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PubMed1969

Renal actions of dihydroergocristine and of phentolamine in anaesthetized cats.

1. Comparison has been made of the effects of dihydroergocristine (DCS) and phentolamine mesylate (phentolamine) on cardiac and respiratory rates, systemic arterial pressure, renal clearances of creatinine (C(Cr)) and of p-amino-hippuric acid (C(PAH)) and on the secretion of Na and K, in cats under chloralose anaesthesia.2. Phentolamine antagonized vasomotor tone and the pressor effect of circulating noradrenaline to comparable extent. The extent of reduction in urine flow, C(Cr), C(PAH) and Na excretion correlated with the fall in mean arterial pressure. Innervated and denervated kidneys responded similarly. Cardiac and respiratory rates rose slightly as arterial pressure fell.3. DCS, 10 to 20 mug/kg per min, did not reduce vasomotor tone, markedly reduced the pressor effect of exogenous noradrenaline, caused bradycardia and respiratory slowing but had little or no effect on renal function.4. DCS, 30 to 40 mug/kg per min, lowered mean arterial pressure by 15-25 mm Hg, decreased C(PAH) but not C(Cr), so raising the filtration fraction and caused a small reduction in urine flow and in Na excretion. Innervated and acutely denervated kidneys responded similarly.5. DCS, 30 to 40 mug/kg per min, raised mean arterial pressure, decreased C(PAH), urine flow and Na excretion but did not alter C(Cr) in animals pretreated with full alpha-adrenergic blocking doses of phentolamine.6. DCS, 30 to 40 mug/kg per min, increased the rate of secretion of sympathetic amines from the adrenal medulla and increased the concentration of renin in renal venous blood.7. Isolated kidneys perfused at constant pressure from pump-oxygenator circuits and in saline diuresis responded to DCS (15-17 mug/120 ml. blood) by diuresis and natriuresis and by a rise in the rate of secretion of renin. Higher concentrations of DCS (125-250 mug/120 ml.) were without effect on renal function and did not influence renin secretion.8. The renal effects of full alpha-adrenergic blocking doses of DCS and of phentolamine were comparable, in the whole animal.9. The evidence indicates that the release of noradrenaline by DCS 30-40 mug/kg per min from nerve terminals supplying the juxtaglomerular apparatus may have caused the enhancement of renin secretion.

Adrenal Medulla↗
PubMed1971

Myocardial and haemodynamic effects of phentolamine.

1. In cats anaesthetized with pentobarbitone, intravenous infusions of phentolamine ((10-50 mug/kg)/min for 5 min) increased heart rate, left ventricular dp/dt max (without increasing end-diastolic pressure), aortic dp/dt, cardiac output, myocardial blood flow and metabolic heat production.2. Phentolamine-induced increases in myocardial contractility occurred irrespective of the direction or magnitude of the blood pressure change and were maintained well beyond the actual infusion period.3. In cats treated with alprenolol, bretylium or reserpine there was no evidence of increased cardiac contractility following phentolamine administration.4. It is concluded that phentolamine, in doses less than those required to produce significant alpha-adrenoceptor blockade, increased myocardial contractility through an effect on the sympathetic nervous system.

Adrenergic beta-Antagonists↗
PubMed1974

Protection by phentolamine against the effects of phenoxybenzamine on transmitter release elicited by nerve stimulation in the perfused cat heart.

