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PubMed1977

Changes in rat hind limb vascular resistance following intracerebroventricular drug administration.

The right hind limbs of rats (which had previously implanted intraventricular guide cannulae) were isolated from the systemic circulation, but with the nerves to the limb remaining intact, and perfused using a constant output blood pump. Using this preparation, changes in vascular resistance, blood pressure and heart rate were monitored following injection of noradrenaline, phentolamine and propranolol into the lateral cerebral ventricles (i.c.v.) of rats anaesthetised with alpha-chloralose. All three drugs lowered blood pressure. Noradrenaline administered i.c.v. induced a nervously mediated vasocilatation and an insignificant fall in heart rate whereas i.c.v. phentolamine administration was followed by a nervously mediated vasoconstriction in the isolated hind limb and a gradual rise in heart rate. After i.c.v. administration of propranolol there was no evidence of an immediate nervously mediated vasodilatation but heart rate fell significantly. Following i.c.v. phentolamine or propranolol vasodilatation did not occur in the hind limb until after the time taken for circulating blood ro reach the isolated vascular bed. The vasodilatatory and hypotensive responses to i.c.v. noradrenaline were not evident following prior i.c.v. injection of phentolamine. These results indicate the suitability of this preparation for investigations of central actions of other drugs.

Animals↗
PubMed1981

Cholinergic component of the excitatory response in the rat anococcygeus muscle.

The effects of neostigmine and atropine on the excitatory response of the rat anococcygeus muscle to field stimulation have been studied. The excitatory responses were inhibited and abolished by 0.1 and 3 micro M phentolamine, respectively. Neostigmine, 1 micro M, by itself and in the presence of 0.1 micro M phentolamine potentiated responses. In the presence of 3 micro M phentolamine neostigmine restored responses to 1-20 HZ. Atropine, 1 micro M by itself, in the presence of neostigmine (1 micro M), and in the presence of neostigmine and phentolamine (0.1 micro M) inhibited the response. Hexamethonium, 100 micro M, had no effect on responses to field stimulation or to exogenously applied (-)-noradrenaline. Responses to (-)-noradrenaline were not altered by neostigmine or atropine. It is suggested that there is a cholinergic component to the excitatory response to field stimulation in the rat anococcygeus muscle.

Acetylcholine↗
PubMed1987

Mechanisms involved in catecholamine effect on glycogenolysis in catfish isolated hepatocytes.

Isolated catfish hepatocytes were treated with epinephrine, norepinephrine, isoproterenol, and phenylephrine in the presence or in the absence of propranolol or phentolamine as beta and alpha inhibitors, respectively. Glycogen phosphorylase a activity and glycogen content, as well as glucose released from cells, were tested. Phosphorylase activity was stimulated by all the catecholamines and was accompanied by a decrease of glycogen content in cells and by an increase in glucose output into the medium. Whereas phentolamine did not affect the catecholamine action on any parameter considered, propranolol inhibited the effect of epinephrine, norepinephrine, and phenylephrine, but hardly altered that of isoproterenol. The effect of epinephrine and norepinephrine, as modified by propranolol and not by phentolamine, is consistent with a beta action of these catecholamines. The fact that propranolol and not phentolamine inhibited the phenylephrine effect indicates that in catfish hepatocytes phenylephrine behaves as a beta agonist and/or that propranolol may also bind to alpha receptors. Results also indicate that in catfish liver cells isoproterenol, whose effect is scarcely influenced by propranolol, is not a pure beta agonist.

Animals↗
PubMed1980

Epinephrine and norepinephrine are cleared through beta-adrenergic, but not alpha-adrenergic, mechanisms in man.

