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PubMed1995

Induction of highly proliferative phenotypes in cultured glomerular mesangial cells by benzo[a]pyrene alone or in combination with methoxamine.

Recent studies have suggested that aromatic hydrocarbons can initiate glomerular mesangial cell (GMC) injury and contribute to the onset of renal disease. The present studies were conducted to assess the impact of benzo[a]pyrene (BaP), a ubiquitous polycyclic aromatic hydrocarbon, on the proliferation of GMCs. Challenge of cultured GMCs with BaP (0.3-30 microM) for 24 h was associated with concentration-dependent decreases in DNA synthesis, a response mediated by selective interference with early G1 cell cycle progression. One cycle of sequential treatment with 3 microM BaP for 24 h followed by challenge with 10 microM methoxamine (MeoA), a growth-promoting alpha 1-adrenergic agonist, for an additional 24 h attenuated the inhibitory response elicited by BaP alone. Following three rounds of sequential treatment with BaP and MeoA, GMCs exposed to BaP alone or BaP/MeoA exhibited enhanced proliferation rates relative to controls. BaP/MeoA cells acquired the greatest proliferative enhancement and exhibited unregulated c-jun and c-fos gene expression under growth-arrested and serum-stimulated conditions. Marked increases in specific AP-1 binding to a synthetic oligonucleotide were observed upon serum stimulation of quiescent cultures of BaP/MeoA cells relative to controls or any of the other treatment groups. These data demonstrate that sequential treatment with BaP in combination with MeoA is associated with induction of highly proliferative phenotypes in GMCs characterized by differential expression of growth-related protooncogenes.

Adrenergic alpha-Agonists↗

PubMed1987

Accumulation of adenosine 3',5'-monophosphate in slices of rat cerebral cortex induced by alpha-adrenergic agonists. I. Responses to methoxamine and norepinephrine in adult and neonatal tissue.

The effects of adrenergic agonists and adenosine on the accumulation of adenosine 3',5'-monophosphate (cyclic AMP) were examined in cerebral cortical slices from adult and neonatal rats. Methoxamine (10 to 100 microM) produced up to a two-fold increase in tissue from adult animals only in the presence of optimal concentrations of adenosine (40 to 100 microM), but had no effect in neonatal tissue. Such responses were inhibited more readily by prazosin than by yohimbine, but the reverse was true for responses to norepinephrine; when tested without the addition of adenosine, however, responses to norepinephrine were somewhat more sensitive to prazosin. Under the latter conditions, norepinephrine induced about twice as much increase in cyclic AMP as did isoproterenol in adult tissue. While always prevented by alpha-adrenergic antagonists, the greater efficacy of norepinephrine was eliminated by methylxanthines only in some instances, but never in tissue from animals known to be less than 60 days of age. At 11 to 15 days of age, responses to norepinephrine were more than fourfold those to isoproterenol, even in the presence of methylxanthines, and were completely suppressed by propranolol. Responses to isoproterenol were enhanced when tested in the presence of adenosine, especially in neonatal tissue. The results suggest that both endogenous adenosine and age-related phenomena may account for some of the discrepancies among earlier studies. Moreover, they indicate that several populations of alpha-adrenergic receptors may be involved in responses to adrenergic agonists in rat cerebral cortical tissue.

Adenosine↗

PubMed1983

Prolonged angina pectoris and persistent negative T waves in the precordial leads: response to atrial pacing and to methoxamine-induced hypertension.

In 18 consecutive patients without a history of myocardial infarction (MI), prolonged angina pectoris with persistent negative T waves in the precordial leads was associated with a high frequency of in-hospital spontaneous angina (14 of 18, 78%), usually accompanied by S-T segment elevation, and occasionally in-hospital MI (4 of 18, 22%). Angina and MI always involved the electrocardiographic leads with negative T waves. Coronary arteriography, performed in 16 patients, revealed greater than or equal to 90% proximal diameter reduction of the left anterior descending (LAD) coronary artery in 14 patients. No patient had severe narrowing of all 3 major coronary arteries, but the 3 who had 100% LAD occlusion lacked collateral circulation. The ejection fraction was greater than or equal to 50% in 13 patients. Atrial pacing performed in 11 patients at an average rate of 142 beats/min produced a 1.0 mm S-T segment change in only 5 patients (45%), 3 of whom had an associated lactate production. Arterial systemic hypertension induced by methoxamine in 14 patients caused reversal of negative T waves without significant S-T segment shifts or chest pain and failed to elicit lactate extraction abnormalities in each of the 5 patients in whom it was determined. Thus, prolonged angina with persistent negative T waves in the precordial leads is almost invariably associated with a critical and proximal LAD obstruction, severe narrowing of 1 or 2 coronary arteries, and poor or absent collateral vessels. The relatively preserved coronary reserve in 55% of our patients suggests that negative T waves do not represent active myocardial ischemia. The study also suggests that transient "positivization" of the negative T waves may not necessarily relate to myocardial ischemia when associated with acute systemic hypertension.