1 The effects of cocaine, phentolamine and phenoxybenzamine on neuronal uptake of [(3)H]-noradrenaline and on (3)H-transmitter and noradrenaline overflow elicited by nerve stimulation were determined in the perfused heart of the cat.2 During perfusion with cocaine 3.4 x 10(-7)M, there was a 2-fold increase in transmitter overflow while neuronal uptake of [(3)H]-noradrenaline was inhibited by 31.3 +/- 2.1%.3 After exposure to phenoxybenzamine 8.7 x 10(-7)M for 20 min and washing with drug-free solution for 165 min there was an 8-fold increase in transmitter overflow during nerve stimulation. Under these conditions neuronal uptake of [(3)H]-noradrenaline was inhibited by only 17.5 +/- 5.4%.4 There was no significant change in transmitter overflow or in neuronal uptake of [(3)H]-noradrenaline, 155 min after a 30 min exposure to phentolamine (3.2 x 10(-5)M).5 Perfusion with phentolamine (3.2 x 10(-5)M) before and during exposure to phenoxybenzamine (8.7 x 10(-7)M), prevented the increase in transmitter overflow observed after perfusion with phenoxybenzamine alone.6 Protection by phentolamine against the effects of phenoxybenzamine supports the view that the effects on transmitter release obtained after perfusion with phenoxybenzamine are due to the blockade of presynaptic alpha-adrenoceptors which regulate transmitter release through a negative feed-back mechanism.

Animals↗
PubMed1980

Blockade of adrenaline-induced hyperglycaemia in the anaesthetized cat by continuous infusion of phentolamine and propranolol.

1 The effects of adrenoceptor blocking drugs on the metabolic responses to adrenaline infusion (1 microgram kg-1 min-1) have been studied in the anaesthetized, fasted cat. 2 Propranolol, in doses (0.25 or 1 mg/kg) which prevented completely adrenaline-induced tachycardia, reduced but did not abolish adrenaline-induced hyperglycaemia. 3 Phentolamine infusion, at a rate (15 micrograms kg-1 min-1 after a priming dose of 2.5 mg/kg) which reversed the pressor effect of adrenaline, reduced but did not abolish adrenaline-induced hyperglycaemia. 4 The continuous infusion of a combination of phentolamine (15 micrograms kg-1 min-1 after a priming dose of 2.5 mg/kg) and propranolol (5 micrograms kg-1 min-1 after a priming dose of 0.25 mg/kg) prevented completely the hyperglycaemia response to adrenaline infusion over a 6 h period. 5 The increase in blood lactate concentration produced by adrenaline was prevented completely by the combined infusion of propranolol and phentolamine but was not modified by phentolamine alone.

Anesthesia↗
PubMed1985

Comparison of the antagonistic effects of phentolamine on vasoconstrictor responses to exogenous and neurally released noradrenaline in vivo.

The antagonistic effects of the alpha-adrenoceptor blocking agent phentolamine on vasoconstrictor responses to intraluminal noradrenaline and lumbar sympathetic nerve stimulation were compared in the hindlimb of the anaesthetized dog. Sympathetic stimulation with 1 pulse or trains of 4-10 pulses at 0.4-40 Hz produced graded vasoconstrictor responses that were matched in amplitude by intra-arterial injections of 10(-8) - 10(-6) g noradrenaline. Phentolamine (0.5 mg kg-1 i.v.) attenuated amplitude-matched responses to both types of stimuli to quite similar extents. The extent of the effect of phentolamine on neurogenic responses was greater with 1 pulse stimulation than with trains, and greater with 4 pulse than with 10 pulse trains. The effect was maximal within 2 min of phentolamine administration and wore off in parallel with that on responses to injected noradrenaline. The results are consistent with the view that transmitter released from noradrenergic vasoconstrictor nerves acts primarily on subjunctional alpha-adrenoceptors.

Animals↗
PubMed1992

Pulmonary artery and aortic pressure changes during high intensity treadmill exercise in the horse: effect of frusemide and phentolamine.

Intravenous frusemide (1.0 mg/kg bwt) or phentolamine (0.33 mg/kg bwt) was given to 7 horses 1 h before exercise and their effects on pulmonary artery and aortic pressure changes during strenuous exercise were examined. Short-term near-maximal treadmill exercise (10 m/sec, 3 degrees incline) produced increases in heart rate, mean pulmonary artery pressure (PAP), mean aortic pressure (AP), and packed cell volume (PCV). Frusemide did not affect heart rate, PAP or PCV during exercise. Frusemide significantly decreased mean AP by 10 to 15 mmHg during exercise. Phentolamine produced an increase in heart rate relative to control only early in exercise but not during later, more strenuous, exercise. Phentolamine had no statistically significant effect on AP, PAP, or PCV, but a significant reduction was observed between 180 and 230 sec of exercise when PAP and AP were standardised against heart rate. Frusemide did not prevent horses from haemorrhaging during exercise in this study. Treatment with phentolamine did not sufficiently reduce the PAP and AP to test our hypothesis that a reduction in PAP and AP would eliminate EIPH.

