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At least 19 recordsLinked to original sources

PubMed1978

Effect of beta-sympatholytic agents on vascular responses to noradrenaline and potassium chloride.

Vasoconstrictory responses to noradrenaline (NA) or high potassium chloride (130 mM) usually show a biphasic behaviour: an initial peak is followed by a lower steady state level. The influence of three beta-sympatholytic agents (propranolol, pindolol, practolol) and a "Ca-antagonist" (verapamil) on this particular behaviour of KCl-induced vasoconstrictions was compared with responses to NA. Studies were performed on the intact vascular bed of an isolated intestinal preparation of the rat. 1. Increases in the concentration of propranolol and pindolol from 10(-10) to 10(-6) M attenuated the vascular responses to high KCl. Practolol, however, distinctly enhanced the KCl-responses. NA (1.3 microgram/ml)-elicited vasoconstriction was found to be influenced in a similar manner by the beta-receptor antagonists used, though lower concentrations of pindolol had an enhancing, higher concentrations a reducing effect on the constrictory responses to NA. 2. The extent to which the biphasic response adjusted to the steady state level was concentration-dependently increased KCl-responses and significantly decreased to a monophasic response to NA, in the presence of the beta-sympatholytic agents. 3. By using a quotient of deltaPs (steady-state phase) to deltaPi (initial vasoconstriction) and by comparing the effect of the three beta-sympatholytic agents with that of verapamil on this quotient showed a concentration-dependent decrease in presence of the beta-sympatholytic as well as of the Ca-antagonistic agents. These myotropic actions, i.e. negative influences on the mechanism of vascular smooth muscle activation ranged in the following sequence: Verapamil greater than propranolol greater than pindolol greater than practolol. 4. The mechanism underlying the biphasic responses to high potassium chloride are concluded to be basically different from the NA-responses because they are inversely affected by beta-sympatholytic agents. The steady-state response to KCl was found to be very sensitive to non-specific pharmacological actions of beta-sympatholytic substances. The myotropic action of the beta-receptor antagonists is compared with that of the Ca-antagonist verapamil and the role of calcium in the mechanism of activation of vascular smooth muscle is discussed.

Adrenergic beta-Antagonists↗

PubMed1991

Sympatholytic interventions and vascular remodelling.

Most of the results on the effects of sympatholytic agents on vascular remodelling came from studies involving hypertensive animals. Therefore, it is often difficult to dissociate the antihypertensive property of the drugs from those caused by the direct action of the drugs on the structure of the blood vessels. However, some general conclusions can be drawn in some areas. Very little information is available on the effects of sympatholytic agents on the structure and function of the endothelial cells, and on the structure of the internal elastic lamina. Necrotic changes of the endothelial cells, and destruction of the internal elastic lamina present in hypertensive animals are prevented with sympatholytic agents, which may be related to the antihypertensive property of the drugs. The density of the fenestrations in the internal elastic lamina is decreased by sympathectomy. In the media, proliferation of vascular smooth muscle cells in growing animals is usually interfered with by sympatholytic drugs, so that the medial mass is normally smaller than that in the untreated control. In most animals, treatment of the animals with sympatholytic agents causes an increase in the biosynthesis, or accumulation of collagen in several types of arteries in the rats and rabbits. In addition to adrenergic nerves, the density of some peptidergic nerves is also reduced by these drugs. The effect of sympathectomy on lumen size is less clear, because lumen size was increased in some studies, and decreased in others. It is clear that remodelling of the vessel wall does occur in some instances, but in general, it is important to distinguish the growth retardation of the animals due to the treatment, from the effect which might be specific to the vessel wall.

Animals↗

PubMed1989

Studies on the mechanism of the sympatholytic effect of 8-OH DPAT: lack of correlation between inhibition of serotonin neuronal firing and sympathetic activity.