Although catecholamines are rapidly removed from the extracellular fluid, the role of adrenergic mechanisms in the clearance of epinephrine and norepinephrine has not been defined. In five normal human subjects, mean (+/- SE) plasma epinephrine concentrations did not change during control infusions, rose from 21 +/- 6 pg/ml to 834 +/- 84 pg/ml during the infusion of epinephrine (50 ng/kg/min) over 180 min and to 853 +/- 112 pg/ml during the infusion of epinephrine plus phentolamine (500 micrograms/min after a 5.0 mg loading dose infused over 2 min), but to 2400 +/- 104 pg/ml during the infusion of epinephrine plus propranolol (80 micrograms/min after a 5.0 mg loading dose infused over 2 min), indicating that beta-adrenergic blockade sharply reduces the clearance of epinephrine in man. In separate studies in seven subjects, similar increments in plasma epinephrine occurred during the infusion of epinephrine alone and the clearance of epinephrine was comparably reduced during the infusion of epinephrine plus propranolol and during the infusion of epinephrine plus propranolol plus phentolamine, suggesting that the reduction of epinephrine clearance produced by beta-adrenergic blockade during epinephrine infusion is not mediated by an alpha-adrenergic reduction of blood flow to organs of epinephrine clearance. Endogenous plasma norepinephrine concentrations doubled during the infusion of phentolamine without propranolol but rose to nearly fourfold higher values during the infusion of phentolamine with propranolol indicating that beta-adrenergic blockade reduces the clearance of norepinephrine as well as that of epinephrine. These findings indicate that epinephrine and norepinephrine are cleared through beta-adrenergic, but not alpha-adrenergic, mechanisms in man.

Adrenergic alpha-Antagonists↗
PubMed1985

Interaction between the baroreflex and anterior hypothalamic stimulation. Demonstration of a noradrenergic involvement.

Cats, anaesthetized with alpha-chloralose, were used to investigate an interaction between the baroreceptor reflex and stimulation of the anterior hypothalamus (AH). In these cats, stimulation of the anterior hypothalamus gave autonomic responses that characterize the defense reaction. Stimulation of the anterior hypothalamus also interacted with the baroreceptor reflex without altering the effectiveness of the vasodepressor component of the reflex (induced by stimulation of the aortic nerves). However, in spinal cats the bradycardia component (induced by angiotensin at 0.097 nmol/kg pe min, i.v.) was inhibited by stimulation of the anterior hypothalamus and the inhibition was augmented by pretreatment with phentolamine (17.7 nmol) in the nucleus tractus solitarius (NTS). Pretreatment with phentolamine (17.7 nmol) in the nucleus tractus solitarius also reduced the sensitivity of the bradycardia component of the reflex and attenuated (3 and 6 nmol) the induced inhibition of the bradycardia induced by stimulation of the anterior hypothalamus. This attenuation induced by NE was abolished by pretreatment with phentolamine (17.7 nmol), but not by pretreatment with sotalol (16 nmol) or haloperidol (12 nmol) in the nucleus tractus solitarius. Additionally, NE was released from the nucleus tractus solitarius during activation of the baroreceptor and during stimulation of the anterior hypothalamus in cats with intact baroreceptor nerves, but not in baroreceptor-denervated cats. Moreover, the baroreceptor reflex attenuated the pressor response evoked by stimulation of the anterior hypothalamus, and also caused the release of NE from the anterior hypothalamus. At this site, injection of NE (3 and 6 nmol) attenuated the pressor response evoked by stimulation of the anterior hypothalamus and this attenuation was abolished by pretreatment with phentolamine (17.7 nmol), but not by pretreatment with sotalol (16 nmol) or haloperidol (12 nmol) in the anterior hypothalamus. It is concluded that NE participates at the nucleus tractus solitarius and the anterior hypothalamus as an attenuator in the interaction between the baroreflex and stimulation of nerve fibers in the anterior hypothalamus that mediate the defense reaction.

Animals↗
PubMed1994

Regional haemodynamic effects of carbachol injected into the hypothalamic paraventricular nuclei of conscious, unrestrained rats.

