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At least 271 records · Page 15Linked to original sources
PubMed1980

Effect of clonidine and phentolamine on self-stimulation behavior in the dorsal and ventral regions of the lateral hypothalamus in mice.

The effects of IP injections of increasing doses of clonidine and phentolamine on self-stimulation behavior (ICSS) in the dorsal and ventral regions of the lateral hypothalamus were studied in C57BL/6 mice. Clonidine specifically stimulates alpha-noradernergic receptors and has two distinct effects on ICSS. Ventral hypothalamic ICSS is immediately depressed at low doses (5 microgram/kg) whereas dorsal ICSS exhibits a discrete increase. At higher doses, ICSS is perturbed at both sites. Phentolamine is a specific blocking agent of alpha-noradrenergic receptors and depresses dorsal ICSS more than that of the ventral region. These observations clearly indicate a noradrenergic influence in the dorsal region of the hypothalamus.

Animals↗
PubMed1979

Blockade of pressor responses to angiotensins I and II and noradrenaline using phentolamine, propranolol and hexamethonium in conscious rabbits.

Angiotensin I is known to have direct agonist activity at some target tissues, independent of its conversion to angiotensin II. Aspects of its possible direct role as a pressor agent were investigated in conscious rabbits. Phentolamine (3 mg/kg i.v.), a dose which did not affect baseline blood pressure, reduced the pressor response to angiotensin II by 17% (P less than 0.05) but did not alter the sensitivity to angiotensin I. Noradrenaline activity was reduced by 56%. Propranolol (2 mg/kg i.v.), a dose which did not affect baseline blood pressure but which substantially reduced the depressor response to isoprenaline, had no effect on the pressor activity of either angiotensin I or II. Noradrenaline potency was reduced by 32%. Hexamethonium (20 mg/kg i.v.), caused a potentiation of the response to angiotensin I and II and noradrenaline. This was probably a non-specific action associated with the decrease in baseline blood pressure. No differential effect of ganglion blockade on the two angiotensins was noted. The dissociation of the effects of phentolamine on angiotensins I and II provides further evidence that pressor actions of these two compounds act through partially different mechanisms.

Angiotensin I↗
PubMed1991

The effects of the combination of phentolamine and vasopressin on hepatic and systemic hemodynamics in cirrhotic portal hypertensive dog model.

The experimental study was aimed at elucidating the effects of phentolamine and vasopressin used separately or in combination on hepatic and systemic hemodynamics in cirrhotic portal hypertensive dogs. The results showed that either of the two drugs used separately could lead to reduction in portal venous pressure and could also influence systemic hemodynamics or lower hepatic blood flow. When phentolamine in combination with vasopressin was administered, no side-effect could be found on hepatic and systemic hemodynamics, suggesting that the drugs used in combination could efficaciously decrease portal hypertension and counteract their respective side-effect. This combination therapy will be useful in treating bleeding from esophageal variceal rupture in cirrhotic patients with portal hypertension.

Animals↗
PubMed1999

Comparison of the synergistic effects of tamsulosin versus phentolamine on penile erection: in vitro and in vivo studies.

In vitro and in vivo studies were performed to determine the potential use of tamsulosin (TAM) versus phentolamine (PHE) for intracavernosal injection (ICI) therapy when mixed with papaverine (PAP) and/or prostagladin E1 (PGE1) or with vasoactive intestinal polypeptide (VIP) for the treatment of erectile dysfunction. We performed isometric tension studies on rabbit (n = 15), dog (n = 5), and human (n = 10) cavernous smooth muscle strips with TAM, PAP, PHE, VIP, PGE1, and the combinations of PAP and PHE; PAP and TAM; VIP and PHE; VIP and TAM; PAP, PGE1 and PHE; and PAP, PGE1 and TAM. TAM-containing trimix (PAP 18.75 mg, PGE1 6.25 micromg, and TAM 0.875 mg per ml) or PHE-containing trimix (PAP, PGE1, and PHE 0.625 mg per ml) were also injected into the cavernous bodies of ten mongrel dogs. Among the single agents, TAM and PGE1 (only in human) had the strongest effect on the relaxation of cavernous muscles in rabbit, dog, and human strips (P<0.05). Relaxation responses to 2- or 3-drug mixtures containing tamsulosin were also significantly better (P<0.05) than PHE-containing ones in rabbit, dog, and human strips. The increase in intracavernosal pressure with a TAM-containing trimix was higher than with a PHE-containing one (0.03 ml; 81.2 vs. 75.8 mm Hg, 0.04 ml; 103.2 vs. 94.3 mm Hg), although not statistically different. The drop in systemic blood pressure was lower after injection of a TAM-containing trimix than a PHE-containing one, although not statistically different. In conclusion, tamsulosin might be a more efficacious and safer agent to use for ICI therapy than phentolamine.