Previous studies indicate that the selective 5-HT1A agonist, 8-OH DPAT, acts in the central nervous system to inhibit sympathetic nerve activity. Based on the observations that: (1) 8-OH DPAT acts at serotonin (5-HT) autoreceptors to inhibit 5-HT neuronal firing; and (2) medullary 5-HT neurons provide a tonic excitatory input to sympathetic preganglionic neurons, we have hypothesized that 8-OH DPAT produces its sympatholytic effects by inhibiting medullary 5-HT neuronal firing and thereby removing an excitatory input to sympathetic preganglionic neurons. The present study was designed to critically test this hypothesis. The sympatholytic effects of 8-OH DPAT were compared in intact animals and in animals which received large electrolytic lesions in the midline area of the lower brainstem. These lesions extended from the obex rostral through the level of the facial motor nucleus and encompassed the brain stem from the dorsal to the ventral surface. The sympatholytic effect of 8-OH DPAT was identical in intact animals and in animals receiving the lesion. The inhibitory effects of 8-OH DPAT on activity recorded simultaneously from the inferior cardiac sympathetic nerve and from medullospinal 5-HT neurons were determined. Medullary 5-HT neurons were identified using criteria modeled after the electrophysiological and pharmacological characteristics previously described for dorsal raphe 5-HT neurons. Medullary 5-HT neuronal activity was more sensitive to the inhibitory effects of 8-OH DPAT than was sympathetic activity. Indeed, low doses of 8-OH DPAT completely suppressed the firing of medullary 5-HT neurons but had little effect on sympathetic nerve activity. These data fail to support the hypothesis that inhibition of 5-HT neuronal firing is responsible for the central sympatholytic effects of 8-OH DPAT. Rather, the data suggest that 8-OH DPAT acts postsynaptically on 5-HT1A receptors located on central sympathetic neurons to inhibit sympathetic nerve activity.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1976

[Study of the influence of the beta-sympatholytic drug KO 1366 (Bunitrolol on lung function (author's transl)].

20 untreated outpatients suffering from chronic obstructive airway disease were tested with a new beta-sympatholytic agent, Kö 1366 (bunitrolol) or placebo in a randomized symptoms of bronchitis, but hacetylcholine inhalation was followed by severe bronchospastic hyperreactivity. The intravenous administration of 2.5 mg Kö 1366 resulted in a rapid and statistically significant (p less than 0.001) marked decrease in heart rate due to the beta-sympatholytic effect. Airway resistance, however, measured by whole-body plethysmography, was not affected. Kö 1366 can be regarded as a cardio-selective beta-sympatholytic drug in so far as i.v. administration is possible in patients with airway disease during a non-obstructive period. Moreover, should a bronchospastic reaction occur immediate control by inhalation of adrenergic or vagolytic drugs is possible.

Adult↗

PubMed1990

Studies on the site and mechanism of the sympatholytic action of 8-OH DPAT.

Studies in our laboratory indicate that the 5-HT1A agonist 8-OH DPAT acts in the central nervous system at postsynaptic receptor sites to inhibit sympathetic nerve activity and lower arterial blood pressure. The present study was designed to investigate possible postsynaptic sites on central sympathetic neurons where 8-OH DPAT might produce its sympatholytic action in anesthetized cats. The sympatholytic effect of 8-OH DPAT was compared in midcollicular transected and sham operated control animals. Administration of 8-OH DPAT (0.01-1.0 mg/kg, i.v.) inhibited sympathetic activity and decreased blood pressure in both the transected and sham animals to a similar degree. The effects of microiontophoretically applied 8-OH DPAT and 5-HT on antidromically identified sympathetic preganglionic neurons were determined. Microiontophoretically applied 5-HT consistently increased the firing rate of sympathetic preganglionic neurons. Iontophoretic 8-OH DPAT failed to affect the firing of sympathetic preganglionic neurons but blocked the excitatory effects of 5-HT. The effects of 8-OH DPAT and 5-HT on the firing of sympathoexcitatory neurons located in the rostral ventrolateral medulla were also determined. Sympathoexcitatory neurons were identified using spike triggered averaging techniques and by their response to baroreceptor activation. Intravenous administration of 8-OH DPAT inhibited the firing of sympathoexcitatory neurons in the rostral ventrolateral medulla. The inhibition of unit firing produced by 8-OH DPAT was exactly paralleled by the shutoff of inferior cardiac nerve activity. Microiontophoretic application of 8-OH DPAT and 5-HT onto sympathoexcitatory neurons in the rostral ventrolateral medulla failed to affect the firing rate of these neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

Effects of amiodarone on cardiac electrophysiology and inducibility of arrhythmias in chronically infarcted dogs: late arrhythmias, haemodynamics, and sympatholytic actions.