Carbachol was injected into the hypothalamic paraventricular nuclei (PVN) of conscious, unrestrained Long Evans rats, chronically instrumented with intravascular catheters and pulsed Doppler probes to assess changes in regional haemodynamics. Bilateral microinjections of carbachol (1 ng-1 microgram) produced increases in blood pressure, bradycardias and vasoconstrictions in renal, superior mesenteric and hindquarters vascular beds. In the presence of phentolamine, the bradycardic and hindquarters vasoconstrictor responses to carbachol were unchanged while the pressor response was smaller due to a reduction in the renal and the superior mesenteric vasoconstriction. In the presence of propranolol, the bradycardic response was reduced, but the pressor and renal vasoconstrictor responses were potentiated, whereas the superior mesenteric and hindquarter vasoconstrictions were not changed significantly. In the presence of phentolamine and propranolol, the heart rate and pressor responses, as well as the renal vasoconstriction, were unchanged, whereas the superior mesenteric vasoconstriction was reduced and the hindquarters vasoconstriction was potentiated. Together these results are consistent with an involvement of the sympathoadrenal system in the pressor response to carbachol injected into the PVN of untreated animals. They indicate that alpha-adrenoceptor-mediated vasoconstriction in the superior mesenteric vascular bed is a particularly important component in that regard. In the presence of the vasopressin antagonist, d(CH2)5(Tyr(Et))DAVP, alone or in combination with phentolamine and propranolol, the pressor response to carbachol was substantially reduced, while the renal and superior mesenteric vasoconstrictor effects were completely abolished; the bradycardia was not significantly affected by this treatment. These results indicate an important involvement of vasopressin in the cardiovascular responses to carbachol injected into the PVN of untreated animals. Moreover, in the presence of the vasopressin antagonist the hindquarters vascular bed showed a vasodilatation following PVN injection of carbachol; this effect was reversed to a vasoconstriction following combined i.v. pretreatment with the vasopressin antagonist, phentolamine and propranolol and hence was possibly due to circulating adrenaline acting on vasodilator beta 2-adrenoceptors. However, there was a residual hindquarters vasoconstriction raising the possibility that non-adrenergic, non-vasopressinergic vasoconstrictor mechanisms were influencing that vascular bed.

Adrenergic alpha-Antagonists↗
PubMed1983

Neuroeffector mechanisms of the defense reaction in the rat.

Electrical stimulation of the dorsal periaqueductal gray matter (DPAG) eliciting flight behavior in awake rats caused an increase in arterial blood pressure (BP), heart rate (HR) and respiration in rats anesthetized with urethane. The hypertension was markedly reduced by 5 mg/kg of intravenously injected hexamethonium or bretylium, virtually abolished by 5 mg/kg of phentolamine and partially antagonized by 0.1 mg/kg of the alpha 1-adrenoceptor blocker, prazosin. The tachycardia induced by DPAG stimulation was partially antagonized by hexamethonium or bretylium and abolished by propranolol (5 mg/kg, IV) or practolol (5 mg/kg, IV), but not affected by N-butylscopolamine (10 mg/kg, IV). Phentolamine increased basal HR and abolished the tachycardic response caused by either brain stimulation or intravenous noradrenaline. Prazosin moderately decreased the response to noradrenaline, but did not affect basal HR or the tachycardia induced by brain stimulation. The increase in respiratory amplitude occurring during brain stimulation was abolished by phentolamine as well as by prazosin, while the increase in respiratory rate was moderately reduced by phentolamine and propranolol. These results demonstrate that the cardiovascular component of the defense reaction of the rat is almost entirely due to a sharp increase in sympathetic tone. They also suggest that the hyperventilation induced by aversive brain stimulation is modulated by central and peripheral adrenergic mechanisms.

Animals↗
PubMed1995

Buthus martensi karsch venom: prejunctional adrenergic activity in the rat isolated anococcygeus muscle.