Adrenergic alpha-Antagonists↗
PubMed1982

Selective modifications in the de novo biosynthesis of retinal phospholipids and glycerides by propranolol or phentolamine.

The effects of propranolol or phentolamine on the metabolism of phospholipids, diacylglycerol, and triacylglycerol were studied in the bovine retina in vitro. Lipid labeling was followed during short-term incubation of intact bovine retinas with [U-14C]glycerol and [1-14C]palmitic acid. Each of these precursors was recovered in the appropriate lipid moiety. Most of the [14C]glycerol appeared progressively in triacylglycerol (TG) through the sequence from phosphatidic acid (PA) to diacylglycerol (DG). Labeled palmitate appeared in much lower quantities than labeled glycerol in all glycerolipids except phosphatidylcholine (PC). Propranolol and phentolamine greatly enhanced the [14C]glycerol specific activities of PA, phosphatidylinositol (PI), and phosphatidylserine (PS), whereas labeling in other glycerolipids was much lower than in controls. The labeling in TG with both precursors was found to be less than 50% of the control values; however, a late increase in DG labeling was observed. The effects of these drugs on broken cell preparations were also described, although lipid synthesis from labeled glycerol in these preparations was only 9% that of intact retinas. It appeared that an amphiphilic cationic structure was necessary to produce these drug effects; propranolol glycol, the hydrophobic moiety of propranolol, did not elicit the same effects. It is suggested that, among other changes, the drugs inhibited phosphatidate phosphohydrolase and redirected the flux predominantly toward PI. Support for the proposed multiple lipid effects elicited by these drugs was provided by the dual changes found in the labeling of DG.

Animals↗
PubMed1984

Antagonism of stimulation-produced antinociception by intrathecal administration of methysergide or phentolamine.

This study examined whether the antinociception produced by electrical stimulation of medullary raphe nuclei is mediated by activation of monoaminergic neurons projecting to the spinal cord. Ninety-four sites distributed about the midline of the medulla were stimulated and their ability to produce antinociception was determined using two different analgesiometric tests. Stimulation of sites in the nuclei raphe pallidus and raphe obscurus did not produce antinociception, but rather, produced tremor and, on occasion, extensor rigidity. In contrast, stimulation at sites located in the nucleus raphe magnus and the adjacent nucleus reticularis paragigantocellularis produced antinociception, as indicated by increased tail flick latencies and decreased responsiveness to noxious pinch applied to the extremities. Intrathecal administration of saline prior to electrical stimulation of these sites did not attenuate either the elevation of tail flick latencies or the decreased responsiveness to pinch. However, intrathecal administration of 30 micrograms of either methysergide or phentolamine prior to stimulation at these same sites significantly attenuated the increase in tail flick latency and restored responsiveness to pinch. Naloxone (1 mg/kg, s.c.) did not attenuate the stimulation-produced antinociception evoked from any of these sites. These data support the postulate that the antinociceptive effect of electrical stimulation of the nucleus raphe magnus and the nucleus reticularis paragigantocellularis is mediated by activation of serotonergic and noradrenergic neurons projecting to the spinal cord. The inability of either methysergide or phentolamine alone to completely antagonize the elevation of tail flick latency further suggests that the serotonergic and noradrenergic bulbospinal systems are coactivated by electrical stimulation of these sites.