Adult↗

PubMed1983

Effects of enhanced afterload (methoxamine) and contractile state (dobutamine) on the left ventricular late-systolic wall stress-dimension relation.

Although the left ventricular (LV) end-systolic pressure-dimension relation is a load-independent, sensitive index of contractile state, its accurate determination requires afterload manipulation. The slope value of the late-systolic stress-dimension relation determined under resting conditions has been suggested as an alternative index of contractility that can be assessed without pharmacologic intervention. To evaluate this relation, 14 normal subjects were studied by M-mode echocardiography, phonocardiography and indirect carotid pulse tracings during infusion of methoxamine to increase afterload. Seven of these subjects were also studied after infusion of dobutamine to increase contractility. Continuous systolic stress-dimension trajectories were computer generated from digitized tracings. The late-systolic portions of these curves were found to be linear and the slope and intercept were determined. The slope value was sensitive to both afterload and contractility, and the magnitude of change in slope value was relatively greater during afterload enhancement than during inotropic stimulation. A strong correlation of slope value with peak systolic stress was found. Thus, the late-systolic stress-dimension relation is linear with a slope value which is dependent on both LV contractility and afterload. Like other ejection phase indexes, the usefulness of this index is limited by its inability to distinguish changes in contractile state from alterations in loading conditions.

Adolescent↗

PubMed1985

Effects of loading conditions and contractile state (methoxamine and dobutamine) on left ventricular early diastolic function in normal subjects.

The influence of changes in preload, afterload and contractile state on left ventricular (LV) filling characteristics were examined. Normal subjects underwent echocardiographic determination of the peak rates of LV dimension change and wall thinning and their respective timing at rest, after preload augmentation with dextran, during increased afterload with methoxamine and during inotropic stimulation by dobutamine. These 2 peak velocities and their timing in diastole correlated well with each other and responded similarly to interventions. Increased preload resulted in higher peak velocities of dimension change and wall thinning, without changing the time in diastole at which they occur. Both peak velocities moved later into diastole with higher afterload; however, the overall change in magnitude was variable and without statistical significance. Inotropic stimulation resulted in faster rates of peak dimension change and wall thinning, which occurred at an earlier point in diastole. Examination of various measures of LV size and function over a wide range of preload and afterload conditions under a constant contractile state revealed a complex set of relations. The ratio of wall thickness-to-dimension at end-diastole showed the most significant relation to the peak rate of dimension change, whereas peak thinning was best correlated with fractional wall thickening. Both velocities were also significantly but more weakly related to other variables of systolic function. The timing of these peak velocities correlated most closely with the end-systolic wall stress and heart rate. Thus, LV filling and wall thinning depend in a complex fashion on loading conditions, heart rate and contractile state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[3H]prazosin binding in the intermediolateral cell column and the effects of iontophoresed methoxamine on sympathetic preganglionic neuronal activity in the anaesthetized cat and rat.

The autoradiographic localization of [3H]prazosin (alpha 1-adrenoceptor ligand) binding sites was determined in cat spinal cord sections. High levels of [3H]prazosin binding were found in the intermediolateral cell column (IML) at thoracic and lumbar levels. The iontophoresis of the alpha 1-adrenoceptor agonist methoxamine onto sympathetic preganglionic neurones (SPNs) in anaesthetized cats and rats caused excitation of 8 cat SPNs and 13 rat SPNs. These results suggest an excitatory role for some of the catecholaminergic innervation of the IML.

