Stimulation Of Sympathetic Ganglia Research Articles

Effect of Electrical Stimulation of Cervical Sympathetic Ganglia on Intraocular Pressure Regulation According to Different Circadian Rhythms in Rats.

PurposeThe purpose of this study was to investigate the relationship between circadian rhythm and intraocular pressure (IOP), and to explore whether electrical stimulation of cervical sympathetic ganglia (SCG) can regulate IOP via neurotransmitter distribution around the Schlemm's canal (SC) in rats.MethodsSprague Dawley rats were housed under normal (N-normal), constant dark (N-dark), and constant light (N-light) rhythms (n = 6 per group). Electrical stimulation (intermittent wave [20 hertz {Hz}, 2 mA, 10 minutes]) was used to stimulate the SCG. Atropine sulfate eye gel was applied three times a day. DiI was injected into the SCG and anterior chamber. The cross-sectional area and circumference of SC were evaluated using hematoxylin-eosin staining. Immunofluorescence staining was used to evaluate dopamine-β-hydroxylase (DβH) expression in SC endothelial (SCE) cells.ResultsN-Dark increased the IOP, decreased the cross-sectional area of SC, and increased DβH levels in SCE cells. Nerve projection between SC and SCG was detected, and electrical stimulation of SCG upregulated DβH expression in SCE cells. Under normal and constant light rhythms, electrical stimulation of SCG increased DβH and decreased the cross-sectional area and circumference of SC, while simultaneously increasing IOP and decreasing IOP fluctuations. After paralyzing the ciliary muscles, electrical stimulation of SCG decreased the cross-sectional area and circumference of SC under normal and constant light rhythms.ConclusionsN-Dark increased DβH in SCE cells, reduced the cross-sectional area of SC, and increased IOP. Under the normal and light rhythms, electrical stimulation of SCG increased DβH in SCE cells, reduced the cross-sectional area and circumference of SC, and in turn elevated IOP and decreased IOP fluctuations.

Effects and underlying mechanisms of human opiorphin on cardiovascular activity in anesthetized rats

The present study was performed to investigate the peripheral cardiovascular effects of opiorphin in anesthetized rats. Intravenous (i.v.) injection of opiorphin (50−500nmol/kg) caused marked dose-dependent increase in blood pressure and heart rate. The pressor and tachycardic responses induced by opiorphin (300nmol/kg, i.v.) were significantly decreased by pretreatment with angiotensin-converting enzyme inhibitor captopril or angiotensin II type 1 (AT1) receptor antagonist valsartan, which suggested that endogenous angiotensin may be involved in the response to opiorphin. Pretreatment with α-adrenoreceptor antagonist phentolamine and β-adrenoceptor antagonist propranolol respectively attenuated the pressor response induced by opiorphin. Propranolol, but not phentolamine, inhibited the tachycardic response. Moreover, reserpine blocked both responses to opiorphin. These findings indicated that the effects of opiorphin to increase blood pressure and heart rate might be due to the stimulation of sympathetic ganglia. Additionally, studies with bilaterally adrenalectomized rats showed that adrenal medulla may be involved in the cardiovascular regulation of opiorphin. In addition, pretreatment with nonselective opioid receptor antagonist naloxone did not modify the cardiovascular responses to opiorphin, suggesting that the effects of opiorphin were not related to the opioid system. Furthermore, radioimmunoassay (RIA) showed that opiorphin significantly increased endogenous levels of angiotensin II and angiotensin III. In summary, all the results indicate that the cardiovascular effects induced by opiorphin are mediated through the renin–angiotensin system (RAS), the sympathetic ganglia and adrenal medulla, but not the opioid system.