Animals↗
PubMed1984

Presynaptic agonist effect of phentolamine in the rabbit vas deferens and rat cerebral cortex.

Clonidine inhibited the electrically-induced twitch response of the rabbit and rat isolated vas deferens preparations and also the K+-evoked release of [3H]noradrenaline from rat cortical slices. This effect of clonidine was antagonized competitively by yohimbine. Phentolamine inhibited the electrically-induced twitch response of the rabbit, but not the rat, vas deferens and in low concentrations (less than 0.1 microM) also inhibited the K+-evoked release of [3H]NA from rat cortical slices. These inhibitory effects of phentolamine were antagonized by yohimbine in a competitive manner but were not antagonized by indoramin, an alpha 1-adrenoceptor antagonist. In the rabbit vas deferens, the effects of phentolamine were shown not to be due to the stimulation of beta-, H1-, H2-, 5-HT- or muscarinic receptors. These results are consistent with the view that phentolamine can act as an agonist at presynaptic alpha 2-adrenoceptors in the rabbit vas deferens and rat cortex but not in the rat vas deferens.

Animals↗
PubMed1978

Competitive antagonism by phentolamine of responses to biogenic amines and the transmitter at a neuroglandular junction.

1. A quantitative study has been made of phentolamine's inhibition of the electrical and secretory responses of the isolated salivary glands of Nauphoeta cinerea Olivier to nerve stimulation and bath applications of agonists. 2. The results suggested that phentolamine is a competitive antagonist having an affinity constant of about 1 micrometer-1 for the receptors for dopamine, noradrenaline, adrenaline and the neurotransmitter. 3. Phentolamine also inhibited responses to 5-hydroxytryptamine in a manner seemingly more complex than competitive antagonism. Attempts to estimate the affinity constant gave values of about 0.08 and 0.015 microgram-1 for inhibition of the secretory and electrical responses respectively. 4. This investigation showed that phentolamine discriminates between two kinds of receptor in this gland, one binding 5-hydroxytryptamine and the other combining with catecholamines and the neurotransmitter.

Animals↗
PubMed1999

Antagonistic effects of phentolamine and octopamine on rhythmic motor output of crayfish thoracic ganglia.

Spontaneous rhythmic motor output of crayfish thoracic ganglia consists of bursts of activity in antagonistic leg motor neurons (MNs), alternating with a rather slow cycle period (typically > or = 20 s). The most common pattern (77% of preparations) consists of long coxal promotor bursts, the duration of which was correlated strongly with cycle period, and relatively short remotor bursts independent of cycle period. Octopamine, at a concentration of 2-30 microM reversibly retarded this rhythm, increasing both cycle period and promotor burst duration. Higher concentrations of octopamine inhibited promotor nerve activity and abolished rhythmic bursting. Phentolamine (10-50 microM) had the opposite effect of decreasing cycle period, mainly by decreasing promotor burst duration. Whereas in the presence of octopamine promotor bursts were lengthened and became even more strongly related to cycle period, phentolamine promoted a more symmetrical rhythm with shorter promotor bursts that were less dependent on cycle period. When octopamine was applied in the presence of phentolamine, there was no significant increase in cycle period or burst duration, although high octopamine concentrations (100 microM) were still capable of inhibiting promotor nerve activity. To our knowledge, pharmacological modulation of a spontaneous locomotor rhythm by an amine antagonist (applied by itself) has not been reported previously. The results raise the testable possibility that phentolamine exerts its modulatory effects by acting as an octopamine antagonist in crayfish thoracic ganglia.

