alpha-Antagonists↗
PubMed1991

Significance of adrenoceptor-mediated atrial natriuretic factor release in normal humans.

To assess the potential role of adrenoceptor-stimulated atrial natriuretic factor (ANF) release in healthy humans, 18 volunteers, divided into groups of six, underwent experiments with infusion of incremental doses of salbutamol with and without beta-blockade with propranolol, propranolol alone, and bolus injections of clonidine before and after alpha-blockade with phentolamine, and phentolamine alone. Since changes in right atrial pressure have been shown to influence ANF release, central venous pressure (CVP) was continuously measured 30 min before, during the 120 min duration of drug infusions, and for 30 min after the bolus injections of the drugs. ANF was serially determined in central venous plasma during all drug infusions, and plasma catecholamines were measured to determine any possible influence of endogenous sympathetic activation on ANF levels. Plasma ANF was unaffected by all individual drugs and drug combinations, despite significant reductions in CVP in the salbutamol, phentolamine and phentolamine + clonidine groups, and a doubling of heart rate during salbutamol administration (p less than 0.01 for all). The results do not suggest a major role for adrenoceptor-mediated ANF release in normal humans, and do not indicate that plasma ANF levels are determined by tonic inhibition or facilitation of the sympathetic nervous system.

Adult↗
PubMed1990

Glucoregulation under beta-adrenergic stimulation by dobutamine and terbutaline in the male rat.

The influence of the beta-adrenoreceptor stimulating agents dobutamine and terbutaline as compared to epinephrine on insulin and glucose levels has been assessed in the male rat. All agents were infused either intravenously or subcutaneously over 6 h at varying dosages. In addition, epinephrine was given concomitantly with the alpha-adrenoreceptor blocker phentolamine. The heart frequency as an estimate of the effects of the adrenergic agents beyond the glucoregulatory system was accelerated in a dose-dependent manner. Serum insulin concentrations were significantly increased by phentolamine and significantly depressed by epinephrine, while they were virtually unchanged at any dosages of dobutamine, terbutaline, or epinephrine, when simultaneously applicated with phentolamine. As for serum glucose levels, these agents, again, did not exert any influence, while glucose levels were significantly depressed under phentolamine and significantly increased under epinephrine application. The data demonstrate, that dobutamine and terbutaline at pharmacologically common dosages do not affect glucose homoeostasis. The study does not support a major effect of beta-adrenergic stimulation on the pancreatic B cell in the male rat.

Adrenergic beta-Agonists↗
PubMed1990

[Effect of intravenous administration of nitroglycerin and regitine on hemodynamics in mitral valve insufficiency].

During exercise in subjects with congestive heart failure and mitral regurgitation the rise in systemic arterial pressure is usually accompanied by increase in systemic vascular resistance. That could cause decrease of cardiac output not only because of a lack of myocardial reserve, but also because of an increase of mitral regurgitant volume. In such situation decrease in left ventricular preload could further increase the regurgitant volume and cardiac output. Whether changes in pre-or afterload can cause significant changes in mitral regurgitation, nitroglycerin and phentolamine was assessed in that group of patients. 22 patients with significant mitral regurgitation (3+,4+) was randomly divided into two groups. The first one received short intravenous infusion of nitroglycerin at a rate of 170 micrograms/min. The second one received phentolamine intravenously 1-1,5 mg/min. Patients underwent right heart catheterization with Swan-Ganz thermodilution catheter. Mean pulmonary, pulmonary capillary wedge, and right atrial pressure were monitored and recorded. Cardiac output was determined by thermodilution technique using iced 5% dextrose. If there were no contraindications (PWP greater than 30 mm Hg) an effort test was performed (cycloergometer, supine position). The same protocol was repeated during administration of nitroglycerin and phentolamine. Nitroglycerin significantly decreased right atrial and capillary wedge pressure (from 22.9 to 15.6 mm Hg). There were no significant differences in cardiac output, pulmonary and systemic vascular resistance. Pulmonary artery pressure decreased after nitroglycerin but the difference was not significant. All above effects of nitroglycerin persisted during effort. Phentolamine decreased significantly right atrial, pulmonary and capillary wedge pressure with simultaneous increase of cardiac output (30%) and decrease of pulmonary and systemic vascular resistance. In summary, nitroglycerin decreases only symptoms and theoretically could worsen forward flow in patients with mitral regurgitation and heart failure, especially in subjects with a significant increase of systemic vascular resistance during effort.