Cardiovascular responses to intravenous administration of human hemokinin-1 and its truncated form hemokinin-1(4-11) in anesthetized rats

Human hemokinin-1 and its carboxy-terminal fragment human hemokinin-1(4-11) have been recently identified as the members of the tachykinin family. The peripheral cardiovascular effects of these two tachykinin peptides were investigated in anesthetized rats. Lower doses of human hemokinin-1 (0.1–3 nmol/kg) injected intravenously (i.v.) induced depressor response, whereas higher doses (10 and 30 nmol/kg) caused biphasic (depressor and pressor) responses. The depressor response is primarily due to the action on endothelial tachykinin NK 1 receptor to release endothelium-derived relaxing factor (NO) and vagal reflex was absent in this modulation. The pressor response is mediated through the activation of tachykinin NK 1 receptor to release catecholamines from sympathetic ganglia and adrenal medulla. Moreover, human hemokinin-1 injected i.v. produced a dose-dependent tachycardia response along with blood pressure responses and the activation of sympathetic ganglia and adrenal medulla are involved in the tachycardia response. Human hemokinin-1(4-11) only lowered mean arterial pressure dose-dependently (0.1–30 nmol/kg) and the mechanisms involved in the depressor response are similar to that of human hemokinin-1. Additionally, human hemokinin-1(4-11) could also produce tachycardia response dose-dependently and the mechanisms involved in the tachycardia response are similar to that of human hemokinin-1 except that bilateral adrenalectomy could not affect the tachycardia markedly, indicating that the tachycardia induced by human hemokinin-1(4-11) is primarily due to the stimulation of sympathetic ganglia. In a word, to a certain extent, human hemokinin-1(4-11) is the active fragment of human hemokinin-1, however, the differences between human hemokinin-1 and hemokinin-1(4-11) involved in the effects of cardiovascular system suggest that the divergent amino acid residues at the N-terminus of human hemokinin-1 produced different activation properties for tachykinin NK 1 receptor.

Cardiovascular responses to rat/mouse hemokinin-1, a mammalian tachykinin peptide: Systemic study in anesthetized rats

Rat/mouse hemokinin-1 is a mammalian tachykinin peptide whose biological functions have not been well characterized. In the present study, an attempt has been made to investigate the effect and mechanism of action of rat/mouse hemokinin-1 on systemic arterial pressure after intravenous (i.v.) injections in anesthetized rats by comparing it with that of substance P. Our data showed that injection of rat/mouse hemokinin-1 (0.1, 0.3, 1, 3 and 10 nmol/kg) lowered systemic arterial pressure dose-dependently. This effect was significantly blocked by pretreatment with SR140333 (a selective tachykinin NK1 receptor antagonist) and the NO synthase inhibitor L-NAME (Nomega-nitro-L-arginine methyl ester hydrochloride), respectively, but was not affected by bilateral vagotomy or the muscarinic receptor blocker atropine. Compared to rat/mouse hemokinin-1, a dose of 3 nmol/kg of substance P caused biphasic changes in systemic arterial pressure (depressor and pressor responses). The results suggest that the mechanism of the depressor response caused by substance P was similar to rat/mouse hemokinin-1 in that it was inhibited by SR140333 and L-NAME, respectively, but that there was a component of the cardiovascular change induced by rat/mouse hemokinin-1 (but not substance P) that was attenuated by SR48968 (a selective tachykinin NK2 receptor antagonist). The depressor response induced by rat/mouse hemokinin-1 (i.v.) might be explained primarily by the action on endothelial tachykinin NK1 receptors to release endothelium-derived relaxing factor (NO) and this effect was not affected by vagal components. In addition, rat/mouse hemokinin-1 could not induce the pressor response through stimulation of sympathetic ganglion like substance P in anesthetized rats.

Neurogenic regulation of cochlear blood flow occurs along the basilar artery, the anterior inferior cerebellar artery and at branch points of the spiral modiolar artery

The cochlea receives its main blood supply from the basilar artery via the anterior inferior cerebellar artery and the spiral modiolar artery. Morphologic studies have shown sympathetic innervation along the spiral modiolar artery of the gerbil and the guinea pig and functional studies in the isolated in vitro superfused spiral modiolar artery of the gerbil have demonstrated norepinephrine-induced vasoconstrictions via α 1A-adrenergic receptors. It is current unclear whether the sympathetic innervation is physiologically relevant. Stimulation of sympathetic ganglia in guinea pigs has been shown to alter cochlear blood flow in situ. Whether these changes originated from local or more systemic changes in the vascular diameter remained uncertain. The goal of the present study was to demonstrate the presence or absence of neurogenic changes in the diameter of the isolated in vitro superfused spiral modiolar artery, anterior inferior cerebellar artery and basilar artery from the gerbil and the guinea pig. Vascular diameter was monitored by videomicroscopy. Electric field stimulation was used to elicit neurotransmitter release. A reversible inhibitory effect of 10 −6 M tetrodotoxin was taken as criterion to discriminate between neurogenic and myogenic changes in vascular diameter. Mesentery arteries of comparable diameter, which are known to respond with a neurogenic vasoconstriction to electric field stimulation, served as controls. Basilar artery, anterior inferior cerebellar artery, spiral modiolar artery and mesentery arteries constricted in response to electric field stimulation. No dilations were observed. Myogenic and neurogenic vasoconstrictions were observed in all vessels. These observations suggest that the sympathetic innervation of the basilar artery, the anterior inferior cerebellar artery and branch points of the spiral modiolar artery is involved in a physiologically relevant control of the vascular diameter in the gerbil and the guinea pig.