Animals↗
PubMed1977

Presynaptic alpha-adenoceptors: the depression of self-stimulation by clonidine and its restoration by piperoxane but not by phentolamine or phenoxybenzamine.

Depression of self-stimulation by clonidine has been ascribed to continuous direct stimulation of alpha-adrenoceptors with consequent disruption of reinforcement signals thought to be conveyed by noradrenergic pathways. This suggestion was tested by administration of alpha-receptor blocking agents (piperoxane, phentolamine and phenoxybenzamine, PBZ) differing in their affinity for pre- and post-synaptic receptor sites. Piperoxane in low doses (0.55-5.0 mg/kg) previously reported to cause specific blockade of pre-synaptic receptors implicated in negative feedback circuits, caused a significant increase in self-stimulation rate and strongly antagonized the depression of self-stimulation by clonidine (0.15 mg/kg). A larger dose of piperoxane (45 mg/kg) and graded doses of phentolamine and PBZ, affecting both pre- and post-synaptic receptors, depressed self-stimulation, and did not antagonize clonidine-induced depression of self-stimulation. It is concluded that depression of self-stimulation by clonidine may depend on clonidine-induced inhibition of NA release exerted via presynaptic receptors, and that the effect of clonidine is not necessarily evidence that noncontingent adrenergic stimulation disrupts reinforcement.

Animals↗
PubMed1978

The plasma cyclic AMP response to catecholamines as potentiated by phentolamine in rats.

Norepinephrine failed to increase plasma cyclic AMP when injected alone into fasted rats, in contrast with sharp increases elicited by isoproterenol, epinephrine or tyramine. In rats pretreated with 6-hydroxydopamine or cocain, however, there was significant increase in plasma cyclic AMP after norepinephrine injection, suggesting that the rapid neuronal catecholamine uptake was at least partly responsible for the lack of norepinephrine action. Phentolamine was very effective in enhancing the epinephrine-, norepinephrine- or tyramine-induced increase in plasma cyclic AMP but without effect on the isoproterenol-induced increase. Blockade of postsynaptic alpha-adrenoceptors, rather than of presynaptic receptors, is likely to be involved in the phentolamine potentiation, since it was even observed in rats treated with 6-hydroxydopamine or cocaine. A discussion is presented regarding the mechanism by which cyclic AMP generation is influenced by the alpha- and beta-adrenoceptor interaction on effector cell membranes.

Animals↗
PubMed1978

The protective effect of phentolamine against cardiac arrhythmias in the rat.

Norepinephrine was given by continuous infusion at a rate of 80 microgram/kg/min for 2 min. Norepinephrine caused the appearance of cardiac arrhythmias, primarily ventricular extrasystoles. The prior administration of phentolamine, even in a dose which did not antagonize the pressor effect of norephinephrine, prevented extrasystole production by norepinephrine. Tolazoline and yohimbine, in doses which did not affect the vasopressor action of norepinephrine, also suppressed extrasystole production. It is concluded that the antiarrhythmic effect of phentolamine, does not require antagonism of alpha-adrenoceptors of the type found in the vasculature, but may involve effects on a different type of alpha-adrenoceptors in the heart.

Angiotensin II↗
PubMed1980

Effect of guanethidine on alpha-adrenoceptor blocking potency of phentolamine in vitro.

The effect of guanethidine on the alpha-adrenoceptor blocking potency of phentolamine was studied using the rabbit aortic strip and rat vas deferens. The agonists used were noradrenaline (in presence of DOCA and cocaine which block uptake mechanisms) and xylometazoline (which is not taken up by uptake mechanisms). Guanethidine augmented the responses to noradrenaline and xylometazoline and increased the pA2 value of phentolamine against both agonists. Increased affinity of alpha-receptors may be partly responsible for the guanethidine-induced supersensitivity to alpha-adrenoceptor agonists.

Animals↗
PubMed1984

The effect of prazosin, indoramin and phentolamine on sympathetic nerve activity.