Anesthesia↗

PubMed1991

Prostaglandin E2 mediates the stimulatory effect of methoxamine on in vivo luteinizing hormone-releasing hormone (LH-RH) release in the ovariectomized female rhesus monkey.

Previously, we found that noradrenergic input through alpha 1-receptors modulates pulsatile release of luteinizing hormone-releasing hormone (LH-RH) in ovariectomized rhesus monkeys in the absence of estrogen. In the present study, the role of prostaglandin E2 (PGE2) in mediating alpha-adrenergic stimulation of LH-RH release is investigated. In the first experiment the effects of the alpha 1-adrenergic agonist methoxamine (MTX) on LH-RH and PGE2 release were examined. Push-pull perfusion of the stalk-median eminence (S-ME) was performed in conscious, ovariectomized monkeys, and perfusate samples were collected on ice. MTX (10(-5) M) was infused into the S-ME through the push cannula for 10 min at 90-min intervals, and LH-RH and PGE2 in aliquots of the same perfusate samples were measured by radioimmunoassay. Infusion of MTX significantly stimulated LH-RH release (n = 12; P less than 0.01) and PGE2 release (P less than 0.05). In the second experiment, the effect of PGE2 infusion on LH-RH release was tested. PGE2 (10(-7) M) was infused using the same protocol as above, and LH-RH was measured in the perfusates. Infusion of PGE2 through the push cannula significantly stimulated LH-RH release (n = 23; P less than 0.05). These results suggest that the stimulatory effect of MTX on LH-RH release is at least partly mediated by PGE2, since MTX stimulated not only LH-RH but also PGE2 release, and since PGE2 itself stimulated LH-RH release. Therefore, PGE2 may be an important endogenous mediator of alpha 1-adrenergic input stimulating pulsatile LH-RH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

Bronchopulmonary effects of phenylephrine and methoxamine in the guinea-pig. Interaction with bronchoconstrictor drugs.

The bronchopulmonary effects of phenylephrine (Phe) and methoxamine (Met) were investigated in vitro on isolated guinea-pig tracheas and lung strips and in vivo on pulmonary airway resistance (Raw) in conscious guinea-pigs. Phe, but not Met, relaxed the isolated trachea precontracted with acetylcholine (ACh); this effect was inhibited by propranolol and ascribed to beta-adrenergic stimulation. In the presence of propranolol, both Phe and Met contracted the isolated trachea (-log EC50 were 3.80 +/- 0.37 and 3.04 +/- 0.25 respectively (n = 5] and this effect was competitively antagonized by phentolamine. Phe and Met contracted the isolated lung strips more strongly than the trachea (-log EC50 were 5.14 +/- 0.23 and 4.30 +/- 0.14 respectively (n = 5]. In contrast with the latter, the maximum response was equivalent to that induced by ACh; this effect was also antagonized by phentolamine. In the conscious guinea-pig, Phe (100 and 300 micrograms/kg) and Met (1 and 3 mg/kg) had no effect on Raw but significantly reduced the bronchoconstriction induced by ACh (25 micrograms/kg), histamine (20 micrograms/kg) and serotonin (15 micrograms/kg); this protective effect was unmodified by propranolol (2 mg/kg), yohimbine (1 mg/kg) or piperoxan (0.3 mg/kg) but was significantly inhibited by prazosin (30 micrograms/kg) or AR- C239 (50 micrograms/kg). These results suggest that alpha-adrenergic vasoconstriction with subsequent shrinkage of the bronchial mucosa is responsible for the protective effect of Phe and Met against ACh-induced bronchoconstriction. In isolated lung strips, vasoconstriction would increase tension.

Acetylcholine↗

PubMed1987

Investigation of the central and peripheral actions of clonidine and methoxamine using a new in vivo rat preparation.