The effect of Buthus martensi Karsch venom (MKV) on adrenergic responses was investigated using the rat isolated anococcygeus muscle (Acm), since several scorpion venoms can cause peripheral sympathetic nerve stimulation with enhanced adrenergic responses. The effects of phentolamine (5 microM), guanethidine (5 microM), tetrodotoxin (2 microM), desipramine (1.5 microM) and reserpine pretreatment in vivo (5 mg/kg s.c. x 24 hr and 5 mg/kg i.p. x 3 hr) on contractile responses of the rat Acm to field stimulation, noradrenaline (3 microM), tyramine (10 microM), crude MKV (2 micrograms/ml), carbachol (3 microM) and potassium chloride (50 mM) were compared. Phentolamine, guanethidine, tetrodotoxin and reserpine pretreatment completely blocked the contractile responses of the Acm to MKV and to field stimulation but desipramine potentiated the responses. The responses to NA were completely blocked by phentolamine, but were potentiated by guanethidine, desipramine and reserpine pretreatment. The contractile responses to tyramine were completely blocked by phentolamine, desipramine and reserpine pretreatment. The low doses (0.1 microgram/ml x 3) of MKV, which did not produce any observable increase in tone of the anococcygeus muscle, potentiated the contractile responses to field stimulation, but not the responses to exogenous NA. Thus, the adrenergic agonist action of MKV in the rat isolated anococcygeus muscle is mediated by some prejunctional mechanism(s) of action, presumably stimulating the release of the neurotransmitter noradrenaline.

Animals↗
PubMed1988

Effects of intrathecal antagonists on the antinociception, hypotension, and bradycardia produced by intravenous administration of [D-Ala2]-methionine enkephalinamide (DALA) in the rat.

DALA is a synthetic pentapeptide that produces inhibition of the tail-flick reflex evoked by radiant heat, as well as hypotension and bradycardia. Two experiments examined the effects of administration of various receptor antagonists into the subarachnoid space of the lumbar spinal cord on the antinociception produced by IV administration of DALA. Experiment 1 showed that intrathecal administration of 30 micrograms of phentolamine produced a significant reduction in the antinociceptive effect of DALA, while naloxone (30 micrograms), methysergide (30 micrograms), or vehicle control had no effect. Experiment 2 showed that intrathecal administration of combinations of either phentolamine and methysergide, or phentolamine and naloxone, were no more effective in reducing the antinociceptive effect of DALA than administration of phentolamine alone. These data demonstrate the involvement of descending noradrenergic systems in the production of antinociception by IV DALA. Further, they indicate that the antinociception produced by DALA is independent of a direct spinal action of the drug.

Analgesics↗
PubMed1983

On the assessment of the potency of antagonists using the rat isolated anococcygeus muscle.

The conditions required for assessing the potencies of antagonists of muscarinic and at alpha-adrenoceptors have been examined using contractility studies with the rat anococcygeus muscle. Physostigmine (5 X 10(-7) M) and atropine (10(-8)-10(-7) M) had no effect on the responses to noradrenaline. The responses to acetylcholine were potentiated by physostigmine and inhibited by atropine. Physostigmine and atropine increased the slopes of the concentration-response curves to acetylcholine. In the presence of physostigmine, atropine at 10(-8) M inhibited the responses without altering the slopes of the concentration-response curves to acetylcholine. The responses to acetylcholine were potentiated by cocaine (greater than 10(-6) M) and inhibited by phentolamine (10(-6) M). Cocaine (10(-6) - 5 X 10(-6) M) potentiated and phentolamine (10(-7) - 10(-6) M) inhibited the responses to noradrenaline. The slopes of the concentration-response curves to noradrenaline were increased by cocaine at 5 X 10(-6) M, but not at 10(-6) - 2 X 10(-6) M, and by phentolamine. In the presence of cocaine (10(-6) M), phentolamine (10(-7) - 5 X 10(-7) M) inhibited the responses and increased the slopes of the concentration-response curves to noradrenaline. These results illustrate that, in the rat anococcygeus muscle, it is possible to assess the potency of muscarinic antagonists with the method described. However, in this tissue, alpha-adrenoceptor blocking activity cannot be determined with noradrenaline as the agonist in the presence of cocaine.

Acetylcholine↗
PubMed1995

Caffeine antinociception in the rat hot-plate and formalin tests and locomotor stimulation: involvement of noradrenergic mechanisms.