Adult↗
PubMed1979

Transmission blockade and stimulation of ganglionic adenylate cyclase by catecholamines.

Isolated rat superior cervical ganglia treated with isoproterenol and related drugs show an increase in ganglionic cyclic adenosine 3':5'-monophosphate (cAMP) and a block of transmission. For isoproterenol, the maximum increase in cAMP occurred at 1 X 10(-6) M, a concentration without effect on transmission. Approximately 5 X 10(-4) M isoproterenol was required to reduce the ganglionic compound action potential by 50%. Dopamine, in contrast to isoproterenol, had no effect on the content of cAMP but depressed transmission. The maximum increase in cAMP produced by norepinephrine occurred with 5 X 10(-4) M, a concentration that reduced transmission by approximately 35%. The effects of isoproterenol on adenylate cyclase and transmission were prevented either by practolol (10(-4) M) or phentolamine (10(-5) M). Dopamine-induced blockade of transmission was antagonized by phentolamine (10(-5) M). Whereas the blockade of transmission by norepinephrine was antagonized by practolol (10(-5) M) or phentolamine (10(-5) M), the stimulation of adenylate cyclase by norepinephrine was prevented by practolol (10(-4) M) but not by phentolamine (10(-5) M). These results show that the blockade of transmission and stimulation of adenylate cyclase are unrelated in rat ganglia and that adrenergic receptor classification is ambiguous. The role of adenylate cyclase in ganglia is unclear.

Adenylyl Cyclases↗
PubMed1987

Effects of alpha 1- and alpha 2-adrenoceptors on basal and adrenaline mediated insulin secretion in rats.

Groups of male rats were injected phentolamine, prazosin or yohimbine and infused with saline or adrenaline for 4 h under pentobarbital anesthesia. Blood samples were taken at 30 min intervals during the infusion, the isovolemia being maintained by replacing the blood volume with the blood obtained from normal donor animals. Plasma glucose and insulin levels were estimated. In saline infused animals a severalfold increase in plasma insulin levels was found after pretreatment with phentolamine, while such increase after prazosin or yohimbine was much less, though significant. In adrenaline infused animals the increased insulinemia after phentolamine pretreatment was still more remarkable than in those infused saline. After prazosin treatment, however, no changes in insulinemia were found during adrenaline infusion, while yohimbine pretreatment resulted in a significant insulin increase in similarly infused rats. It is concluded that alpha 2-receptors apparently play a major role in mediating inhibitory effects of adrenaline on insulin secretion. However, even some participation of alpha 1-receptors in the complex regulation of insulin secretion in vivo cannot be excluded, since the effect of phentolamine pretreatment on either basal or adrenaline induced insulinemia was higher than that of yohimbine, though a higher molar dose of the latter was used. In addition, no changes in insulinemia were found during the infusion of adrenaline only which may be explained by a prevailing effect of inhibitory alpha-adrenoceptor tone over a stimulatory beta-adrenoceptor tone under the conditions of unblocked adrenoceptors.

Animals↗
PubMed1985

Alpha-adrenoceptor antagonists and the release of noradrenaline in rabbit cerebral cortex slices: support for the alpha-autoreceptor hypothesis.