Reduction of the pressor response to nicotine in the guinea pigs by a histamine (H3) agonist is attenuated by an inhibitor of nitric oxide synthesis.

We examined whether a histamine (H3)-agonist, (R) alpha-methylhistamine, [(R) alpha-MeHA] reduced the pressor responses induced by nicotine in urethane-anesthetized guinea pigs treated by atropine. Nicotine dose-dependently increased the basal mean arterial pressure (MAP) and the heart rate (HR) of the preparation. Both effects were due to stimulation of sympathetic ganglia, since muscarinic receptors were blocked. Adrenalectomy did not affect either the hypertension or the tachycardia to nicotine. Nicotine (7 micrograms kg-1) evoked a transient hypertension of approximately 30 mm Hg and a tachycardia by approximately 20 beats/min. (R) alpha-MeHA dose-dependently inhibited the increase in mean arterial pressure and the increase in HR to nicotine but not those produced by exogenous norepinephrine (NE). The inhibitory effects of (R) alpha-MeHA were dose-dependently antagonized by the H3-antagonist thioperamide, but not by combined mepyramine/cimetidine. They were also suppressed by a nitric oxide (NO)-synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME); this suppression was reversed by L-arginine. Histamine in the presence of mepyramine and cimetidine induced a similar inhibition of the hypertension to nicotine but a less potent inhibition of the tachycardia. These findings indicate that postganglionic noradrenergic nerve fibers are endowed with presynaptic H3-receptors, the stimulation of which inhibits NE release through an NO mechanism.

Is nociceptor activation by alpha-1 adrenoreceptors the culprit in sympathetically maintained pain?

In certain patients, pain depends on sympathetic activity in the affected area. Sometimes referred to as reflex sympathetic dystrophy or causalgia, this disease is termed sympathetically maintained pain (SMP). Several lines of evidence support the hypothesis that in this disease alpha-1 adrenoreceptors develop in peripheral tissues (possibly at terminals of nociceptors), such that the release of norepinephrine from the sympathetic terminals activates the nociceptors and leads to the sensation of pain. This hypothesis stems from previous work with regional guanethidine block, stimulation of sympathetic ganglia, application of norepinephrine to the affected area, and oral sympatholytic drugs. Recent results from alpha-adrenergic agonists and antagonists in patients with and with-out SMP support this hypothesis. Intravenous phentolamine, a short-acting, competitive alpha-adrenergic antagonist, produced pain relief that was highly correlated with relief obtained with a local anesthetic block of the sympathetic ganglia. This experiment supports the contention that SMP is mediated by an alpha-adrenoreceptor. Topical application of the alpha-2 agonist, clonidine, relieved hyperalgesia at the site of application presumably by reducing the release of norepinephrine. Injection of norepinephrine and the alpha-1 agonist phenylephrine into the clonidine-treated area produced marked pain and hyperalgesia. These results implicate the alpha-1 adrenoreceptor as the culprit in SMP.

Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana

To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phentolamine, atropine and alpha,beta-methylene ATP had no effect on the response to vagal stimulation. Both epinephrine (EPI) and norepinephrine (NE) increased CVR, with EPI being more potent than NE. The minimum concentrations of EPI and NE required for a significant change in CVR were much higher than plasma catecholamine levels reported for resting bullfrogs. Phentolamine antagonized, but propranolol had no effect on, the responses to the catecholamines. Isoproterenol caused small decreases in CVR which were abolished by propranolol. Acetylcholine was a weak vasodilator. The results indicate that the cutaneous vasculature has two types of vasomotor nerves: sympathetic nerves that are probably adrenergic, and other nerves that are non-adrenergic/non-cholinergic and which do not use ATP as a transmitter. Although catecholamines are vasoactive, the sensitivity of the cutaneous vasculature to EPI and NE is probably too low to allow a direct regulatory role of these hormones on CVR. There is no evidence for cholinergic regulation of CVR. Both alpha- and beta-adrenoceptors are present in the cutaneous vasculature. alpha-Adrenoceptors mediate the constrictor responses to sympathetic nerve stimulation and catecholamine administration. It is unlikely that beta-adrenoceptors play a significant role in regulating CVR.

Mapping of ventricular tachycardia induced by thoracic neural stimulation in dogs.

To investigate ventricular tachycardias produced in healthy canine myocardium by stimulation of sympathetic ganglia or cardiac nerves, we simultaneously recorded a surface ECG and 63 ventricular electrograms in anesthetized open-chest dogs. Isochronal and isopotential maps were generated off-line by computer. Ventricular tachycardia with uniform beat-to-beat morphology was induced in 13 or 22 dogs by electrical stimulation of the left stellate ganglion (five experiments), the left middle cervical ganglion (four experiments), the left caudal pole cardiopulmonary nerve (two experiments), or the ventrolateral cardiac nerve (eight experiments). It was not inducible by stimulation of the right-sided major cardiopulmonary nerves or ganglia. In most instances the earliest measured electrical excitation occurred on the posterior aspect of the ventricles. Isochronal maps demonstrated a radial spread of the impulse away from the area of earliest excitation. Changes in the region of earliest excitation and (or) activation pattern were accompanied by changes in QRS morphology. The potential gradients measured between areas displaying positive and negative T waves on the anterior and left lateral aspects of the ventricles were significantly increased by ventrolateral cardiac nerve stimulation. However, the ventricular regions where these potential gradients existed differed from the regions of earliest excitation during ventricular tachycardia. These results demonstrate that the thoracic autonomic nervous system can induce repetitive ventricular excitation originating from consistent loci.

Effect of sympathetic impulses on parafollicular cells (C cells) of the thyroid gland

Reaction of K-cells (detectable by the Savitsky method) to stimulation of the superior cervical sympathetic ganglia or to their removal was examined in experiments on male rabbits. Stimulation of the sympathetic ganglia attained as a result of application to them of a ringlet made of solid silver wire produced a marked rise of the number and size of K-cells, with the serotonin content in the thyroid gland being significantly increased as compared to the initial level. Bilateral cervical sympathectomy entailed a reduction in the serotonin content and in the size of K-cells. In the course of hyperthyroidization the functional activity of the thyroid epithelium decreased and K-cells underwent a pronounced reduction.

Effect of tilting on the pressor responses to McN-A-343, a muscarinic sympathetic ganglion stimulant.

1 In anaesthetized cats and dogs treated with mecamylamine, the pressor response to McN-A-343 was increased when the animals were changed from a supine to a head-up, tilted position. This potentiation was not seen in rats. 2 The potentiation of the McN-A-343 pressor response was not affected by propranolol, destruction of the brain, or removal of the intestines, spleen or adrenal glands. It was promptly abolished by applying pressure to the lower half of the tilted animal. No increase in the pressor response to McN-A-343 occurred when cats were tilted head down. The potentiated response in tilted cats was abolished by atropine. 3 The pressor effects of adrenaline, noradrenaline, tyramine and angiotensin in cats treated with mecamylamine were either reduced or unchanged when the animal was changed from the supine to the tilted position. In one cat not treated with mecamylamine in which orthostatic hypotension occurred, tilting potentiated the pressor responses to dimethyl phenylpiperazinium iodide. 4 In cats anaesthetized with chloralose, the reflex pressor response to bilateral carotid occlusion was reduced by tilting. After mecamylamine treatment the residual atropine-sensitive response to carotid occlusion was potentiated when the animal was placed in the tilted position. 5 These results suggest that muscarinic stimulation of sympathetic ganglia by McN-A-343 raises blood pressure by predominantly reducing venous capacity, in contrast to noradrenaline and angiotension which increase blood pressure mainly by arterial vasoconstriction. 6 It is not clear whether this is a general property of sympathetic ganglionic stimulation or is restricted to stimulation of muscarinic sites.