Adrenergic alpha-Agonists↗
PubMed1997

Phentolamine prevents adaptation to ischemia during coronary angioplasty: role of alpha-adrenergic receptors in ischemic preconditioning.

BACKGROUND: Experimental studies indicate that alpha-adrenergic receptors are involved in ischemic preconditioning. Their role in humans is unknown. METHODS AND RESULTS: Eighteen patients undergoing angioplasty for an isolated stenosis of the left anterior descending coronary artery were randomized to receive intravenous infusion of phentolamine or placebo during the procedure. Intracoronary ECG and cardiac pain were determined at the end of the first two balloon inflations. Average peak velocity in the contralateral coronary artery during balloon occlusion, an index of collateral recruitment, was also assessed by using a Doppler guide wire. In both phentolamine- and placebo-treated patients, average peak velocity significantly increased from baseline to the end of the first inflation (P<.01), but it did not show any further increase during the second inflation. In phentolamine-treated patients, ST-segment changes and cardiac pain severity during the second inflation were similar to those observed during the first inflation (13+/-9 versus 12+/-8 mm, P=NS, and 51+/-34 versus 54+/-32 mm, P=NS, respectively), whereas in placebo-treated patients, they were significantly less (6+/-4 versus 13+/-7 mm, P<.01, and 26+/-20 versus 49+/-22 mm, P<.05, respectively). CONCLUSIONS: The adaptation to ischemia observed in humans after two sequential coronary balloon inflations is abolished by phentolamine and is independent of collateral recruitment. Thus, it occurs due to ischemic preconditioning and is, at least in part, mediated by alpha-adrenergic receptors.

Adrenergic alpha-Antagonists↗
PubMed1980

Effects of intravenous phentolamine on hemodynamics and resting pulmonary gas exchange in man.

The influence of intravenous phentolamine on hemodynamics, ventilation, and blood gases were studied in 22 patients with cardiac disease. Phentolamine produced a significant increase in the heart rate and cardiac index and a significant decrease in the mean arterial pressure, mean pulmonary artery pressure, left ventricular end diastolic pressure, peripheral vascular resistance, and pulmonary vascular resistance. There was no significant change in the arterial pH, PO2, PCO2, alveolar-arterial PO2, and the dead space-tidal volume ratio. The favorable hemodynamic responses are attributable to the fact that the vasodilator effect of phentolamine is predominately on the arteriolar resistance bed and much less on the venous capacitance bed. In addition, phentolamine has a positive inotropic action which is indirect and dependent on the release of norepinephrine.

Adolescent↗
PubMed1994

Phentolamine sympathetic block in painful polyneuropathies. II. Further questioning of the concept of 'sympathetically maintained pain'.

To test for the presence of "sympathetically maintained pain" (SMP), we administered placebo-controlled phentolamine sympathetic blocks to 14 patients with painful polyneuropathies. Six received i.v. infusion of saline for 30 minutes, followed by phentolamine (35 mg). In eight patients, the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second saline phase, and then the other active drug. We measured magnitudes of spontaneous pain and mechanical hyperalgesias on a 0-to-10 pain scale every 5 minutes and monitored sensory and sympathetic effects clinically and through quantitative thermotest and thermography. Five patients reported significant diminution of pain (> 50%), all in response to placebo. Neither phentolamine nor phenylephrine provided relief, although all patients had signs of physiologic abnormalities reputed to be determinants or predictors of SMP. These results complement previous studies demonstrating the nonexistence of SMP among "reflex sympathetic dystrophy" patients and further question the concept of SMP.

Adult↗
PubMed1993

The safety of intravenous phentolamine administration in patients with neuropathic pain.