Slices of rabbit cerebral cortex were preincubated with [3H]-noradrenaline and then superfused and stimulated electrically twice for 2 min each (S1, S2) at various frequencies (0.2-3 Hz). The stimulation-evoked overflow of tritium (S1) increased with increasing frequency and was higher when cocaine (10 microM) was present. In the absence of cocaine, tetraethylammonium (TEA; 100 and 300 microM), added before S2, increased the stimulation-evoked overflow of tritium to about the same extent, irrespective of the frequency. In contrast, rauwolscine (0.1 and 1 microM) and idazoxan (0.1-10 microM) increased the evoked overflow much more, the higher the frequency of stimulation. Phentolamine (0.1 and 1 microM) reduced the overflow elicited at 0.3 and 1 Hz, and (1 microM) caused an increase only at 3 Hz. In slices superfused throughout with cocaine 10 microM, rauwolscine (1 microM) and idazoxan (1 and 10 microM) again increased the evoked overflow of tritium more, the higher the frequency of stimulation. For a given frequency, rauwolscine and idazoxan enhanced the evoked overflow to a greater extent in the presence than in the absence of cocaine. Idazoxan (1 and 10 microM) and rauwolscine (1 microM) counteracted the inhibition that phentolamine (0.1 microM) produced at low frequency. The increases caused by rauwolscine (1 microM) and TEA (300 microM) were approximately additive, but those caused by rauwolscine (1 microM) and idazoxan (10 microM) were not. The effects of rauwolscine, idazoxan and phentolamine depend on the experimental conditions (frequency, cocaine) in a manner compatible with the operation of a presynaptic alpha 2-adrenoceptor-mediated autoinhibition of noradrenaline release. When given at sufficient concentrations, these antagonists enhance the release of noradrenaline more, the higher the biophase concentration of the transmitter and the stronger, hence, the autoinhibition. In the case of the partial alpha 2-adrenoceptor agonist phentolamine, a low perineuronal noradrenaline concentration even reverses facilitation to inhibition. This pattern differs markedly from the pattern of effects of TEA which increases the release of noradrenaline by a mechanism other than alpha-adrenoceptor blockade.

Adrenergic alpha-Antagonists↗
PubMed1988

Enhanced endogenous neurotransmitter overflow in the isolated perfused rat kidney after chronic epinephrine administration: lack of a prejunctional beta adrenoceptor influence.

This study examines stimulus-induced overflow of endogenous catecholamines from the isolated perfused kidney of rats after epinephrine (EPI) administration at 100 micrograms/kg/hr for 6 days via s.c. implanted osmotic minipumps. This regimen resulted in the incorporation of EPI into renal catecholamine stores and the co-release of EPI with norepinephrine during periarterial nerve stimulation. Stimulus-induced (1 Hz) absolute and fractional overflows of neurotransmitter were significantly greater in the EPI-treated rats. These differences in overflow were not altered by uptake blockade. Alpha adrenoceptor blockade with phentolamine (10(-9)-10(-5) alone increased overflow in a dose-dependent manner in both groups, although to a greater extent in the EPI-treated group. However, in the presence of 1 microM propranolol the effect of phentolamine in the EPI-treated group was greatly reduced such that, in the presence of propranolol, phentolamine was less effective in the EPI-treated vs. vehicle-treated rats. Beta adrenoceptor blockade alone with propranolol (10(-9)-10(-6) M) did not alter stimulus-induced overflow in either group but propranolol dose dependently reduced fractional overflow in the EPI-treated rats when the experiments were done in the presence of 10 microM phentolamine. It is concluded that the enhanced fractional overflow observed in the kidneys of EPI-treated rats was not due to beta adrenoceptor activation, but rather, a reduced influence of the prejunctional alpha adrenoceptor-mediated negative feedback loop. Beta adrenoceptor activation by neurally released EPI does not appear to modulate stimulus-induced overflow unless the dominant inhibitory alpha adrenoceptor mechanism is inactivated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of one derivative of 2-aminotetralin on the alpha-adrenergic receptors of isolated vessels.

