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PubMed1977

The transient anti-hypertensive effect of phentolamine in patients receiving beta-blocker treatment.

In seven hypertensives receiving beta-blocker drugs, and additional reduction in standing blood pressure occurred between 60 and 90 minutes after 40 mg phentolamine by mouth. The occurrence of the postural hypotensive effect was delayed in relation to the reported time of peak plasma concentration of unchanged phentolamine. Supine blood pressure and heart rate were unaffected. Phentolamine has no clinically useful anti-hypertensive effect in conjunction with beta-blockers in patients with essential hypertension.

Adult↗
PubMed1989

Characterization of a novel alpha 1-adrenoceptor antagonist, SGB-1534, in contractile response of isolated canine arterial and venous smooth muscle to exogenous noradrenaline: comparison with prazosin, phentolamine and yohimbine.

The pharmacological properties of SGB-1534, 3-[2-[4-[(o-methoxyphenyl)-1-piperazinyl]ethyl]-2,4(1H,3H)- quinazolinedione monohydrochloride, a selective alpha 1-adrenoceptor antagonist, compared with prazosin, phentolamine and yohimbine, were examined in contractile responses of isolated canine mesenteric arteries and veins and femoral arteries and veins to exogenous noradrenaline. The arteries and veins concentration-dependently contracted when exposed to noradrenaline. The sensitivity to noradrenaline, when compared in terms of pD2 values, was significantly higher in the veins than in the arteries. Phentolamine and yohimbine were competitive antagonists against noradrenaline in the arteries and the veins. SGB-1534 and prazosin caused a parallel shift to the right of the concentration-response curves for noradrenaline only in the arteries: the two antagonists were less effective in the veins than in the arteries when low concentrations of noradrenaline were applied. The pharmacological characteristics of SGB-1534 resemble those of prazosin. The pA2 values for SGB-1534 against noradrenaline in the arteries were much higher than those for prazosin, phentolamine and yohimbine. The result indicates that SGB-1534 may predominantly act upon arterial resistance vessels rather than the venous side, resulting in potent hypotension.

Adrenergic alpha-Antagonists↗
PubMed1977

[Effect of phentolamine on the catecholamine output from the perifused pig adrenal medulla in response to infusions of acetylcholine (author's transl)].

The effect of phentolamine (regitine) on the in vitro release of catecholamines from adrenal medulla has been studied. Firstly, a continuous flow incubation (perifusion) system was developed in which secretory responses of adrenal medulla to acetylcholine were characterized by serial fluorimetric assay of catecholamine in the effluent medium. There was an initial massive release of catecholamine, which in the absence of acetylcholine, declined to a low basal level. The basal level was stable. Following 2.5 h preincubation, catecholamine release rose abruptly after addition of 10(-2) M acetylcholine to the medium and returned promptly to baseline after withdrawal. Pretreatment of pig adrenal medulla with 10(-2) M phentalamine blocked the increase of catecholamine overflow by 10(-2) M acetylcholine. It was also found that phentolamine, itself, caused no effect on catecholamine release from adrenal medulla. These results show that phentolamine blocked the catecholamine release from perifused pig adrenal medulla in response to acetylcholine infusion.

Acetylcholine↗
PubMed1988

Augmentation of glucose induced insulin secretion by pertussis vaccine, phentolamine and benextramine: involvement of mechanisms additional to prevention of the inhibitory actions of catecholamines in rats.