Association of the Acetylcholine-phosphatidyl Inositol Effect with a “Receptor” Proteolipid from Cerebral Cortex

A striking effect of acetylcholine is the stimulation of phosphatidyl inositol turnover in nervous1–3 and other tissues1,4 as witnessed by the increased incorporation of 32P and isotopically labelled inositol. The effect has been observed in vitro in brain slices1,2 and in brain homogenates5–7 and has been localized in subcellular fractions rich in nerve endings8. More recently a marked increase in the 32P incorporation into phosphatidyl inositol, but not into other phospholipids, was demonstrated in electrically stimulated slices of cerebral cortex9. Preganglionic stimulation of sympathetic ganglia also resulted in an increased phosphatidyl inositol turnover and indirect evidence was presented that the effect occurred at the postsynaptic membrane10,11. These and other findings imply that phosphatidyl inositol may play a special part in synaptic transmission but the mechanisms involved in the acetylcholine effect are as yet unsolved.

Effects of nicotine, DMPP and McN-A-343 administered into the AV node artery of the dog.

The perfusion of the AV node artery in eight dogs in situ was performed under constant pressure of 100mm Hg. Ganglionic stimulating agents, i.e., nicotine, DMPP and McN-A-343 were administered into the AV node artery. Doses above 3μg of nicotine always induced complete AV block. DMPP induced also complete AV block, but frequently followed by nodal tachycardia. These AV blocks were completely prevented by atropine or tetrodotoxin, and nodal tachycardia was blocked by propranolol. On the contrary, McN-A-343 at doses from 10μg to 1mg had entirely no effect on the AV conduction. The authors conclude that the complete AV block induced by nicotine or DMPP is due to the stimulation of parasympathetic ganglia and that nodal tachycardia following initial AV block induced by DMPP is due to catecholamine release from sympathetic nerve endings and not by stimulation of sympathetic ganglia, because McN-A-343 causes neither AV block nor nodal tachycardia.

Pharmacologic actions at various neuroeffectors of single and combined administration of EPN and malathion

Effects of single and combined administrations of two anticholinesterase insecticides, EPN and malathion, were studied in dogs and cats with regard to autonomic and somatic synapses, and to differences in EEG. When the drugs were administered intravenously, EPN had maximum effect only after a latent period of 30 min, while malathion acted almost immediately. EPN and malathion, given singly, facilitated responses to preganglionic stimulation of sympathetic ganglia, to the stimulation of the cardiac vagus nerve and of the chorda tympani nerve, and to intravenously injected acetylcholine. EPN was more potent than malathion in all these cases, but the potency ratio differed from test to test. Even with regard to two sympathetic ganglia, the cervical and stellate, the potency of the two agents as well as the ratio of potency differed widely. EPN and malathion, given singly, were weak and inconsistent in ability to increase muscle twitch and to produce EEG arousal in atropinized animals. Upon combined administration of EPN and malathion, more than additive action arose at several neuroeffectors, particularly at the neuromyal junction and in the central nervous system. Potentiation was absent in the case of several autonomic neuroeffectors. At the neuromyal junction and in the central nervous system, potentiation arose whether EPN was administered 30 to 45 min before, or after, malathion. The potentiation was less in the latter case. The doses of combinations sufficient to cause neuromyal and EEG effects approximate the LD 50 values of the combinations. It is suggested, therefore, that the lethality of combinations is due to neuromyal and central actions. The differential neuroeffector actions of EPN and malathion and of their combinations were discussed. The possibility was stressed that potentiation arising at several neuroeffectors from joint actions of EPN and malathion may depend on factors other than interference of one compound with the metabolism of the other.

Effect of neuroactive drugs on production of fibrinolytic activity.