Experiments were made to test the effects of originally synthesized piperazine derivative of 2-aminotetralin (P11) on the alpha-adrenergic receptors of isolated vessels. Inhibition of the contracting effects of exogenously introduced noradrenaline into isolated rabbit ear artery was found at concentrations of P11 and phentolamine 1 X 10(-8) to 1 X 10(-4) M. IC50 for P11 is 0.68 microM, for phentolamine -- 0,40 microM. There is a certain shift to the right of the concentration effect curves for noradrenaline in isolated strip of rabbit aorta when P11 and phentolamine are applied in concentrations of 1 X 10(-7) to 1 X 10(-5) M. pA2 for P11 is 7.31, for phentolamine -- 8.04. Potentiation of the maximum effect of noradrenaline is observed after P11 1 X 10(-5) M, which decreases upon preliminary administration of cocaine 1 X 10(-5) M and propranolol 1 X 10(-6) M. The tested compound manifests alpha-adrenergic blocking action in the organs studied.

Animals↗
PubMed1986

Characterization of alpha 1-adrenergic receptor subtypes in rat brain: a reevaluation of [3H]WB4104 and [3H]prazosin binding.

[3H]Prazosin and [3H]WB4101 [2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4 benzodioxane] have both been proposed to label alpha 1-adrenergic receptors in the rat central nervous system. As many discrepancies between the binding of these two ligands have arisen, we conducted these studies in order to reevaluate their binding characteristics and resolve the similarities and differences in the pharmacological characteristics of their respective binding sites. [3H]Prazosin binding is characterized by a monophasic saturation isotherm. Prazosin, indoramine, and dihydroergocryptine competitions with [3H]prazosin are steep and monophasic, and model best to a single binding site. In contrast, phentolamine and WB4101 competition curves are shallow in rat cortex, exhibiting Hill coefficients significantly less than 1.0, and model to two binding sites of approximately equal proportions. The higher and lower affinity components are defined as alpha 1A and alpha 1B, respectively. [3H]WB4101 also labels two binding sites in rat cortex and hippocampus with picomolar and nanomolar affinity, respectively. However, the nanomolar binding site is serotonergic and not adrenergic. The picomolar site (KD = 150 pm) has characteristics of an alpha 1-receptor binding site: prazosin, WB4101, and phentolamine affinities for this [3H]WB4101 binding site correlate with their affinities for the highest affinity component (alpha 1A) of [3H]prazosin binding. In addition, the Bmax of this [3H] WB4101-labeled site is equal to one-half of the total [3H]prazosin Bmax. Agonist competitions with [3H]prazosin binding are multiphasic with pseudo-Hill slopes less than 1.0 and with a rank order of affinity of epinephrine greater than norepinephrine greater than phenylephrine. When binding to the alpha 1A component is blocked by a 30 nM phentolamine mask, the same rank order of agonist affinities is preserved. Although the affinities of epinephrine and norepinephrine at the two subtypes are identical, phenylephrine is weaker at the alpha 1B site. The ratio of the potency of phentolamine versus prazosin is about 4 at the alpha 1A component but about 80 at the alpha 1B binding site. We discuss these data in relation to the reported potencies of these antagonists in blocking alpha 1-receptor-mediated responses which may correlate with our designation of alpha 1A or alpha 1B binding sites.

Animals↗
PubMed1980

Inhibition of exocrine pancreatic secretion by alpha-adrenergic blocking agents in conscious rats.

The effects of the alpha-adrenergic blocking agents, phentolamine and phenoxybenzamine were tested on the exocrine pancreatic secretion of conscious rats. Phentolamine (0.156 mg/kg to 1.25 mg/kg) and phenoxybenzamine (1.25 and 2.5 mg/kg) strongly inhibited basal volume and protein secretion. On the other hand, phentolamine had no effect on the cholecystokinin-pancreozymin or urecholine stimulated exocrine pancreatic secretion. The infusion of phentolamine (1.25 mg/kg/hr) greatly impaired the stimulatory effect on protein secretion induced by soybean trypsin inhibitor and oleic acid. These experiments suggest that alpha-adrenergic blocking agents inhibit pancreatic secretion of the conscious rat by impairment of cholecystokinin-pancreozymin release either by a direct inhibitory action or by blocking a still unknown alpha-adrenergic stimulatory reflex present in the duodenal mucosa.

