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At least 217 records · Page 12Linked to original sources
PubMed1998

Effects of radiocontrast and endothelin administration on systolic blood pressure and renal damage in male spontaneously hypertensive and Wistar Kyoto rats with phentolamine-induced adrenergic blockade.

RATIONALE AND OBJECTIVES: The systemic administration of hypertonic solutions may activate the adrenergic system, thus triggering vasomotor reactions that may result in renal failure. In this study, the effects of diatrizoate meglumine sodium radiocontrast agent Hypaque-76 on systolic blood pressure (BP) and renal damage were determined in male spontaneously hypertensive (SH) rats and Wistar Kyoto (WKY) rats under adrenergic blockade. METHODS: The systolic BP was measured in ketamine-anesthetized male SH and WKY rats after administration of saline solution, radiocontrast, or endothelin during adrenergic blockade with phentolamine. Then the left kidney was removed and examined histologically. RESULTS: The fall in systolic BP after phentolamine was not influenced by saline solution or radiocontrast in WKY rats but was restored partially by radiocontrast in SH rats. Endothelin produced an elevation in BP toward baseline levels in both strains. Only moderate renal damage was observed in the kidneys of WKY rats given radiocontrast or endothelin, but very severe damage was produced by these agents in SH rats. CONCLUSIONS: Adrenergic blockade with phentolamine did not prevent the elevation in systolic BP in SH rats by radiocontrast or by endothelin in SH and WKY rats, nor did it protect against renal damage by radiocontrast or by endothelin in SH rats.

Adrenergic alpha-Antagonists↗
PubMed1976

Hydrallazine or phentolamine as adjuncts to beta-adrenoceptor blockade/thiazide therapy in hypertension.

Ten patients not maximally controlled on an oxprenolo/cyclopenthiazide regimen for moderately severe hypertension were treated in a double blind crossover trial with either hydrallazine (75-150 mg/day) or phentolamine (60-120 mg/day) or placebo in addition to their other therapy. Additional phentolamine therapy did not lower blood pressure significantly when compared with placebo. Additional hydrallazine (75-150 mg/day) produced an approximate 10 mm, Hg fall in diastolic blood pressure, but no significant fall in systolic blood pressure. Pulse rates did not alter with the addition of hydrallazine or phentolamine. In patients who fail to attain optimal blood pressure response to beta-adrenoceptor blocking drugs it is suggested that the addition of hydrallazine is a useful measure.

Adult↗
PubMed1989

The effect of phentolamine on basal and pethidine-induced inhibition of gastric emptying in healthy volunteers.

1. The effect of phentolamine 5 mg i.v. on basal and pethidine-induced inhibition of gastric emptying of semisolid TC-99m labelled Chelex-100 resin/oatmeal was studied in ten healthy volunteers. 2. Each volunteer acted as his/her own control. 3. Basal gastric emptying remained unchanged after administration of phentolamine. 4. Administration of phentolamine reversed the pethidine-induced inhibition of gastric emptying.

Adult↗
PubMed2007

The classical competitive antagonism of phentolamine on smooth muscle preparations, investigated by two procedures.

1. In isolated smooth muscle tissues taken from rats, rabbits and guinea-pigs, all at 37.5 degrees C, the equilibrium dissociation constant (K(beta)) of the competitive, reversible alpha-adrenoceptor antagonist phentolamine varied between 4 and 28 nm. 2. The concentration of the antagonist required to inhibit contractions to direct- or indirect-acting alpha-adrenenoceptor agonists by 50% (IC50) also varied between 5 and 30 nm. 3. From one tissue to another, the IC50/K(beta) ratio of the blocker varied from 1 to 2.5, the values being close to those predicted by classical receptor theory based on the law of mass action. 4. At 27.5 degrees C, using phenylephrine as the spasmogen in rat aorta, the IC50/K(beta) ratio for phentolamine was 3.1. 5. A significantly higher IC50 compared with K(beta) for phentolamine indicates that the procedures for estimating affinity constants for a competitive antagonist are not equivalent.