The electrophysiological and antiarrhythmic effects of acute (2 and 10 mg/kg i.v.) and chronic (400 mg/day p.o. for 28 days) amiodarone (AM) treatment were compared in anaesthetised dogs with 5-6-day-old myocardial infarcts. Intravenous AM prolonged the RR interval, sinus node recovery time, the PR interval, and atrial to His conduction time by 36, 33, 25, and 36%, respectively. Corresponding increases after oral amiodarone were 50, 57, 12, and 26%. Atrial and His-Purkinje conduction times were unchanged. Atrial and ventricular refractory periods were increased especially after oral treatment. Oral AM additionally prolonged QRS, QT, and paced QT (by 4, 34, and 19%, respectively). Effects of oral AM on ventricular repolarisation and on the fast inward sodium current were confirmed in vitro. Both modes of AM administration protected against inducible arrhythmias, an effect that was more marked during normal sinus rhythm than during pacing in orally treated dogs. Oral amiodarone failed to protect against spontaneous late arrhythmias 24 h after infarction whilst both modes of administration noncompetitively inhibited isoprenaline-induced tachycardia. Oral AM reduced blood pressure (13%) and LV dP/dt/P (24%) whereas cardiac output was maintained by an increase in stroke volume. It was concluded that oral AM is haemodynamically well tolerated and that prolonged ventricular repolarisation enhanced by bradycardia together with sympatholytic actions may be important mechanisms for antiarrhythmic efficacy, whereas the mechanisms involved in i.v. efficacy are less clear but may depend, at least partly, on sympatholytic actions and perhaps (tentatively) on sodium channel block in Purkinje tissue.

Action Potentials↗

PubMed1985

Mechanisms underlying changes in the contents of neuropeptide Y in cardiovascular nerves and adrenal gland induced by sympatholytic drugs.

Neuropeptide Y (NPY) is a recently isolated vasoactive peptide, which is present, together with catecholamines, in sympathetic nerves and in the adrenal medulla. In the present study, we report that pretreatment with sympatholytic agents influences the tissue levels of NPY-like immunoreactivity (NPY-LI) in the guinea-pig. Thus, 24 h after reserpine not only noradrenaline (NA), but also NPY-LI, was depleted in the heart, spleen and the adrenal gland. The levels of NPY-LI in the vas deferens and stellate ganglia, however, were unaffected by reserpine in spite of marked depletions of NA. The reserpine-induced depletion of NPY-LI was probably caused by enhanced nerve-impulse flow and subsequent release from cardiovascular nerves in excess of resupply, since it could be prevented by the ganglionic-blocking agent chlorisondamine. Long-term (6 days) treatment with chlorisondamine reduced the levels of NPY-LI in the stellate ganglion. Short-term treatment (48 h) with guanethidine partially prevented the reserpine-induced depletion of NPY-LI, probably due to inhibition of NPY release. Long-term guanethidine treatment depleted not only NA, but also NPY-LI from the spleen. Pretreatment with the alpha-receptor antagonist phenoxybenzamine did not influence the NA levels but reduced the content of NPY-LI in the spleen via a mechanism that was dependent on intact ganglionic transmission. Since NPY has several cardiovascular actions, changes in NPY mechanisms may contribute to the pharmacological and therapeutical effects of sympatholytic agents.

Adrenal Glands↗

PubMed1991

Role of ventrolateral medulla in sympatholytic effect of 8-OHDPAT in rats.