The present study examined antinociception produced by systemic administration of caffeine in the rat hot-plate (HP) and formalin tests and addressed several aspects of the mechanism of action of caffeine. Locomotor activity was monitored throughout. Caffeine produced a dose-related antinociception the HP (50-100 mg/kg) and formalin tests (12.5-75 mg/kg). When observed during the formalin test, caffeine stimulated locomotor activity between 12.5 and 50 mg/kg; this was followed by a depression in activity at 75 mg/kg. Caffeine did not produce an anti-inflammatory effect as determined by hindpaw plethysmometry, suggesting that antinociception was not secondary to an anti-inflammatory action. Peripheral co-administration of caffeine with the formalin did not produce antinociception, suggesting a predominant central rather than peripheral site of action for caffeine. Naloxone (10 mg/kg) did not reduce the antinociceptive or locomotor stimulant effects of caffeine, suggesting a lack of involvement of endogenous opioids in these actions. Phentolamine (5 mg/kg) enhanced antinociception by caffeine in both the HP and formalin tests, but inhibited locomotor stimulation. Prazosin (0.15 mg/kg) mimicked the action of phentolamine on locomotor stimulation, but idazoxan (0.5 mg/kg) mimicked the action of phentolamine on antinociception in the formalin test. These observations suggest an involvement of different alpha-adrenergic receptors in the two actions of phentolamine. Microinjection of 6-hydroxydopamine (6-OHDA) into the locus coeruleus, which depleted noradrenaline (NA) in the spinal cord and forebrain, inhibited the action of caffeine in the HP test. This was mimicked by intrathecal 6-OHDA which depleted NA in the spinal cord, but not by microinjection of 6-OHDA into the dorsal bundle which depleted NA in the forebrain. These results suggest an integral involvement of noradrenergic mechanisms in the antinociceptive action of caffeine in the HP and formalin tests and in locomotor stimulation, but the nature of this involvement differs for the 3 end points.

Adrenergic alpha-Antagonists↗
PubMed1995

Effect of alpha adrenergic blockade on thermoregulation in adrenal demedullated burned rats.

This study in burned rats studied at two ambient temperatures (22 degrees and 28 degrees C) and housed at 28 degrees C was designed to investigate the role of catecholamines in the maintenance of thermal homeostasis following burn injury. Two weeks prior to burn or sham burn, animals underwent adrenal medullectomy or sham adrenal medullectomy. Between postburn days 9 and 13, simultaneous direct and indirect calorimetry was performed following administration of 2mg/kg of phentolamine (alpha adrenergic blocking agent) via a carotid arterial line. Following administration of phentolamine, heat production and body temperature decreased and heat loss increased immediately. The cooling slopes for the burn groups were significantly steeper than for the control groups, within ambient temperatures. Within ambient temperatures, the presence or absence of the adrenal medulla had no discernible effect on the cooling slope of the burns or the controls. The burned animals cooled 1.9-3.5 times faster at 22 degrees than at 28 degrees C, and controls cooled 2.0-3.9 times faster at 22 degrees than at 28 degrees C. Phentolamine produced a several-fold increase in serum concentrations of both norephinephrine (NE) and epinephrine (E), indicating a gross overlap in alpha and beta adrenergic receptor utilization for E and NE. The progressive cooling of the adrenal demedullated burn group at 22 degrees C following phentolamine administration seems to indicate that norepinephrine is calorigenic for rats under these experimental circumstances. These experimental results indicate a relatively non-essential role for catecholamines in the maintenance of thermal homeostasis within the thermal neutral zone in the rat.

Adrenal Medulla↗
PubMed1985

Morphine and specific changes in the sensitivity of noradrenergic receptors within the "limbic" part of the feline caudate nucleus: a behaviour study.