A cross-circulation technique was developed in rats to distinguish central from peripheral cardiovascular actions of drugs. The right common carotid arteries were ligated, and the left common carotid arteries and left and right external jugular veins of two pentobarbital-anesthetized rats were connected with PE tubing so that peripheral blood from one rat, A, supplied the head of another rat, B, and then returned to the body of A, and vice versa, for peripheral blood from rat B. Each rat was artificially ventilated with O2, the chest was opened, and both subclavian arteries were ligated. The distribution of blood flow was verified by the microsphere technique. Prior to ligation of the subclavian arteries, blood flow from rat A supplied its own brain and both brain hemispheres but not the brain stem of rat B. Following subclavian artery ligation, blood flow from rat A did not supply A's brain, but supplied both hemispheres and the brain stem of rat B. The head of each rat was, therefore, rendered dependent on the carotid arterial blood supply from another rat. The i.v. injection of clonidine (25 micrograms/kg) into rat A significantly increased mean arterial pressure and slightly, but not significantly, decreased heart rate in rat A, whereas it significantly decreased mean arterial pressure and slightly, but not significantly, decreased heart rate in rat B. Conversely, i.v. injection of methoxamine (25 micrograms/kg) in rat A significantly increased mean arterial pressure and decreased heart rate in rat A, and significantly increased mean arterial pressure and slightly, but not significantly, increased heart rate in rat B. Therefore, this rat cross-circulation preparation can be used to separate the central and peripheral cardiovascular actions of drugs.

Animals↗

PubMed1988

Vascular reactivity to methoxamine in conscious sinoaortic denervated rats.

Alterations in vascular alpha-adrenoceptor responsiveness following sinoaortic denervation was studied in conscious rats. The arterial hypertension observed in baroreceptor denervated rats decreased progressively during the 30 days of observation. A pressor hyperresponsiveness to methoxamine (10-80 micrograms/kg, iv), was observed 3 to 7 days after baroreceptor denervation followed by a gradual normalization of the vascular reactivity. The results indicate a possible participation of an enhanced alpha 1-adrenoceptor-mediated vasoconstrictor component in the early phase of neurogenic hypertension.

Animals↗

PubMed1998

Intracavernous methoxamine in the treatment of priapism.

Methoxamine is an alpha-adrenergic drug, its unique pharmacokinetics and mechanism of action on alpha-1 receptors lead to consider it, similarly to phenylephrine, as a first-choice drug for treating drug-induced or veno-occlusive priapism. The experience obtained with its use in the management of three cases of priapism lasting over 7 h and one case of sustained rigid erection caused during anesthetic induction are reported.

Adrenergic alpha-Agonists↗

PubMed1993

Coronary artery spasm with ventricular tachycardia after administration of methoxamine during cervical epidural anesthesia--a case report.

Coronary artery spasm occurred during thoracotomy under cervical epidural anesthesia in a 60-year-old male patient who had no prior history of myocardial ischemia. It is most likely that the administration of methoxamine induced the spasm. Hypotension and venodilatation induced by the epidural anesthesia and increased vagal tone might also contribute to the spasm.

Anesthesia, Epidural↗

PubMed1986

Hypersensitivity to methoxamine in atria isolated from streptozotocin-induced diabetic rats.

The reactivity to methoxamine (Met) of atria isolated from the hearts of normal and from acutely streptozotocin-diabetic rats has been studied. Met (1 X 10(-6) M) increased the tension of both normal and diabetic atria, but in diabetic atria, the dose-response curve to Met was shifted to the left and the efficacy of Met was enhanced. Inhibitors of alpha-adrenoceptors blocked, in a competitive manner, the positive inotropic effect induced by Met in both types of atrial preparations. Inhibitors of the cyclo-oxygenase pathway for arachidonic acid metabolism blocked the atrial response to Met in non-diabetic as well as in diabetic atria. The inhibition of prostacyclin synthetase prevented the effect of Met in normal atria, while blockers of thromboxane generation inhibited it in diabetic ones. Agents that inhibit the activity of lipoxygenase(s) significantly reduced the positive inotropic action induced by Met in diabetic atria but failed to modify it in non-diabetic preparations. These results show that diabetic atria are more sensitive to Met than normal atria. In diabetes the response to alpha-adrenoceptor stimulation could be mediated by oxidative product generated via thromboxane synthetase and lipoxygenase(s) activities; whereas in normal preparations the action of Met may involve the release of prostacyclin.

Adrenergic alpha-Antagonists↗

PubMed1994

Inhibition of substance P-induced microvascular leakage by inhaled methoxamine in rat airways.