Pertussis vaccine, pertussis toxin, and the alpha-adrenoceptor blocking drug phentolamine augment glucose-induced insulin secretion. The present study was carried out to determine the relationship between this action and the ability of these agents to prevent the inhibitory actions of adrenaline. Pertussis vaccine augmented glucose-induced insulin secretion in rat islets ex vivo and prevented the inhibitory actions of adrenaline and clonidine. Incubation of islets with phentolamine or the irreversible alpha-adrenoceptor blocking agent benextramine also augmented glucose-induced insulin secretion. However, the alpha-adrenoceptor blocking drugs idazoxan, yohimbine or phenoxybenzamine, in concentrations that prevented the inhibitory effects of adrenaline and/or clonidine, did not modify glucose-induced insulin release in vitro. Benextramine (1 X 10(-5) mol/l) blocked the inhibitory effect of clonidine, whilst having no significant effect on the response to adrenaline. It is concluded that stimulation of insulin secretion by certain alpha-adrenoceptor blocking drugs can be dissociated from their alpha-adrenoceptor properties. The ability of pertussis vaccine, phentolamine or benextramine to augment glucose-induced insulin release in vitro is unlikely to be due to the prevention of the inhibitory action of endogenous catecholamines.

Adrenergic alpha-Antagonists↗
PubMed1980

Effects of tiodazosin, praxosin, trimazosin and phentolamine on blood pressure, heart rate and on pre- and postsynaptic alpha-adrenergic receptors in the rat.

Subcutaneous administration of tiodazosin (0.1-3 mg/kg), prazosin (0.01-1 mg/kg), trimazosin (10-30 mg/kg) and phentolamine (0.1-3 mg/kg) to conscious spontaneously hypertensive rats (SHR) produced graded decreases in blood pressure with the order of potency being prazosin > tiodazosin > phentolamine > trimazosin. Heart rate was elevated predominantly only by phentolamine and this was consistent with the activity of this agent for both pre- and postsynaptic alpha-adrenergic receptors. In contrast, tiodazosin, prazosin and trimazosin showed selectivity only for postsynaptic alpha-adrenergic receptors. Acute oral administration of tiodazosin and prazosin indicated tiodazosin to be about 1/2 as potent as prazosin. However, chronic administration of equivalent doses of the two compounds for 25 and 52 days via the drinking water indicated approxiately equivalent, sustained reductions in blood pressure. Furthermore, at the end of the 52-day chronic dosing period tiodazosin caused appreciably less alpha-adrenergic receptor antagonist activity than prazosin as assessed by the norepinephrine dose-pressor response profiles. These results indicate that following chronic dosing with tiodazosin in the rat other mechanisms besides alpha-adrenergic receptor antagonist activity are probably contributing to the antihypertensive effect in the rat.

Administration, Oral↗
PubMed1976

Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood.

The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

Animals↗
PubMed1979

Primary pulmonary hypertension treated with oral phentolamine.

A patient with symptomatic primary pulmonary artery hypertension underwent therapeutic trials with parenteral and oral phentolamine. Before drug therapy, he manifested marked increases in pulmonary artery pressure and pulmonary arteriolar resistance during exercise. This hypertensive response to exercise was significantly attenuated by parenteral phentolamine. He also manifested sustained hemodynamic improvement with the same degree of attenuation of exercise-induced increases in pulmonary artery pressure and pulmonary arteriolar resistance 7 months after initiation of therapy with oral phentolamine. Twenty months after initiation of therapy, the patient continues to enjoy symptomatic improvement with a marked increase in exercise tolerance.

Administration, Oral↗
PubMed1976

[Mechanism of the cardiotonic effect of alpha-adrenoblockade by phentolamine].

In canine experiments with recording intraventricular pressure and its first derivative, with electromagnetic flowmetry and thermodilution it has been demonstrated that controlled Phentolamine-induced alpha-adrenergic block results in an increase of the cardiac output, heart rate, myocardial contractility index, and, at the same time, in a reduction of the total vascular resistance, arterial pressure, intraventricular pressure and heart work. The beneficial chronotropic effect of Phentolamine was shown not to depend on its suggested "central" action, to be not determined by reflex stimulation of the cardiac activity due to systemic hypotension, but to be brought about by a block of the myocardial alpha-adrenergic receptors and a moderate activation of beta-adrenergic receptors. The concept of the untoward chronotropic effects being mediated by myocardial alpha-adrenoreceptors is being substantiated. The mechanism of the beneficial inotropic effect of Phentolamine may be based on the stimulation of beta-receptors, concomitant tachycardia, and, probably, the effect of the "centrai" action of the drug.