The safety of intravenous (i.v.) infusion of large doses of phentolamine as an outpatient diagnostic tool for sympathetically maintained pain was studied retrospectively in 100 consecutive patients (73 females and 27 males) with chronic pain. All patients were pretreated with i.v. fluids followed, in most cases, by propranolol, 1-2 mg i.v. (n = 95). Ten minutes later the phentolamine infusion commenced, lasting for 20 min. In 90 patients, the dose of phentolamine was 35 mg. Two patients received 25 mg, and 8 patients received larger doses of 50-75 mg. No major complications occurred during or after the test, and only small changes in arterial blood pressure or heart rate were observed. All patients developed mild nasal stuffiness, but no decline in oxygen saturation was observed. Five patients developed one of the following minor complications for a brief duration, that resolved spontaneously: sinus tachycardia, premature ventricular beats, dizziness, or wheezing. We conclude that i.v. phentolamine administration is safe in patients with neuropathic pain.

Age Factors↗
PubMed1982

Effects of ecarazine, prazosin, phentolamine and hexamethonium on the vasopressor reflexes induced by bilateral carotid artery occlusion and head-up tilting in cats.

In order to examine clinical potential for ecarazine, prazosin, phentolamine and hexamethonium to cause orthostatic hypotension in man, the effects of these drugs on the vasopressor reflexes induced by bilateral carotid artery occlusion (BCO) or head-up tilting (Tilt) have been investigated in gallamine-immobilized cats. Ecarazine at doses of 0.1 to 10 mg/kg i.v. decreased blood pressure in a dose-dependent way whereas at 0.1 to 1 mg/kg it did not affect the pressor response to BCO or Tilt and at 10 mg/kg it suppressed only the response to BCO slightly. On the other hand, prazosin, phentolamine and hexamethonium, at hypotensive doses, not only decreased blood pressure but also inhibited pressor responses to both BCO and Tilt. Because ecarazine lacks in producing orthostatic hypotension, it seems likely that the clinical propensity of drugs to cause such side effect is correlated with the inhibition of Tilt response rather than with that to BCO. The results of comparison of the inhibition by these drugs of Tilt response indicate that ecarazine is the most favorable drug among these four drugs and that phentolamine has the highest incidence of orthostatic hypotension. With respect to the effects of prazosin, phentolamine and hexamethonium, statistically significant correlation between the inhibition of the response to BCO and that to the compensatory reflex to Tilt has been observed. Hence it is suggested that the agents which decrease blood pressure by affecting peripheral sympathetic mechanisms might depress each efferent sympathetic pathway to the same degree.

Animals↗
PubMed1981

Low cardiac output states after open heart surgery. Comparative hemodynamic effects of dobutamine, dopamine, and norepinephrine plus phentolamine.

The hemodynamic effects of dobutamine, dopamine, and a combination of norepinephrine-phentolamine were compared in nine patients with low cardiac output state after open heart surgery. Using a Latin square design for drug sequence, each patient was given each drug at three levels by continuous intravenous infusion. For dobutamine and dopamine the doses were 2.5, 5.0 and 10.0 microgram/kg/min; for norepinephrine, 0.02, 0.05 and 0.10 microgram/kg/min with phentolamine in the ratio of 1 (norepinephrine) to 2.5 (phentolamine). Dobutamine and dopamine both produced an increase in heart rate, mean arterial pressure, cardiac index, and stroke volume index. Both drugs reduced total pulmonary and systemic vascular resistance in the dose range of 5.0 to 10.0 microgram/kg/min. When the maximum tolerated doses were compared, the drugs equally increased cardiac index and stroke volume index, but dopamine did so at a smaller dose than dobutamine. At equivalent doses, dobutamine tended to produce less tachycardia and vasoconstriction than dopamine. The norepinephrine-phentolamine combination resulted in increases in both systemic arterial pressure and vascular resistance with no significant increase in cardiac index. Its unique feature was its predictable vasopressor response with absence of chronotropic effects and ventricular irritability.

Cardiac Output, Low↗
PubMed1978

Effects of prazosin and phentolamine on cardiac presynaptic alpha-adrenoceptors in the cat, dog and rat.