Adrenergic alpha-Antagonists↗
PubMed1977

Effect of intrahypothalamic phentolamine on hypothermia produced by peripheral noradrenaline in the pigeon.

1 The effect of intrahypothalamic phentolamine (1 and 1 microliter of a 10 microgram/microliter solution) on hypothermia induced by intramuscular injection of noradrenaline (NA, 2 mg/kg) at different times (2, 10, 20 min) after phentolamine was investigated in pigeons. 2 Administration of phentolamine shortly before NA was shown to attenuate hypothermic responses to NA. 3 It is suggested that the attenuation is due to blockade of central hypothermic effects of intramuscular NA. 4 The mapping of injection sites in the brains was carried out.

Animals↗
PubMed1979

Potentiation of the diabetogenic effect of streptozocin by phentolamine in the rat.

The effect of alpha- and beta-adrenoceptor blocking agents and a beta2-agonist, salbutamol, on the diabetogenic effects of streptozocin (threshold doses) was investigated in the rat. Phentolamine and salbutamol potentiated the diabetogenic effect of streptozocin but phenoxybenzamine, tolazoline, oxprenolol and propranolol were without effect. The potentiating effect of phentolamine was blocked by oxprenolol. Potentiation of the diabetogenic effect by phentolamine is not related to alpha-adrenoceptor block, vasodilatation or insulin release. But it may be related to its ability to stimulate beta-adrenoceptors.

Animals↗
PubMed1987

Inhibition of basal and insulin-stimulated gastric acid secretion by phenoxybenzamine or phentolamine.

The present study in the rat was undertaken to investigate the possible involvement of alpha- and beta-adrenoceptors in mediating gastric acid secretion in response to insulin-hypoglycaemia. Phenoxybenzamine, 15 mg kg-1, depressed the basal acid secretion to a level similar to that associated with vagotomy; phentolamine, 15 mg kg-1, had a similar effect. Insulin (1 unit kg-1) significantly stimulated gastric acid secretion. Vagotomy or phenoxybenzamine or phentolamine, 15 mg kg-1 prevented this action. The beta-adrenoceptor blocking drug, propranolol, 5-15 mg kg-1, had no significant effect on the basal acid secretion or its stimulation by insulin. The similarity in action between vagotomy and large doses of phenoxybenzamine and phentolamine suggests that, in the rat, vagal alpha-adrenoceptor stimulation is involved in the mechanisms of basal and insulin-stimulated gastric acid secretion.

Animals↗
PubMed1978

Effect of propranolol and phentolamine on myocardial necrosis after subarachnoid haemorrhage.

A study was set up to assess the effect on the clinical course of subarachnoid haemorrhage (SAH) of giving propranolol 80 mg eight-hourly plus phentolamine 20 mg three-hourly by mouth for three weeks. Out of the 90 patients studied, 14 died. Two of the deaths occurred in an open pilot study of 10 patients, the remaining 12 deaths occurring in patients in a randomised double-blind placebo-controlled study. Postmortem examination was carried out on 12 of the patients, six of whom had been receiving placebo and six propranolol plus phentolamine. Necrotic myocardial lesions were present in the hearts of all six patients (age range 30-59 years) who died while taking placebo (all had had abnormal electrocardiograms (ECGs). In contrast, no necrotic lesions were found in the hearts of the six patients (age range 28-59) who died while receiving the drugs (all had previously had normal ECGs). We conclude that the necrotic myocardial lesions were induced by catecholamines and that propranolol had a cardioprotective effect. While death from a further haemorrhage in cases of SAH is not affected by propranolol and phentolamine, propranolol may have a beneficial effect in other potentially lethal stresses.

Adult↗
PubMed1977

Electrophysiological properties of phentolamine in man.