1. The effect of the inhaled alpha-adrenoceptor agonist, methoxamine (MTX), was studied on experimental airway oedema induced by injection of substance P (SP) in the rat. Sprague-Dawley rats (300-350 g) were anaesthetized with sodium thiopentone, tracheotomized and artificially ventilated. 2. MTX or its vehicle was administered by inhalation. Airway resistance and blood pressure were monitored continuously. Evans Blue dye (EB, 20 mg kg-1) was injected through a jugular catheter 1 min before SP (14.8 nmol kg-1). Airways were dissected out, weighed and placed in formamide for EB extraction and determination by spectrophotometry. 3. EB extravasation induced by SP was significantly reduced in distal intraparenchymal bronchi by inhaled MTX at doses of 50 micrograms kg-1 (58 +/- 9 vs 96 +/- 9 ng EB mg-1 tissue after vehicle, P < 0.001) and 100 micrograms kg-1 (69 +/- 11 vs 137 +/- 26 ng EB mg-1 tissue after vehicle, P < 0.01). Inhaled MTX by itself (100 micrograms kg-1) increased blood pressure: 172 +/- 6 vs 132 +/- 10 mmHg baseline (P < 0.02), but neither induced extravasation nor increased airway resistance. 4. In another set of experiments without SP, MTX was administered intravenously 1 min after EB. At 100 micrograms kg-1, i.v. MTX increased blood pressure to a similar extent as inhaled MTX (180 vs 147 mmHg baseline, P < 0.01), increased airway resistance and caused leakage of plasma proteins in distal intraparenchymal bronchi (79 +/- 7 vs 47 +/- 1 ng EB mg-1 tissue, P < 0.02). 5 Similarly, after sequential i.v. injections of doubling doses of MTX (50-800 microg kg-1), a marked EB extravasation was found in the airways. This was abrogated by pretreatment with prazosin (100 microg kg-1)but not with propranolol (2 mg kg-1).6 These results suggest that microvascular leakage and airway oedema induced by i.v. MTX may be linked to an increase in pressure in the pulmonary circulation, resulting from vasoconstriction of the pulmonary vasculature and acute cardiac dysfunction due to systemic hypertension.7 Our results with inhaled MTX show that direct deposition of MTX at the bronchial vasculature induces a reduction in SP-induced microvascular leakage in rat airways and that inhaled MTX does not share the untoward effect of i.v. MTX inducing airway oedema.

Administration, Inhalation↗

PubMed1991

Repetitive nonsustained monomorphic ventricular tachycardia aborted by methoxamine and sleep "heart rate dependent ventricular tachycardia".

Methoxamine, an alpha adrenoreceptor agonist, and sleep abolished repetitive nonsustained monomorphic ventricular tachycardia in a 41-year-old man without detectable underlying heart disease. Detailed pacing studies revealed that the occurrence of ventricular tachycardia was totally dependent on the basic heart rate. Sleep and the alpha adrenoreceptor agonist abolished the ventricular tachycardia by slowing the basic heart rate. Verapamil, propranolol, and disopyramide were able to decrease the upper limit of the tachycardia-initiating heart rate, but none of them were able to increase the lower limit (75/min). Failure to increase the lower limit of the tachycardia-initiating heart rate was a major reason why these conventional antiarrhythmic drugs were unable to suppress his daytime episodes of repetitive ventricular tachycardia.

Adult↗

PubMed1984

Effects of methoxamine, and alpha-1 adrenoceptor agonist, and prazosin, an alpha-1 antagonist, on the stages of the sleep-waking cycle in the cat.

In these experiments the effects of alpha 1-adrenoceptor agonism and antagonism were studied on the stages of the sleep-waking cycle of the cat, in order to determine optimal levels of alpha 1-adrenergic transmission for these stages. Polygraphic 16-h recordings showed that prazosin, an alpha 1-adrenoceptor antagonist, at 1 mg/kg i.p., increased paradoxical sleep (PS) time from 15.3% to 26.4% (p less than 0.001) of total time, and the number of PS episodes from 30.4 to 43.6 (p less than 0.001). The effect was prompt, reaching a maximum during the first 4 h with a shortening of PS latency from 40.4 min to 11.0 min (p less than 0.001). Prazosin at doses of 0.5 and 3.0 though not at 10.0 mg/kg also slightly, but significantly, increased PS. Methoxamine, and alpha 1-adrenoceptor agonist, at doses of 0.5 and 3.0 mg/kg, increased aroused waking time (low voltage mixed frequency EEG) during the first 4 h from 23.5% to 33.3% (p less than 0.05) and to 50.3% (p less than 0.01), and decreased PS. Prazosin potentiated dose-dependently clonidine-induced drowsiness ( hypersynchronized 4-8 Hz EEG), whereas the decrease in deep slow wave sleep and PS were potentiated only at the largest dose of it. These results indicate that moderate inhibition of cerebral alpha 1-adrenergic transmission facilitates paradoxical sleep in the cat. Furthermore, they suggest that the level of cerebral alpha 1-adrenergic transmission is high during aroused waking and low during drowsy waking.