The present study describes the behaviour effects of intracerebral injections of the noradrenergic (NE) agonist oxymetazoline and the NE antagonist phentolamine into the "limbic" part of the caudate nucleus of cats primed 24 hr earlier and/or treated acutely with morphine (5 mg/kg, IP). Drug-induced changes in the morphine-specific behaviour served as dependent variables. Experiments were performed during two different periods of the year, each of them marked by a characteristic sensitivity of alpha-like NE receptors to NE agents, viz. the so-called NE "antagonist" period during which the NE receptors were sensitive to the NE antagonist phentolamine and the so-called NE "agonist" period during which the NE receptors were sensitive to NE and the NE agonist oxymetazoline. The present study demonstrates that morphine reversed the initial sensitivity to oxymetazoline respectively insensitivity to phentolamine in animals tested in the NE "agonist" period. In animals tested in the NE "antagonist" period morphine did not reverse the initial insensitivity to oxymetazoline resp. sensitivity to phentolamine. Furthermore, evidence is provided that the initial sensitivity to NE agents did not conspicuously determine the animal's response to the acute administration of morphine. The data are discussed in view of the concept that the firing rate of NE fibres determines the actual sensitivity of presynaptic and postsynaptic NE receptors to NE agonists and antagonists.

Animals↗
PubMed2005

A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase.

PURPOSE: To examine prospectively the incidence of digital infarction and phentolamine rescue in a large series of patients in whom local anesthesia with adrenaline was injected electively into the hand and fingers. There continues to be a commonly held belief that epinephrine injection is contraindicated in the finger despite a lack of valid evidence to support this concept in the literature. METHODS: From 2002 to 2004 there were 9 hand surgeons in 6 cities who prospectively recorded each consecutive case of elective hand and finger epinephrine injection. They recorded each instance of skin or tissue loss and the number of times phentolamine reversal of adrenaline vasoconstriction was required. RESULTS: There were 3,110 consecutive cases of elective injection of low-dose epinephrine (1:100,000 or less) in the hand and fingers and none produced any instance of digital tissue loss. Phentolamine was not required to reverse the vasoconstriction in any patients. CONCLUSIONS: The true incidence of finger infarction in elective low-dose epinephrine injection into the hand and finger is likely to be remote, particularly with the possible rescue with phentolamine.

Canada↗
PubMed2001

Desensitization of insulin secretory response to imidazolines, tolbutamide, and quinine. II. Electrophysiological and fluorimetric studies.

Prolonged in vitro exposure (18 h) of pancreatic islets to insulin secretagogues that block ATP-dependent K(+) channels (K(ATP) channels), such as sulfonylureas, imidazolines, and quinine, induced a desensitization of insulin secretion (Rustenbeck et al., pages 1685-1694, this issue). To elucidate the underlying mechanisms, K(ATP) channel activity, plasma membrane potential and the cytosolic Ca(2+) concentration ([Ca(2+)](i)) were measured in mouse single B-cells. In B-cells desensitized by phentolamine or quinine (100 microM each) K(ATP) channel activity was virtually absent and could not be elicited by diazoxide. Desensitization by alinidine (100 microM) induced a marked reduction of K(ATP) channel activity, which could be reversed by diazoxide, whereas exposure to idazoxan (100 microM) or tolbutamide (500 microM) had no lasting effect on K(ATP) channel activity. Correspondingly, phentolamine-, alinidine-, and quinine-desensitized B-cells were markedly depolarized, whereas B-cells that had been exposed to tolbutamide or idazoxan had an unchanged resting membrane potential. The increase in [Ca(2+)](i) normally elicited by phentolamine and alinidine was suppressed after desensitization by these compounds, whereas the [Ca(2+)](i) increase by re-exposure to quinine was markedly reduced and that by tolbutamide only minimally affected as compared with control-cultured B-cells. The increase in [Ca(2+)](i) elicited by a K(+) depolarization was diminished in secretagogue-pretreated B-cells, the extent depending on the secretagogue. This effect was closely correlated with the degree of depolarization after pretreatment with the respective secretagogue. In conclusion, the apparently uniform desensitization of secretion by K(ATP) channel blockers is due to different effects at two stages located distally in the stimulus-secretion coupling: either at the stage of [Ca(2+)](i) regulation, where the increase is depressed as a consequence of a persistent depolarization (e.g. in the case of phentolamine or alinidine) and/or at the stage of exocytosis, which responds only weakly to substantial increases in [Ca(2+)](i) (in the case of tolbutamide).