The effects of phentolamine, 0-3 mg/min given intravenously for 15 minutes, on His bundle electrograms were studied in 11 patients with heart disease. Recordings were made at varied heart rates, using atrial pacing. Phentolamine significantly reduced the AH interval in every patient but it had no effect on the HV interval. Functional and effective refractory periods were measured with the use of the atrial extrastimulus technique. The effective refractory period of the atrium and atrioventricular node as well as the functional refractory period of the atrioventricular node all significantly decreased after phentolamine infusion. This improvement in conduction is probably mediated by a release of catecholamines.

Adolescent↗
PubMed1987

Comparative effects of rauwolscine, prazosin, and phentolamine on blood pressure and cardiac output in anesthetized rats.

The endogenous role of the alpha-adrenergic system in the maintenance of mean arterial pressure (MAP), total peripheral resistance (TPR), cardiac output (CO) and its distribution, and plasma norepinephrine and epinephrine release was investigated by the administration of selective alpha-adrenoceptor antagonists to halothane-anesthetized rats. The blockade of alpha 1-, alpha 2-, and both alpha 1- and alpha 2-receptors was accomplished by i.v. infusions of prazosin, rauwolscine, and phentolamine, respectively. The microsphere technique was used for the determination of CO and its distribution. Since the infusions of the three antagonists caused similar decreases of MAP and heart rate, the results suggest that postjunctional alpha 1- and alpha 2-receptors are both important in the control of MAP. During the infusion of prazosin, TPR was decreased but CO was not changed. In contrast, CO was decreased but TPR was not changed during the infusions of rauwolscine and phentolamine. Thus, CO was reduced after the blockade of alpha 2- but not alpha 1-receptors. All three antagonists caused an increase in percent distribution of CO to the lungs and muscle, suggesting that the sympathetic nervous system plays the greatest vasoconstrictor influence in the lungs and muscle via stimulations of both subtypes of alpha-adrenoceptors. The administration of either prazosin or rauwolscine caused little change in plasma catecholamine levels. In contrast, phentolamine caused large increases in both epinephrine and norepinephrine levels. Therefore catecholamine release was only increased after concurrent blockade of both alpha 1- and alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1982

Dogfish pressor response to potassium blocked by magnesium and phentolamine.

In vivo infusion of MgCl2 blocks the dogfish pressor response to K+. This action of Mg2+ was contrasted to phentolamine in in vivo and in vitro experiments. Mg2+ blocks the spontaneous release of catecholamines from dogfish chromaffin tissue but does not alter the norepinephrine-induced contraction of the isolated dogfish artery. In vivo infusion of Mg2+ causes a significant decrease in resting catecholamine levels and diminishes the catecholamine release caused by K+ challenge. Both Mg2+ and phentolamine block the pressor action of K+, Mg2+ by preventing the K+-induced release of catecholamines and phentolamine by preventing the circulating catecholamines from interacting with alpha-adrenergic receptor sites.

Animals↗
PubMed1975

Effects of phentolamine on the adrenergic-induced changes in arterial plasma potassium.

Phentolamine was used as a pure alpha-adrenergic blocking agent in the study of the arterial plasma potassium responses to adrenergic stimulation in dogs. Both the hyperkalemia and hypokalemia evoked by the intravenous infusion of noradrenaline, 5 mug/kg-min-1, were reduced by phentolamine (1-3 mg/kg), the response being completely abolished by increasing the dose of this alpha-blocker (9 mg/kg). The decrease of both parts of this dual response was parallel, and it was not possible to abolish the secondary hypokalemia without abolishing the early rise. The secondary decrease in arterial plasma potassium evoked by the intravenous infusion of the same dose of adrenaline was reduced, but not abolished, by the pretreatment with increasing doses of phentolamine, although the initial increase was completely abolished. These results agree with those that attribute an alpha-adrenergic nature to the adrenergic-evoked hyperkalemia, and a complex origin to the secondary hypokalemia. The different interpretations of the results obtained for these kalemotropic adrenergic effects are discussed, in the light of the Ahlquist hypothesis for adrenergic receptors. It is concluded that the alterations in the metabolic state of the effector cells observed during the administration of either adrenergic agonists or antagonists may influence the results obtained and may be considered as one of the factors responsible for interpretative difficulties described.