Adrenergic alpha-Antagonists↗
PubMed1980

Interaction between alpha and beta adrenergic receptors and cholinergic receptors in isolated perfused rat heart: effects on cAMP-protein kinase and phosphorylase.

The ability of acetylcholine to antagonize catecholamine-induced activation of myocardial cyclic AMP dependent protein kinase and glycogen phosphorylase activity was assessed using isolated perfused rat hearts. Perfused hearts were treated with either saline, epinephrine, epinephrine plus phentolamine or isoproterenol. After 1 minute of infusion of the indicated drug a second infusion containing acetylcholine was started. After an additional minute hearts were frozen and analyzed for cyclic nucleotide content and enzyme activity. In the presence of the alpha receptor blocking agent, phentolamine, epinephrine is a more effective activator of protein kinase than in its absence. Under these conditions the antagonistic action of acetylcholine on protein kinase activation is more pronounced. In the presence of epinephrine plus phentolamine or in the presence of isoproterenol the antagonistic action of acetylcholine on phosphorylase activity can be accounted for by a reduction in cyclic AMP-protein kinase. This same action of acetylcholine on epinephrine-stimulated phosphorylase in the aabsence of phentolamine, however, cannot be totally accounted for by a reduction in cyclic AMP content or in protein kinase activity.

Acetylcholine↗
PubMed1984

Blockade of ganglionic afterdischarges by tyramine may be mediated by endogenous catecholamines.

Tyramine reduced the compound postganglionic action potential from preganglionic stimulation of the golden hamster isolated stellate ganglion at 0.2 Hz. This action of tyramine was only slightly reduced by phentolamine (10(-5)M), an alpha adrenoceptor antagonist. Tyramine also reduced the postganglionic discharges after preganglionic stimulation at 30 Hz for 2 sec in the presence of hexamethonium. The blockade of afterdischarges by tyramine was markedly reduced by phentolamine. Furthermore, tyramine was much less effective in blocking ganglia from reserpine-pretreated hamsters (6 mg/kg, 4 hr before isolation). Blockade of afterdischarges by norepinephrine was reduced by phentolamine, but not by reserpine. These results indicate that the blockade of afterdischarges with tyramine is mediated by endogenous catecholamines. The blocking action of tyramine was not reduced by cocaine (10(-5)M). Cocaine did reduce the afterdischarges, and this action of cocaine was partially antagonized by phentolamine and reserpine. These results suggest that the blockade of afterdischarges by tyramine and cocaine is due to inhibition of catecholamine uptake which potentiates the actions of endogenous catecholamines.

Action Potentials↗
PubMed1983

Cholinergic and adrenergic effects on diffusional water flux in the toadfish, Opsanus beta.

Intraperitoneal injections of adrenaline resulted in increased tritiated water efflux rate in the toadfish, Opsanus beta. Adrenaline-stimulated water flux was inhibited by the beta-adrenergic blocker, propranolol, but not by the alpha-adrenergic blocker, phentolamine. Propranolol on its own had no effect but phentolamine significantly stimulated water flux; this action was attributed to a beta-mimetic effect of the drug. The cholinergic neurotransmitter acetylcholine, had no effect while the parasympathico-mimetic carbachol, significantly stimulated water flux. Arguments were advanced to explain the similarity in the effects of the adrenergic and cholinergic drugs although they are both known to produce opposing vascular haemodynamic effects in fish gills. Adrenaline substantially stimulated tritiated water flux in the toadfish, Opsanus beta. The adrenaline-stimulated water flux exhibited a linear dose-response curve up to an adrenaline dosage of 750 micrograms kg-1; wt. At higher doses there was apparently a desensitization of the beta-adrenergic receptor sites. The adrenaline effect was inhibited by the beta-blocker propranolol, but not by the alpha-blocker, phentolamine. This suggests that the adrenaline-stimulated water flux was due predominantly to beta-receptor site stimulation. Stimulation of water flux by phentolamine on its own could be due to the stimulation of endogenous catecholamine release by the drug. We have proposed that the beta-stimulated water efflux could be due to an increase in surface area of the branchial epithelium, a decrease in water to blood diffusion distance, a direct metabolic effect or any combination of these effects by adrenaline. Carbachol caused an increase in tritiated water efflux. The carbachol-stimulated water flux was inhibited by atropine thus suggesting that the drug acts via muscarinic receptor sites. We have suggested that the action of the drug on hydraulic water conductivity, water to blood diffusion distance, hydrostatic pressure or a direct effect on membrane diffusion coefficient.