In cats, dogs and rats, clonidine (20.0 microgram/Kg, i.v.) reduced the sustained tachycardia evoked by a continuous electrical stimulation of cardiac sympathetic nerve fibres. This effect of clonidine resulting from stimulation of cardiac presynaptic alpha-adrenoceptors could be completely antagonized by phentolamine and prazosin in the dog and the cat, whereas in the rat, prazosin, unlike phentolamine, failed to effectively inhibit the clonidine induced reduction in heart rate. The calculated doses of phentolamine and prazosin needed to produce a 50% antagonism were of similar magnitude in the dog, but in the cat prazosin was about three times less potent than phentolamine. As opposed to clonidine, LD 3098, a potent vascular postsynaptic alpha-adrenoceptor stimulating imidazoline, and phenylephrine (20.0 microgram/Kg, i.v.) did not significantly alter the sympathetic tachycardia in the pithed rat and the spinal dog. These results indicate that compounds stimulating postsynaptic alpha-adrenoceptors may be inactive as agonists of cardiac presynaptic alpha-adrenoceptors within the same animal species. Furthermore, a compound showing selective activity as an antagonist of vascular alpha-adrenoceptors in one species may not necessarily exert the same selective effects in other animals as demonstrated here for prazosin.

Animals↗
PubMed2004

Phentolamine bioequivalence study.

OBJECTIVE: To assess the bioequivalence of 2 tablet formulations of phentolamine (Regitine phentolamine 40 mg tablet formulation by Novartis, Brazil, as test formulation, and Vasomax, phentolamine 40 mg tablet formulation by Schering Plough S.A., Brazil, as reference formulation). METHODS: A single 40 mg oral dose of each formulation was administered to 36 male healthy volunteers. The study was conducted after screening, using an open, randomized, 2-period crossover design, a 7-day interval between doses, and wash-out period of at least 4 weeks. Plasma samples for determination of phentolamine were obtained predose and at intervals over 720 min postdose. Plasma concentrations were quantified by reversed-phase liquid chromatography coupled to tandem mass spectrometry (LC-MS-MS) with positive ion electrospray ionization using multiple reactions monitoring (MRM) method. Precision of the method was evaluated using calibration curves and plasma quality control samples. The subjects were monitored throughout the study. Systolic and diastolic blood pressure and pulse rate measurement were taken predose and at intervals up to 720 min. Tolerance of both products was good. No serious adverse reactions were reported. The pharmacokinetic parameters calculated for both compounds included: AUC(0-720 min), AUC(0-infinity), C(max), Ca and k(e). RESULTS: The maximum concentrations reached (C(max)) were compared. Regitine 40 mg formulation C(max) geometric mean ratio was 108.29% (90% CI = 98.58-118.96) of Vasomax 40 mg formulation. The areas under the curve (AUC(0-720 min)) were compared. Regitine 40 formulation (AUC(0-720 min)) geometric mean ratio was 102.33% (90% CI = 97.21-107.72) of Vasomax 40 mg formulation. CONCLUSION: Since the 90% CI for both C(max) and AUC ratio where inside the 80 to 125% interval proposed by the Food and Drug Administration, it is concluded that Regitine 40 mg tablet is bioequivalent to Vasomax for the rate and extent of absorption.

Administration, Oral↗
PubMed1989

[Phentolamine in cases of liver cirrhosis with bleeding from esophageal variceal rupture].

The aim of this study is at establishing cirrhotic portal hypertension with common bile duct ligation in 9 mongrel dogs to measure the plasma catecholamine level. On the basis of experimental study, phentolamine, the alpha-adrenoceptor antagonist, was used to treat 14 patients with liver cirrhosis complicating bleeding from esophageal variceal rupture. The results had been shown that the levels of noradrenaline (NE) in both portal and inferior caval vein were increased more significantly in the cirrhotic stage than in the precirrhotic stage. The mechanism of the NE elevation might be due to increased release from enhancement of sympathetic nervous activity. Our clinical data have also been demonstrated that the effect of phentolamine on the 12 cases of variceal hemorrhage is markedly efficacious with no longer bleeding. Only 2 patients had showed no good reaction neither to phentolamine nor to pituiterin, eventually died of liver failure. It is conceivable that phentolamine has the same efficacy in treatment of esophageal variceal bleeding as pituitrin. But less side effect than the latter.

Animals↗