Animals↗
PubMed1979

Kinetics of alpha-adrenoreceptor blockade by phentolamine in the normal and denervated rabbit aorta and rat vas deferens.

The rates of onset and offset of alpha-adrenoreceptor blockade by phentolamine (5 X 10(-7) M) have been studied on the normal and denervated rabbit aorta and rat vas deferens. Removal of the adventitia with its accompanying sympathetic nerve component results in an approximately threefold increase in the rate of onset of alpha-adrenoreceptor blockade by phentolamine in the rabbit aorta. The rate of offset of blockade by the antagonist on the aorta is likewise faster after the adventitia has been removed (approximately threefold faster for loss of 90% of the antagonist from the region of the receptors). This effect is not likely to be attributed to the absence of sympathetic nerve terminals since surgical denervation of the rat vas deferens has no effect on the kinetics of receptor blockade in this densely innervated organ. These data suggest that the adventitia of the rabbit aorta may serve as a diffusion barrier which limits the antagonist's access to, and efflux from, the region of the receptors. The dissociation constant of phentolamine (calculated from the equilibrium dose ratio) on the alpha-adrenoreceptor is unaltered by denervation in either tissue and is identical in both tissues. It is suggested that alpha-adrenoreceptors in the rabbit aorta and rat vas deferens are of a single type and are not significantly affected, with respect to antagonist affinity, by denervation.

Animals↗
PubMed1991

Reduction of sympathetic influences on penile erection by phentolamine.

The lumbosacral sympathetic trunks seem to play a major role in penile detumescence. In animal experiments an erection induced by cavernous nerve stimulation can be abolished by neurostimulation of the canine sympathetic trunks. This canine experiment was designed to study the possible reduction of the sympathetic effect by intravenous injection of phentolamine. The aborted erection by sympathetic trunks stimulation was partially antagonized by phentolamine. The arterial flow to the penis as well as the intracavernous pressure were elevated by this drug. As an expected side effect the systemic arterial blood pressure decreased by 4-14 cm H2O after phentolamine injection.

Animals↗
PubMed1994

Comparison of a mixture of papaverine, phentolamine and prostaglandin E1 with other intracavernous injections.

OBJECTIVE: evaluation of a self-injection program with a mixture of papaverine, phentolamine and prostaglandin E1 (PGE1). METHOD: a self-injection program for erectile dysfunction was started by 48 patients, using a 1-ml mixture of 4.5 mg papaverine, 0.2 mg phentolamine and 1.5 micrograms PGE1. Patients completed a questionnaire at 6 weeks and at 3 months and were followed at the Outpatients Department for an average of 1 year. RESULT: of these patients 25 had previous experience with 20 micrograms PGE1 for intracavernous use and 22 patients had previously used 30 mg papaverine with 1 mg phentolamine. None of these 3 self-injection drugs is obviously superior in its ability to induce erections. Priapism occurred twice on a total of 1,290 injections. After 1-year follow-up, 4 patients had developed problems with fibrosis of the corpora, 2 of whom had encountered this problem also in a previous self-injection program. CONCLUSION: this triple mixture has the disadvantage of causing fibrosis and priapism in susceptible patients.

Alprostadil↗
PubMed1982

The effects of cigarette smoke and nicotine on platelet thrombus formation in stenosed dog coronary arteries: inhibition with phentolamine.