Animals↗
PubMed1997

[Effect of phentolamine on portal pressure in cirrhotic patients with portal hypertension].

Changes of hepatic venous wedge pressure (WHVP) and portal venous pressure (PVP) in fourteen patients with postnecrotic cirrhosis proved pathologically and seven patients with colon carcinoma without hepatopathy were observed before and after the infusion of alpha-adrenergic receptor antagonist phentolamine from peripheral venous. The results indicate that phentolamine can reduce WHVP and PVP of cirrhotic patients with portal hypertension efficiently (0.56-0.63 kPa, 0.42-0.50 kPa, respectively, P < 0.01), but it effects arterial diastolic pressure and heart rate simultaneously (arterial diastolic pressure reduced by 0.94-10.7 kPa, while heart rate increased by 8.67-10.67 per minute). Phentolamine doec not reduce portal pressure on patients without portal hypertension.

Adrenergic alpha-Antagonists↗
PubMed1999

Chronic neurogenic facial pain: lack of response to intravenous phentolamine.

AIMS: Chronic neurogenic facial pain is commonly resistant to treatment and is often the source of significant patient morbidity. Adrenergic mechanisms are postulated to play a role in producing this type of pain, and adrenergic blocking agents are frequently used in clinical practice for pain control therapy. The analgesic effectiveness of an adrenergic blocking agent, intravenous phentolamine, was compared to saline and intravenous lidocaine in the present study using a single-blind protocol in patients with chronic neurogenic facial pain. METHODS: Thirty patients were studied whose common clinical features included pain for more than 6 months, unilateral trigeminal distribution, constant dysesthesia, and no evidence of pathology or known etiology. Phentolamine (30 mg), lidocaine (100 mg), and saline were each infused over periods of 5 to 10 minutes. Pain ratings were assessed every 4 minutes throughout each study period using a 10-point pain intensity scale. RESULTS: No patient reported subjective improvement of pain during or immediately following phentolamine or saline infusions alone. Sixteen of the 30 patients reported decreased pain following lidocaine infusion. In the majority of the patients, the duration of lidocaine analgesia was less than 30 minutes; however, some patients reported decreased pain for a longer time. CONCLUSION: The results do not support an adrenergic mechanism for chronic neurogenic facial pain. The response to lidocaine, a nonadrenergic, membrane-stabilizing agent, suggests that it may have clinical effectiveness in certain neurogenic facial pain patients.

Adrenergic alpha-Antagonists↗
PubMed1978

[Comparison of the effects of phentolamine and trinitrine in the treatment of left ventricular failure during the acute phase of myocardial infarct].

Two groups of 10 patients with left ventricular failure during the acute phase of myocardial infarction were studied. One group were given phentolamine, the other trinitrin. The infusion rate was regulated so that the heart rate was not increased by more than 10 beats per minute, and to obtain a pulmonary arterial diastolic pressure less than 18 mmHg with a mean systemic arterial pressure remaining greater than or equal to 80 mmHg. The dose of phentolamine was 5 +/- 3 mcg/kg/mn, but using trinitrin the initial optimal dose of 0.39 +/- 0.22 mcg/kg/mn had to be progressively increased during the first 24 hours. The haemodynamic study done before treatment and after an hour at the optimal infusion rate showed that, for a similar reduction in the pulmonary arterial diastolic pressure, the mean systemic arterial pressure was reduced less by trinitrin than by phentolamine, while the stroke work index was not appreciably altered by either drug. In patients with low systemic arterial pressure, trinitrin appears to be preferable and warrants use after the possible setting up of circulatory assistance by aortic counter-pulsation.

Adult↗
PubMed2001

[Intracavernous auto-injection therapy with papaverine phentolamine via an auto-injection pen for patients with an erectile dysfunction: similar results achieved in family practice and urology].