Acetylcholine↗
PubMed1983

Antagonism and supersensitivity to phenylephrine-induced chronotropic responses.

Right atria from rats were analyzed for chronotropic responses to phenylephrine in face of various drugs and procedures. Propranolol, 10(-8) M, produced a competitive antagonism against the agonist which concentration-effect curve was closely similar to that obtained from reserpinized animals. Prazosin, but not phentolamine (both 10(-6) M) showed inhibition of the phenylephrine-induced changes in heart rate, as judged by their -log EC50. Either of the alpha-adrenoceptor antagonists exhibited a greater steepness in the curve slope with respect to control. The simultaneous exposure of tissues to phentolamine and propranolol proved to effectively antagonize the chronotropic effect of the agonist. This held true for phentolamine assayed in atria from reserpine-pretreated rats. Previous incubation of tissues with papaverine, 10(-5) M, brought about supersensitivity to phenylephrine which was thoroughly inhibited by either phentolamine or propranolol. These results strongly suggest that beta-adrenoceptor stimulation of heart rate by phenylephrine takes place indirectly via norepinephrine release. There is also alpha 1-adrenoceptor stimulation (blocked by prazosin). Finally, it is hypothesized that supersensitivity develops by papaverine-enhanced Ca2+ influx, since numerous evidences are against a phosphodiesterase inhibition-dependent cAMP accumulation mechanism triggered by papaverine in the presence of phenylephrine.

Animals↗
PubMed1984

Selective activation by LY-141865 and apomorphine of presynaptic dopamine receptors in the rat kidney and influence of stimulation parameters in the action of dopamine.

The presence and physiological role of presynaptic dopamine receptors in the isolated-perfused rat kidney was assessed by determining the effects of several agonists and antagonists on the release of [3H]norepinephrine elicited during periarterial nerve stimulation. In the presence of cocaine, dopamine caused a concentration-dependent inhibition of stimulus-induced release of [3H]norepinephrine at 0.5 and 2 Hz. Phentolamine as well as sulpiride caused partial antagonism of the inhibitory action of dopamine at 0.5 Hz (20 sec) and a combination of both of these agents was required to completely antagonize the action of dopamine. The inhibition of [3H]norepinephrine release caused by dopamine at 2 Hz (20 sec) was completely antagonized by sulpiride alone and phentolamine had no effect on the inhibitory action of dopamine. These results suggest that dopamine-induced inhibition of norepinephrine release depends on the conditions of stimulation, i.e., during lower frequencies of sympathetic nerve stimulation, inhibition occurs by simultaneous activation of both presynaptic dopamine receptors as well as alpha adrenoceptors, whereas only presynaptic dopamine receptors are responsible for the inhibition of neurotransmitter release caused by dopamine at the higher frequency of nerve stimulation. The dopamine receptor agonists apomorphine and LY-141865 caused concentration-dependent inhibition of [3H]norepinephrine release elicited during periarterial nerve stimulation at 0.5 Hz, which was antagonized by sulpiride but not by phentolamine, suggesting that selective stimulation of presynaptic dopamine receptors accounted for inhibitory actions of these compounds. In the presence of cocaine, norepinephrine also inhibited stimulus-induced release of [3H]norepinephrine at 0.5 Hz, which could be antagonized by phentolamine but not sulpiride.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