In halothane-anesthetized, paralyzed, and artificially ventilated rats, the putative 5-hydroxytryptamine1A receptor agonist 8-OHDPAT (13.1 micrograms/kg iv) produced hypotension (-14.6 +/- 1.3 mmHg, n = 35), reduced lumbar sympathetic nerve discharge (SND, -17.8%, n = 35), and slowed the discharge rate of sympathoexcitatory neurons recorded in the rostroventrolateral medulla (RVLM, -17.6%, n = 20). The gain of the baroreflex was unaffected by the drug, but SND and RVLM unit discharges were silenced at significantly reduced levels of mean arterial pressure (MAP; 153 vs. 171 mmHg for SND, 155 vs. 172 mmHg for RVLM cells). Subsequent intravenous administration of the alpha 2-adrenergic receptor agonist clonidine (5.3 micrograms/kg) produced an additional decrease in MAP (-21.2 +/- 1.9 mmHg, n = 24) and SND (-24%, n = 24), Bilateral microinjections of 8-OHDPAT into the RVLM (1 nmol/side, n = 9) or into the raphe pallidus-obscurus (2 injections of 1 nmol each, n = 7) also produced hypotension (-22.9 +/- 3.2 and -14.4 +/- 2.8 mmHg, respectively) and sympathoinhibition (-39.1 and -24.6%, respectively). Bilateral microinjection into RVLM of the alpha 2-adrenergic antagonists idazoxan (16 nmol/side, n = 6) or rauwolscine (2 nmol/side, n = 6) attenuated the sympatholytic effect of both 8-OHDPAT (13.1 micrograms/kg, iv) and clonidine (5.3 micrograms/kg iv). These results suggest that 8-OHDPAT may exert a portion of its central sympatholytic effect by activating alpha 2-adrenergic receptors in the rostroventral medulla.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1976

Angina in hypertensive patients. With particular reference to the negative chronotropic effects of sympatholytic therapy.

There was no significant difference in the blood pressure and heart rate response of hypertensive patients with and without angina to standardised exercise on a treadmill before and after anti-hypertensive treatment. There was no improvement in exercise tolerance in the hypertensive patients with angina treated with bethanidine, debrisoquine or guanethidine despite a reduction of resting and exercise heart rates after treatment. The negative chronotropic effect of these sympatholytic drugs was less than that of oxprenolol or propranolol, but the hypotensive response was greater. Both of these beta-receptor blocking drug produced an an improvement in exercise tolerance in patients with angina either alone or in combination with other hypotensive therapy. The best control of blood pressure and angina was often achieved by a combination of a sympatholytic drug and beta-receptor blocking drug. In hypertensive patients treated for several years, angina at presentation was occassionally reduced by reduction of blood pressure. Later onset of angina appeared to be unrelated to control of hypertension but to be due to coincidental coronary occlusion. There was no evidence that myocardial infarction was precipitated by postural or exercise hypotension although these effects occasionally precipitated angina.

Adrenergic beta-Antagonists↗

PubMed1991

Sympatholytic action of yohimbine mediated by 5-HT1A receptors.

The present study determined the mechanism by which yohimbine inhibits sympathetic nerve activity in the anesthetized cat. Low i.v. doses of yohimbine increased inferior cardiac nerve discharge as a result of the alpha 2-adrenoceptor antagonist properties of the drug. Higher doses of yohimbine (0.8-1.6 mg/kg) inhibited sympathetic nerve discharge. The inhibition of nerve activity was reversed by i.v. administration of the 5HT1A receptor antagonist spiperone. Similarly we have previously observed spiperone reversal of the sympatholytic effects of the 5-HT1A agonist 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin) but failed to affect nerve activity when given alone. Spiperone failed to reverse the sympatholytic effect of clonidine. These data indicate that high doses of yohimbine inhibit sympathetic nerve activity via a 5HT1A agonist action.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

[Cardiovascular reactivity to isometric stress in patients with stable and borderline hypertension and in normotensive subjects. Effects of alpha sympatholytics and beta blocking agents].

Aim of the study was to evaluate blood pressure (BP) and heart rate (HR) variability during isometric handgrip test (IHT) in 20 ambulant non-obese male adults affected by sustained hypertension (SH) WHO I and II, 20 borderline hypertensive (BH) and 20 normotensives (C) of comparable sex, age and BMI. SBP and DBP were assessed by "Random Zero" sphygmomanometer, HR by ECG registration. IHT was performed at 30% of maximal effort for 3 min. IHT was carried out: 1) after 7 days placebo, 2) after 7 days propranolol treatment (80 mg/day) and, following 10 days wash-out, 3) after 7 days prazosin treatment (0.5 mg/day). After placebo IHT caused increases of SBP, DBP and HR values insignificantly different in the 3 groups. After propranolol IHT induced significantly more elevated SBP and DBP increases in SH than in BH or in C. These increases were significantly more elevated in comparison with those observed, in advance, in the same group of SH subjects after placebo. After prazosin treatment SBP increase induced by IHT was, on the contrary, significantly more elevated in BH than in SH or in C. This increase is more significant in comparison with that observed in the same BH group after placebo treatment. As for DBP variations induced by IHT after alpha sympatholytic therapy we have observed that SH subjects show significantly lesser diastolic variations as compared with those obtained in BH or in C groups after this treatment. In conclusion, enhanced IHT induced SBP elevation after propranolol and dampened DBP reactivity after prazosin suggest an overriding alpha stimulation in SH subjects. SBP hyperreactivity induced by IHT after alpha sympatholytic treatment and DBP hyporeactivity after betablockers emphasize the role of beta stimulation in BH individuals. Inhibition of BP reactivity to IHT in C after prazosin suggest that this one is mediated by alpha adrenergic receptors.