This study was undertaken to examine in vivo the effects of cigarette smoke on cyclic reductions in coronary flow due to platelet thrombus formation in the stenosed coronary arteries of anesthetized dogs. The circumflex coronary artery of 21 mongrel dogs was stenosed 60 - 80%, with blood flow measured with an electromagnetic flow probe. After the administration of cigarette smoke, plasma epinephrine was elevated nine times the control level (p less than 0.001) and peak mean blood pressure was elevated one and one-half times control (p less than 0.01). The hematocrit increased several percent (p less than 0.01) with cigarette smoke, although blood gases and pH remained unchanged. In all 21 dogs, spontaneous reductions in coronary blood flow were greatly exacerbated in the stenosed circumflex artery as evidenced by the number of flow reductions, the increased size of the reductions and the rate of flow reduction. Nicotine administered intravenously in doses comparable to those achieved through absorption of cigarette smoke by the lungs provoked similar responses of alpha-adrenergic stimulation and potentiation of the platelet thrombus formation. An alpha-adrenergic antagonist, phentolamine, was given (3 mg/kg) intravenously to inhibit the exacerbated platelet thrombus formation due to cigarette smoke or infused nicotine. In 18 of 21 dogs, an acute occlusive platelet thrombus was prevented 15 minutes after phentolamine and after phentolamine and after a cigarette smoke or nicotine challenge. This study confirms a link between cigarette smoking, platelet formation, and the potential for humans to develop an acute occlusive platelet thrombus in a diseased and stenotic coronary artery.

Animals↗
PubMed1977

Comparison of nitroglycerin-, nitroprusside-, and phentolamine-induced changes in coronary collateral function in dogs.

The recent use of vasodilators to improve ventricular function in acute myocardial infarction led us to investigate the effects of nitroglycerin, nitroprusside, and phentolamine on coronary collateral flow. Dogs were studied 2-4 wk after an ameroid constrictor was placed around the left anterior descending (LAD) coronary artery. Retrograde flow and peripheral coronary pressure were measured from a cannula inserted in the LAD distal to the ameroid. Systemic arterial pressure was held constant by an aortic cuff. When administered intracoronary (i.c.), nitroglycerin, 0.3-100 mug/min, or nitroprusside, 3-100 mug/min, produced quantitatively similar, dose-dependent increases in retrograde flow. Neither drug, i.c., changed peripheral coronary pressure. Nitroglycerin, 3-300 mug/min, intravenous (i.v.), produced dose-dependent increases in retrograde flow; nitroprusside, i.v., increased retrograde flow only in high doses (100-300 mug/min). Nitroglycerin and nitroprusside, i.v., produced similar increases in peripheral coronary pressure. Phentolamine, 1-300 mug/min, i.v., decreased retrograde flow, and did not change peripheral coronary pressure. Nitroprusside was considerably more potent than nitroglycerin in decreasing systemic arterial pressure and in reducing total coronary resistance. Thus, (a) although i.c. nitroglycerin and nitroprusside produce similar effects on collateral function, i.v. nitroglycerin is more effective than i.v. nitroprusside in augmenting collateral flow; (b) phentolamine has deleterious effects on collateral function; and (c) the relative vasodilator potencies of nitroglycerin and nitroprusside vary in different vascular beds; thus, for a given reduction in systemic arterial pressure, nitroprusside is less effective in increasing retrograde flow.

Animals↗
PubMed1979

Hemodynamic effects of phentolamine in mitral stenosis and congestive cardiomyopahty.

Nine patients with alcoholic cardiomyopathy and 8 patients with mitral stenosis were studied by right and left heart catheterization. Hemodynamic observations were made during control period and during the infusion of phentolamine at a rate of 0.3 mg per minute. The patients with the cardiomyopathy responded to phentolamine with a significant decline in the left ventricular filling pressure, pulmonary artery mean pressure, peripheral resistance, and arteriovenous oxygen difference. There was a significant increase in the cardiac index. The patients with mitral stenosis did not show any hemodynamic improvement after phentolamine infusion.

Cardiac Output↗