Adrenergic alpha-Agonists↗

PubMed1976

Effects of angiotensin, vasopressin, and methoxamine on cardiac function and blood flow distribution in conscious dogs.

A comparison was made of the effects of vasopressin (ADH), methoxamine (MX), and angiotensin II (AN) on coronary and left ventricular dynamics, cardiac output, and regional blood flow distribution in intact, consci9us dogs. At an equal percent pressure elevation, ADH reduced cardiac output and cardiac rate the most, while AN had the least effect. After denervation of arterial baroreceptors, ADH still reduced heart rate, while AN increased it, suggesting nonbaroreceptor negative and positive chronotropic effects, respectively. A differential pattern on peak dP/dt was also observed, with ACH causing a greater reduction than MX while AN did not decrease dP/dt. With heart rate held constant, AN did not reduce dP/dt, suggesting a direct positive inotropic effect since dP/dt should have fallen slightly due to reflex mechanisms, as was observed with MX and ADH. ADH induced the greatest increase in coronary resistance (140%), while the least (46%) was observed with AN, which could be explained, in part, by the differential effects observed on cardiac rate and contractility. The greatest increase in resistance in the iliac bed occurred with ADH (30%), and the least with AN (34%). Conversely, the greatest constriction in the renal bed occurred with AN (95%), and lesser amounts were observed with ADH (36%) and MX (35%). Thus ADH, MX, and AN exert potent yet differential vasoconstricting actions on peripheral beds. In addition, while all three agents elicited coronary vasoconstriction, the differential effects on coronary vascular resistance appeared to be due predominantly to a difference in chronotropic and inotropic actions.

Angiotensin II↗

PubMed1988

Inhibitory effects of nitroglycerin on contractile responses to methoxamine and clonidine in isolated rabbit renal and femoral arteries.

The inhibitory effect of nitroglycerin (NG) on contractile responses to methoxamine (MO) and clonidine (CL) was investigated in isolated rabbit renal and femoral arteries. NG (10(-7)-10(-5) mol/l) inhibited the responses to MO and CL in a noncompetitive manner and its inhibitory effect on CL-responses was much greater than that on the MO-responses. In the presence of phenoxybenzamine, however, NG (10(-5) mol/l) markedly inhibited the residual response to MO. Contractile responses to KCl or added Ca2+ in a Ca2+-free medium containing KCl were slightly inhibited by NG. In the presence of nifedipine, NG (10(-5) mol/l) markedly inhibited residual responses to CL but it only slightly inhibited the response to MO. In a Ca2+-free medium with EGTA, MO (10(-5) mol/l) or CL (10(-5) mol/l) induced a phasic contraction. NG had a greater inhibitory effect on the response to CL than MO. In a Ca2+-free medium with EGTA, nifedipine and MO (10(-5) mol/l) or CL (10(-5) mol/l), Ca2+ induced a tonic contraction. NG inhibited the Ca2+-response in the presence of CL, but it had little or no effect on the Ca2+-response in the presence of MO. These results suggest that in rabbit renal and femoral arteries, the potent inhibitory effect of NG on the responses to CL as compared to MO may be due to differences in the amount of receptor reserves that exist for both the agonists. In addition, the inhibition of voltage-dependent Ca2+ channels may not play a major role in the vasoinhibitory action of NG. Further, NG inhibits contractile responses due to mobilization of intracellular Ca2+ much more than the responses due to receptor-activated, nifedipine-insensitive Ca2+-movement.

Animals↗