The failure of alpha 1-adrenoceptor antagonists, prazosin and indoramin, to cause a reflex tachycardia was investigated in the anaesthetised cat. Recordings were made of preganglionic sympathetic nerve activity from the third or fourth white ramus communicans, femoral arterial conductance, heart rate and blood pressure. A 1 h infusion of prazosin or indoramin caused falls in preganglionic sympathetic nerve activity, heart rate and blood pressure. Infusion of phentolamine differed, in that there was an increase in preganglionic sympathetic nerve activity and heart rate along with a fall in blood pressure. Indoramin differed from prazosin and phentolamine in that it only caused a small increase in femoral arterial conductance. It is suggested that the ability of prazosin and indoramin to cause a reduction in central thoracic sympathetic outflow may explain the failure of these drugs to cause a reflex tachycardia in man and experimental animals.

Animals↗
PubMed1989

Hypotension and bradycardia after intrathecal ketanserin and phentolamine in the rat.

Intrathecal administration of ketanserin and phentolamine elicited dose-dependent falls in arterial blood pressure and heart rate in anaesthetized rats without attenuation of the pressor responses to i.v. injections of phenylephrine. It is concluded that both ketanserin and phentolamine can decrease arterial blood pressure by acting within the spinal cord.

Animals↗
PubMed1987

Effect of phentolamine on wakefulness and sleep during recovery from REM sleep deprivation in cats.

Adult cats with permanent EEG, EMG, EOG, and PGO electrodes were recorded for 24 hours started at the end of a 72-hour REMS deprivation induced by a platform-water-tank procedure and after receiving IP injections of phentolamine (20 mg/kg) or saline. Exposure of the cats to the platform-REMS deprivation procedure increased the percentage of REMS during the subsequent 24 hours. Phentolamine interacted with the platform REMS deprivation causing the peak of REMS percentage to occur during recovery hours 5-12. These findings indicate that blockade of alpha-receptors has an additive effect on platform-REMS deprivation induced REMS rebound in cats.

Animals↗
PubMed1991

Intravenous phentolamine test: diagnostic and prognostic use in reflex sympathetic dystrophy.

In some patients, ongoing and evoked neurogenic pain is relieved by pharmacological or destructive block of the sympathetic innervation of the affected part. In others, sympatholysis is ineffective. The present report shows that these two groups of patients can be distinguished by a safe and simple diagnostic test. Individuals in whom the pain was transiently relieved by intravenous phentolamine (Regitine) were very likely to respond favourably to subsequent sympatholytic treatment with i.v. regional guanethidine. Individuals in whom the phentolamine test was negative did not enjoy pain relief from this type of sympatholysis.

Adolescent↗
PubMed1986

Effect of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--I. Growth hormone.

In this report the effects of various receptor blockers on desimipramine (DMI)-induced growth hormone (GH) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker: methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). DMI-induced GH stimulation was not significantly different after DMI i.v. alone (n = 12) than after three days' pretreatment with 12 mg methysergide p.o. in another group of subjects (n = 12). Following combined administration of DMI and propranolol (15 mg i.v.), GH secretion was significantly increased by 25 mg DMI (p less than 0.05) and 50 mg DMI (incomplete block design, n = 18). GH secretion was significantly lower (p less than 0.01) after DMI in combination with 60 mg phentolamine i.v. compared to that after administration of DMI alone in the same group (n = 12). Following 10 mg yohimbine i.v. in combination with DMI (n = 6), the DMI-induced GH increase was also significantly less (p less than 0.05) than that after DMI alone. The DMI-induced GH increase following DMI plus 1 mg prazosin p.o. (n = 12) was comparable to that after DMI alone. The results indicate that the GH-stimulating effect of DMI is primarily related to the ability of DMI to inhibit noradrenaline (NA) reuptake. Should serotonergic receptors be involved in the DMI-induced GH secretion at all, they transmit a positive stimulus. The alpha-1 receptors are most likely not (or not essentially) involved, whereas alpha-2 receptors affect the DMI-induced secretion positively, and beta receptors have an inhibitory effect.

Adolescent↗
PubMed1986

Effects of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--II. Prolactin.