Adult↗

PubMed1976

The influence of some sympatholytic, parasympatholytic and serotonin-synthesis-inhibiting agents on the ultrastructure of the rabbit pineal organ.

The influence of certain drugs on the ultrastructure of rabbit pinealocytes was studied. The results obtained after administration of p-chlorophenylalanine and p-chloroamphetamine support the hypothesis proposed earlier that the smooth endoplasmic reticulum in the light pinealocytes is involved in indoleamine synthesis. The administration of either one of the sympatholytic agents, 6-hydroxydopamine or alpha-methyl-p-tyrosine, induced typical fine structural changes corresponding to those observed after surgical sympathectomy.

5-Hydroxytryptophan↗

PubMed1986

7-(Trifluoromethyl)-4-aminoquinoline hypotensives: novel peripheral sympatholytics.

A family of 7-(trifluoromethyl)-4-aminoquinolines that are hypotensive agents and that act by a novel sympatholytic mechanism is described. Structure-activity relationships in this series have been elucidated. Some of the more potent hypotensives were evaluated for safety in the mouse. A candidate, 1-[(4-fluorophenyl)sulfonyl]-4-[4-[[7-(trifluoromethyl)-4- quinolinyl]amino]benzoyl]piperazine hydrochloride (losulazine hydrochloride) has been selected for clinical development. Losulazine hydrochloride is a hypotensive agent in the rat, cat, and dog. At acute effective hypotensive doses, it does not block the response of the sympathetic nervous system to stimuli. Both animal pharmacology and clinical experience suggest that losulazine hydrochloride may be free of the clinically limiting side effects that often plague compounds that decrease blood pressure by interfering with autonomic neurogenic function.

Aminoquinolines↗

PubMed1990

Omega-conotoxin GVIA, the N-type calcium channel inhibitor, is sympatholytic but not vagolytic: consequences for hemodynamics and autonomic reflexes in conscious rabbits.

We investigated the effects of the N-type calcium channel blocking agent, omega-conotoxin GVIA, on the resting hemodynamics and on some autonomic reflexes in the conscious rabbit. omega-Conotoxin 3 and 10 micrograms/kg i.v. reduced mean arterial blood pressure by 16 +/- 2 and 25 +/- 3 mm Hg, respectively, over 30 min accompanied by a tachycardia. Renal vascular conductance (Doppler flowmeter) increased by 27.6 +/- 3.7 and 38.6 +/- 10.3% at 30 min after omega-conotoxin 3 and 10 micrograms/kg, respectively. Vasodilatation was also observed but to a lesser extent in the hindquarter and mesenteric vascular beds. The baroreceptor-heart rate reflex was evoked by a drug method (bolus injection of sodium nitroprusside and phenylephrine) and by inflation of perivascular balloons implanted on the thoracic vena cava and aorta. omega-Conotoxin (3 micrograms/kg) abolished the sympathetic component of the cardiac baroreceptor reflex without affecting vagal efferent activity. In addition, marked vagal-mediated bradycardia from (a) the "Bezold-Jarisch-like" reflex evoked by serotonin (1-10 micrograms/kg i.v.) and (b) the nasopharyngeal reflex evoked by cigarette smoke were unaffected by omega-conotoxin (3-10 micrograms/kg). We conclude that omega-conotoxin-induced N-type calcium channel blockade abolishes sympathetic but not vagal cardiac efferent activity. The hypotension and peripheral vasodilatation are probably due to the prejunctional sympatholytic action of the peptide. These N-type calcium channels are thus limited to the sympathetic varicosities in the rabbit.

Analysis of Variance↗

PubMedDate not supplied

The effects of sympatholytic drugs on the cardiovascular response to tilting in anaesthetized cats.