OBJECTIVE: To determine the results of an auto-injection therapy with papaverine-phentolamine (using an auto-injection pen) prescribed by a GP or a urologist, in patients with erectile dysfunction. DESIGN: Prospective, comparative, descriptive. METHOD: A total of 603 men with erectile dysfunction who were prescribed papaverine-phentolamine auto-injection by 59 GPs and 76 urologists participated in the study. The physician completed a questionnaire at the first visit and during the three follow-up visits (the last at 6 months) and the patient kept a diary and gave a satisfaction score on a nine-point scale. RESULTS: The cause of the erectile dysfunction was most commonly psychogenic/mixed somatic-psychogenic in the GP group and most commonly vascular in the urologist group (p > 0.05). The somatic comorbidity was the same (70%), whereas the prevalence of psychological symptoms differed (GP group: 6%; urologist group: 7%; p < 0.001). Attendance at all of the follow-up examinations was 38% for the GP group and 17% for the urologist group. The mean starting dose in the GP group was 0.49 ml and in the urologist group 0.70 ml (p < 0.001). The mean end dose was the same (about 1 ml). The frequency of adverse reactions was 9%: haematoma (5%), prolonged erection (1.8%). During the course of the investigation, 38% of the patients (31% in the GP group; 40% in the urologist group) discontinued the treatment owing to a limited effect, adverse reactions, difficult administration or problems related to the partner. In both the GP and the urologist group, 72% of the patients and 77% of the partners were satisfied or very satisfied with the auto-injection pen treatment. The patient's mean satisfaction score was 7.2. CONCLUSION: Whether the patient was treated by a GP or a urologist, the auto-injection therapy with papaverine-phentolamine for erectile dysfunction, using an auto-injection pen, was well tolerated and was highly appreciated by both the patients and their partners. Nevertheless one third of the patients discontinued the treatment prior to the end of the study. The mean end dose of the medication was the same in both groups.

Adrenergic alpha-Antagonists↗
PubMed1975

The morphologic effects of simultaneous infusion of levarterenol and phentolamine on the canine myocardium.

The effect of simultaneous administration of levarterenol and phentolamine on the myocardium over a 3 hour period was studied in 15 adult mongrel dogs. All animals receiving levarterenol alone had moderate-to-severe subendocardial hemorrhage and necrosis. Four of the 6 animals receiving the simultaneous infusion of levarterenol and phentolamine had little or no hemorrhage or necrosis. These differences are significant (p less than 0.02). It is concluded that the administration of phentolamine simultaneously with levarterenol affords a significant protective effect on the myocardium.

Animals↗
PubMed1992

Protective effects of berberine and phentolamine on myocardial reoxygenation damage.

The protective effects of berberine and phentolamine against anoxia and reoxygenation damage in isolated rat hearts have been investigated. Incorporation of berberine (24.5 mumol/L) in both anoxic and aerobic perfusion media resulted in a significant reduction of CPK release during the reoxygenation period, and the ultrastructural damage was reduced as compared with the control group; the myocytes in the berberine-treated group displayed mild intracellular edema, well-registered myofibrils without contracted bands, and swollen mitochondria with partially broken cristae but without dense bodies. Berberine did not inhibit calcium and sodium accumulation or magnesium and potassium loss. Treatment with phentolamine (6.6 mumol/L), an alpha-adrenoceptor antagonist, had similar effects, though the CPK release profile was shifted to the right and downwards. These results suggest that although berberine and phentolamine have some beneficial effects on myocardial reoxygenation injury, they may not abolish the injury. Therefore alpha-adrenoceptor stimulation may not be the major mechanism behind the injury.

Adrenergic alpha-Antagonists↗
PubMed1990

[Effect of phentolamine in combination with pituitrin on the hepatic and systemic hemodynamics].