In this report the effects of various receptor blockers on desimipramine (DMI)-induced prolactin (PRL) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker: methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). Following administration of methysergide (12 mg p.o., n = 12), a significantly lower (p less than 0.01) DMI-induced PRL secretion compared to DMI alone in another group of subjects (n = 12) was observed. Combined administration with propranolol (15 mg i.v.) significantly enhanced the DMI-induced PRL secretion compared to DMI 50 mg i.v. alone (n = 18, incomplete block design) (p less than 0.01). Neither combined administration with phentolamine (60 mg i.v., n = 12), yohimbine (10 mg i.v., n = 6), nor prazosin (1 mg p.o., n = 12) significantly influenced the DMI-induced PRL secretion compared to DMI alone in the same subjects. The results of the present study, especially the inhibitory effect on DMI-induced PRL secretion of methysergide, indicate that the primarily noradrenaline (NA) and lesser serotonin (5-HT) reuptake inhibiting antidepressant DMI stimulates PRL secretion via 5-HT neurons. Furthermore, the significantly enhanced PRL release following combined administration of DMI and propranolol suggests that a noradrenergic inhibitory effect also may be involved in the transmission of the PRL stimulus.

Blood Glucose↗
PubMed1986

Effects of receptor blockers (methysergide, propranolol, phentolamine, yohimbine and prazosin) on desimipramine-induced pituitary hormone stimulation in humans--III. Hypothalamo-pituitary-adrenocortical axis.

In this report the effects of various receptor blockers on the desimipramine (DMI)-induced cortisol (ACTH) secretion in healthy male subjects are presented. Each trial consisted of two administrations: one of DMI i.v. alone and one of DMI i.v. in combination with the respective receptor blocker, i.e. methysergide (serotonin (5-HT) receptor blocker), propranolol (beta receptor blocker), phentolamine (alpha-1/alpha-2 receptor blocker), yohimbine (alpha-2 greater than alpha-1 receptor blocker), and prazosin (alpha-1 receptor blocker). In addition, the effect of prazosin on DMI-induced ACTH stimulation was examined. DMI-induced cortisol stimulation was not significantly different after DMI alone (n = 12) from that after three days pretreatment with methysergide (12 mg p.o.) in another group of subjects (n = 12). Neither the combination of DMI plus propranolol (15 mg i.v. n = 18, incomplete block design) nor that of DMI plus phentolamine (60 mg i.v. n = 12) had a significant influence on DMI-induced cortisol secretion. Following combined administration with yohimbine (10 mg i.v.), cortisol secretion was higher compared to that after DMI alone in the same group (n = 6). DMI-induced cortisol secretion was significantly lower (p less than 0.01) following combined administration with prazosin (1 mg p.o. n = 12), as was DMI-induced ACTH secretion (p less than 0.05) in these subjects. The findings of these trials, especially those of the prazosin trial, indicate that DMI-induced stimulation of cortisol and ACTH secretion is attributable to the noradrenaline (NA) reuptake inhibiting effect of DMI, and that the stimulus is transmitted with the aid of noradrenergic alpha-1 receptors. Alpha-2 receptors possibly exert a negative influence on this effect.

Blood Glucose↗
PubMed1990

Epinephrine-induced vasospasm reversed by phentolamine digital block.

A case of profound digital vasoconstriction caused by the accidental injection of epinephrine from a commercial bee sting kit is reported. One hour later the patient had a cold, painful, blanched finger. A digital block using a 2-mg dose of phentolamine mixed with 2% lidocaine was performed. Thirty minutes after treatment, the finger was pink and warm. The patient reported a marked decrease in pain. Reexamination 12 hours later showed only mild tenderness at the fingertip. No tissue necrosis occurred. One month after injection, there were no apparent sequelae. Although the use of alpha-adrenergic blocking agents by regional infiltration to treat accidental infusion or extravasation of epinephrine has been suggested, no reports of this technique are found in the emergency medicine literature. The mechanism of digital vasoconstriction and the action of phentolamine are discussed.

Accidents↗