Animals↗
PubMed1997

Different contributions of ATP and noradrenaline to neurotransmission in the isolated canine intermediate auricular artery.

Vasoconstrictor responses elicited by periarterial electrical nerve stimulation were analyzed pharmacologically in the canine isolated, perfused intermediate auricular artery. Phentolamine (10 microM) significantly inhibited the vasoconstrictor responses to stimulation at 5 Hz and over but not those to stimulation at frequencies below 5 Hz. Additionally administered alpha, beta-methylene ATP (1 microM) abolished the phentolamine-resistant vasoconstrictions at all frequencies used in this study. In contrast, suramin (100 microM) inhibited the vasoconstrictor responses to stimulation at 5 Hz and below but not those to stimulation at frequencies higher than 5 Hz. Phentolamine abolished the suramin-resistant vasoconstriction at all frequencies. Phentolamine and alpha, beta-methylene ATP selectively abolished the vasoconstrictor responses to exogenous noradrenaline and ATP, respectively. These results show that the co-transmission of noradrenaline and ATP exists at sympathetic nerve terminals in the canine intermediate auricular artery, and that purinergic transmission is mainly involved in the vasoconstrictor responses to low-frequency nerve stimulation.

Adenosine Triphosphate↗
PubMed1997

Nociception from blood vessels is independent of the sympathetic nervous system under physiological conditions in humans.

To test the hypothesis that vascular pain depends on sympathetic drive under physiological conditions we studied the effects of both alpha-adrenoceptor stimulation by noradrenaline and alpha-adrenoceptor blockade by phentolamine on the intensity of physicochemically evoked pain from veins in humans. In seven healthy volunteers, a vascularly isolated hand vein segment was perfused continuously with noradrenaline (6 x 10(-9)-6 x 10(-6) M), or phentolamine (1.24 x 10(-4) M). Pain was evoked by intraluminal electrostimulation or by injection of hyperosmolar saline during control perfusion of isoosmolar saline and after each noradrenaline concentration, as well as after perfusion of phentolamine. Subjects rated pain intensity continuously on an electronically controlled visual analogue scale (VAS) between 0% VAS (no pain) and 100% VAS (tolerance maximum). Intravenous electrostimulation as well as hyperosmolar solutions evoked pain in each subject. The intensity of pain was neither influenced by noradrenaline, nor by phentolamine, so that nociception from blood vessels is unlikely to be modulated by the sympathetic nervous system under physiological conditions in humans.

Adrenergic alpha-Agonists↗
PubMed1991

Pharmacologically induced erections among geriatric men.

Intracavernous injection of vasoactive drugs for the treatment of erectile impotence has become a standard therapeutic technique. Previous reports detailing experience with this treatment are based on patient populations significantly younger than most patients who suffer from impotence. The geriatric population, which comprises the majority of patients with importance, is unique due to the physical, psychological and social changes associated with the aging process. To characterize better elderly men with impotence, and determine whether intracavernous injection therapy is safe and effective in this age group, a retrospective analysis was performed upon patients attending the male sexual dysfunction clinic at our university medical center who received a standard papaverine and phentolamine mixture (30 mg. papaverine and 1.0 mg. phentolamine per ml.). The etiology of impotence, degree of patient satisfaction and complication rate of 65 patients 65 years or older (mean age 70 years) undergoing papaverine plus phentolamine self-injection therapy were compared to a similar size group of impotent men approximately 20 years younger (mean age 47 years). Significant differences in etiology of impotence were evident between the 2 groups. Treatment response rates were equal for the 2 age groups although elderly patients required a higher dose of papaverine and phentolamine to obtain an erection, and used the medication less frequently. Complications were few, of minimal consequence and occurred with equal frequency between the 2 age groups.

Adult↗