This experimental study was aimed at the effect of phentolamine used separately or in combination with pituitrin on hepatic and systemic hemodynamics in cirrhotic portal hypertensive dogs. The results showed that either of these drugs used separately could lead to reduction of portal venous pressure. Each of the drugs could also cause by-effect on systemic hemodynamics, or reduce hepatic blood flow. When phentolamine was used in combination with pituitrin no side effect was found in hepatic and systemic hemodynamics. It was suggested that phentolamine used in combination with pituitrin could efficiently decrease portal hypertension and counteract the side-effects. It would be useful in treatment of bleeding from esophageal variceal rupture in cirrhotic patients with portal hypertension.

Animals↗
PubMed1975

Effects of phentolamine on dibutyryl cyclic AMP and norepinephrine in rats anesthetized with amobarbital.

In vitro evidence demonstrated that norepinephrine (NE) increased endogenous levels of cyclic AMP in brain tissue. In vivo findings showed that in rats anesthetized with amobarbital, NE certrally administered prolonged narcosis whereas exogenous dibutyryl cyclic AMP shortened it. Phentolamine, an alpha adrenergic receptor inhibitor, administered centrally prolonged narcosis but did block all symptomatology accompanying its administration. Phentolamine added to dibutyryl cyclic AMP dose-relatedly antagonized the shortening of the duration of narcosis. Such ovservations suggest that whereas the inhibitory action of phentolamine affects NE at the alpha adrenergic receptor site, it antagonizes cyclic AMP at other sites as well.

Amobarbital↗
PubMed1991

[Combination of phentolamine and angelicini in cholestasis and severe type of chronic active hepatitis B].

Among 60 patients with chronic active hepatitis B, 43 were of the severe type, 17 were of cholestasis type. Each type was divided randomly into two groups: therapeutic and control. The former received both conventional supporting therapy and combination of phentolamine (20-30 mg/day) and angelicini (150-450 mg/day). The latter was only treated with conventional supporting therapy. Digital subtraction angiography (DSA) and platelet agglutination test were performed in 10 patients respectively. DSA demonstrated that liver sinusoids were expanded and the vascular bed round the sinusoids were also enlarged in diameter following instillation of phentolamine. It was also shown that angelicini could suppress the second phase of platelet agglutination. These indicated that phentolamine and angelicini could improve the liver microcirculation in different way. The incidence of survival between therapeutic and the control group was 57.14% and 31.82% respectively (P less than 0.05).

Adult↗
PubMed1985

Effect of alpha-adrenoceptor antagonists (phentolamine, nicergoline and prazosin) on reperfusion arrhythmias and noradrenaline release in perfused rat heart.

Rat isolated hearts were perfused through the left atrium with a modified Krebs-Henseleit solution or mounted on a Langendorff perfusion system. The hearts were prelabelled with [3H]-noradrenaline [( 3H]-NA) and the left main coronary artery was ligated for 10 min after which reperfusion followed. The liberation of [3H]-NA and the development of ventricular tachycardia and fibrillation were monitored throughout. During the occlusion period, ventricular arrhythmias did not occur and heart rate was not significantly altered in the control series. In contrast, reperfusion was followed by ventricular fibrillation and ventricular tachycardia in all the hearts in the control series (Langendorff or 'working' models). The alpha-adrenoceptor antagonists phentolamine (7.1 X 10(-6) M and 7.1 X 10(-5) M) and nicergoline (3.1 X 10(-6) M) diminished or prevented reperfusion arrhythmias. However, prazosin (5.2 X 10(-6) M) was not effective. The lower concentration of phentolamine did not alter the pattern of [3H]-NA release, whereas, high doses of phentolamine and nicergoline increased the release of [3H]-NA. Prazosin (5.2 X 10(-6) M) caused a very marked increase in release of [3H]-NA but was not antiarrhythmic. A 'membrane-stabilizing' effect seems the most appropriate explanation for these antiarrhythmic effects of alpha-antagonist agents.

Adrenergic alpha-Antagonists↗