1. Using cats anaesthetized with chloralose and urethane, comparison was made of the abilities of several antihypertensive and sympatholytic drugs to lower systemic blood pressure, and to depress the compensatory cardiovascular responses to bilateral carotid occlusion and to 45 degrees head-up tilting. Similar comparisons were also made of the effects of these drugs on the perfusion pressure of the vascularly isolated autoperfused hindquarters, and the response of this to carotid occlusion and tilting. The effects of bilateral vagotomy and haemorrhage on these responses were also studied. 2. It was found that hypotensive doses of both bretylium and guanethidine (3.0 mg/kg, i.v.) markedly depressed the ability of cats to restore their systemic blood pressure and to constrict their hindquarters vasculature during tilting. Both drugs depressed the carotid occlusion reflex in the systemic, but not in the hindquarters, circulation. Neither propranolol, 2.0 mg/kg, i.v., nor bilaterial vagotomy had any effect on these parameters and haemorrhage sufficient to cause marked hypotension was without effect on the systemic responses to carotid occlusion or tilting. 3. Clonidine (1.0, 5.0 and 25 microgram/kg, i.v.), xylazine (62.5, 125 and 250 microgram/kg, i.v.) and reserpine (0.5 and 2.0 mg/kg, i.v.) all caused considerable hypotension but had no effect on the response to tilting of the systemic circulation, apart from somewhat prolonging recovering time. The highest dose of clonidine moderately depressed the hindquarters perfusion pressure, and the response of this to tilting. 4. Clonidine (5.0 and 25 microgram/kg, i.v.) and xylazine (125 and 250 microgram/kg, i.v.) depressed the systemic pressor responses elicited by the ganglion stimulants DMPP and McN-A-343. This may indicate that the ability of clonidine to prolong the pressure recovery during tilt may be due to impaired peripheral sympathetic transmission. 5. It is concluded that drugs which significantly reduce the compensatory pressure reponses to tilting in anaesthetized cats may also cause postural disturbances in man, whilst drugs which merely prolong the period required for pressure compensation seem much less likely to cause serious clinical impairment of orthostatic reflexes. It appears that the cardiovascular response to bilateral carotid occlusion may not provide a good index of the integrity of orthostatic reflexes.

Animals↗

PubMed1988

Side effects of sympatholytic antihypertensive drugs.

Antihypertensive drugs with pharmacological action due to sympatholytic activity have been second only to diuretics in their use and efficacy in normalizing blood pressure. Their pharmacological actions have resulted in the notable absence of chemical toxicity, but because of symptomatic side effects, their use has been limited relative to some of the newer antihypertensive agents. Most prominent among undesirable side effects are the central nervous system findings of sedation, altered thought process, depression, and orthostatic or exercise hypotension. Sexual problems, especially in men, are also prominent. Special toxicity is discussed with reference to methyldopa, clonidine, monoamine oxidase inhibitors, and metyrosine.

Female↗

PubMedDate not supplied

[The effect of sympatholytics and adrenergic receptor blockade on the histophysiology of the insular apparatus of the pancreas and insulin sensitivity of white rats].

Experiments were conducted on 200 male albino rats. It was shown that prolonged administration of sympatholytics (ornide or actadine) and also of a blocker of the alpha-adrenorecptors with phentholamine or of beta-adrenoreceptors with inderal led to the accumulation of zinc in the cytoplasm of beta-cells, reduction of the content in them of specific aldehyde-fuchsinophilic granularity, neoformation of the islands of Langerhans and to increase in the animal sensitivity to the exogenous insulin.

Animals↗

PubMed1975

Effects of sympatholytic agents on amanita phalloides toxicity in the rat.

Some sympatholytic agents have been tested for the ability to counteract either the hepatotoxic or the lethal effect of A. phalloides in rats. Propranolol displayed a marked preventive action on the liver damage induced by the poison, but only a moderate influence on the lethality. Reserpine was uneffective in terms of liver derangement, but exerted some protection against the general toxic effect of A. phalloides. Other alpha- or beta-adrenolytic compounds failed to afford any significant protection with respect to both liver injury and lethality. It is suggested that propranolol might interfere with transport or binding of phallotoxins to the liver.

Acid Phosphatase↗