Neuroactive drugs were investigated for their ability to produce a blood plasma fibrinolysin in experimental animals. Following intravenous injections of these drugs, blood samples were drawn and the plasma studied for fibrinolytic activity as indicated by the Astrup fibrin plate technique. Drugs inducing a small degree of fibrinolytic activity in dogs were acetylcholine hydrochloride, epinephrine hydrochloride, carbamylcholine chloride, physostigmine salicylate and prostigmine methylsulfate. The possible mechanism of drug-induced fibrinolysin as compared with the biological activation of profibrinolysin is interpreted on the basis of stimulation and release of catecholamines resulting from stimulation of sympathetic ganglia and the adrenal medulla.

A ganglion-stimulating principle present in peptone.

One of us (W. T. B.) has previously described a pressor effect of peptone in the rat. This effect was considered secondary to a release of sympathin by the stimulation of sympathetic ganglia. The present experiments show that peptone causes contraction of guinea-pig ileum and inferior eyelid of the rat which is antagonized by hexamethonium. Atropine inhibits equiactive doses of peptone and acetylcholine on the guinea-pig ileum and eserine potentiates them. Boiling peptone in concentrated hydrochloric acid or N sodium hydroxide destroys its activity; incubation with proteolytic enzymes (trypsin, pepsin, and chymotrypsin) has no effect on its activity. It is concluded that peptone acts upon the intramural ganglia of the guinea-pig ileum and on sympathetic ganglia which supply the inferior eyelid of the rat.

The pressor effect of peptone in the rat.

Peptone normally causes a rise of blood pressure in rats. Since the pressor response was not abolished or even diminished by adrenalectomy, it could not have been caused by a release of pressor substances from the adrenal glands. The group of drugs (dibenamine, dihydroergotamine, ergotamine, tolazoline, nicotine and hexamethonium) which antagonize or block the peptone-induced pressor action suggests that the pressor effect may be secondary to a release of sympathin by the stimulation of sympathetic ganglia. Since it was not possible to duplicate the pressor response to peptone by either 48/80 or histamine, the hypothesis that peptone acts by liberating histamine can be ruled out.

Cardiovascular action of 1, 1-dimethyl-4-phenylpiperazinium iodide (DMPP): A ganglion stimulating agent useful in the diagnosis of pheochromocytoma

1. 1. DMPP (1,1-dimethyl-4-phenylpiperazinium iodide) stimulated sympathetic ganglia more powerfully than nicotine and tetramethylammonium iodide and had less ganglion paralyzing action than nicotine in dogs, cats, rabbits and man. It differed from nicotine also in that its vasopressor action was largely independent of carotid and aortic chemoreceptor function. Respiratory stimulation, however, depended in part upon stimulation of these chemoreceptors. 2. 2. The pressor effect of DMPP depended upon release of epinephrine and/or norepinephrine from the adrenal glands and liver and stimulation of sympathetic ganglia with resultant vasoconstriction and cardioacceleration. The drug had no prominent direct action on blood vessels, at least in the perfused denervated dog's leg. 3. 3. Stimulation of parasympathetic ganglia caused initial transient bradycardia and fall in blood pressure that tended to inhibit the pressor action of DMPP. This opposing action was especially prominent after spinal cord section at C 6 and was eliminated by atropine or section of the vagus nerves. 4. 4. Section of the spinal cord at C 6 or paravertebral sympathectomy augmented the pressor action of DMPP, since these procedures also augment the pressor action of epinephrine and nor-epinephrine. 5. 5. TEAC, nicotine and hexamethonium all inhibited the ganglion-stimulating action of DMPP. The adrenergic blocking agents, priscoline, regitine and RO 2-3248, inhibited the pressor action of DMPP to a degree directly dependent on the inhibition of pressor response to nor-epinephrine. 6. 6. Response to DMPP was not altered by production of chronic neurogenic hypertension in dogs by section of the carotid sinus and aortic depressor nerves. But during the acute hypertension immediately following section of the buffer nerves the late sustained pressor action of DMPP was often replaced by a pronounced depressor effect. The significance of this difference is unknown, other than it may be listed with other observations suggesting that the two forms of hypertension depend on different mechanisms. 7. 7. DMPP has proved useful in the diagnosis of pheochromocytoma because of its strong and specific action on ganglia and adrenal medullary tissue. It ensures a high secretory activity of the tumor, the effect of which is specifically inhibited by adrenergic blocking agents.