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PubMedDate not supplied

Prostaglandins and the renal responses to haemorrhage, angiotensin II and methoxamine in conscious rabbits.

The responses to 20% haemorrhage were examined in conscious rabbits with or without inhibition of prostaglandin production by indomethacin (5 mg/kg + 0.5 mg/kg per h i.v.). In rabbits not pretreated with indomethacin, haemorrhage lowered mean arterial pressure by 6.3 (s.e.m. = 1.6) mmHg, renal blood flow by 22.8 (s.e.m. = 3.4) ml/min and glomerular filtration rate (GFR) by 3.4 (s.e.m. = 0.6) ml/min, and raised plasma renin activity by 5.2 (s.e.m. = 1.0) ng/ml per h. Pretreatment of the rabbits with indomethacin did not significantly alter the responses to haemorrhage. Mean arterial pressure fell by 10.9 (s.e.m. = 1.8) mmHg, renal blood flow by 24.9 (s.e.m. = 3.9) ml/min and GFR by 4.2 (s.e.m. = 1.8) ml/min and plasma renin activity rose by 3.2 (s.e.m. = 0.5) ng/ml per h. In a separate group of 5 rabbits, angiotensin II was infused at 10, 25 and 50 ng/kg per min i.v. or methoxamine was infused at 10 and 25 micrograms/kg per min i.v. After indomethacin pretreatment, angiotensin II caused a significantly greater rise in mean arterial pressure and greater fall in renal vascular conductance, but there was no effect on the GFR response. In contrast, methoxamine caused significantly smaller falls in GFR, renal blood flow and renal vascular conductance after indomethacin pretreatment. Indomethacin significantly lowered resting GFR but not renal blood flow or arterial pressure. Thus, indomethacin pretreatment accentuated the renal vasoconstriction to angiotensin II, reduced the renal vasoconstriction to methoxamine and had no effect on the responses to haemorrhage. The results therefore suggest that prostaglandins do not act to lessen the renal effects of all vasoconstrictor stimuli, but that the prostaglandin response depends on the nature of the ischaemic stimulus.

Angiotensin II↗
PubMedDate not supplied

Enhancement of methoxamine-induced contractile responses of rat ventricular muscle in streptozotocin-induced diabetes is associated with alpha1A adrenoceptor upregulation.

AIM: To clarify the time-related changes in cardiac function and the mechanism underlying the cardiac dysfunction present in diabetes mellitus, we studied mechanical responses induced by alpha(1)- and beta-adrenoceptors, the Ca(2+)-entry promoter Bay K 8644- and ryanodine (an agent known to inhibit Ca(2+) release from the sarcoplasmic reticulum) in papillary muscles from streptozotocin (STZ)-induced diabetic and age-matched control rats. METHODS: Male Wistar rats received a single injection of STZ (60 mg kg(-1)) via the tail vein to induce diabetes. For the mechanical studies, papillary muscle preparations were suspended in an organ bath and isometric contractions were measured in 1-, 4-, and 10-week STZ-induced diabetic and age-matched control rats. RESULTS: In 1-week diabetic rats, the contractions induced by isoproterenol, methoxamine and Bay K 8644 were unchanged (vs. age-matched controls). In 4-week diabetic rats, (a) the isoproterenol- and Bay K 8644-induced contractions were impaired, (b) sensitivity to ryanodine was reduced, whereas (c) the methoxamine-induced contraction was unchanged. In 10-week diabetic rats, the isoproterenol- and Bay K 8644-induced contractile responses were impaired and the sensitivity to ryanodine was reduced, but in sharp contrast the methoxamine-induced contraction was enhanced. Both the mRNA level for the alpha(1A) adrenoceptor (but not the alpha(1B) or alpha(1D) mRNAs) and alpha(1A) adrenoceptor protein were increased in 10-week diabetic rats (vs. age-matched controls). CONCLUSION: These results suggest that impairments of beta-adrenergic and Ca(2+)-handling mechanisms occur early in the development of cardiomyopathy in STZ-induced diabetic rats, and that this is followed by augmentation of alpha(1A) adrenoceptor-mediated inotropy due to alpha(1A) adrenoceptor upregulation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Evidence for regionally selective changes in response to potassium chloride but not vasopressin or methoxamine in vasculature from diabetic rats.

In the present study we examined the contractile responses of aortae and mesenteric and femoral arteries taken from rats treated 3 weeks previously with streptozotocin (55 mg/kg, i.v.) or saline (1 mL/kg, i.v.) to vasopressin, potassium chloride, and methoxamine. The dose-response curves obtained with vasopressin and methoxamine were not significantly different between control and diabetic animals. However, both the diabetic mesenteric and femoral arteries showed a significantly (p less than 0.05) greater maximum response to potassium chloride as compared with their respective controls. The reactivity of the diabetic aortae to this agonist was not different. It is concluded that while the contractile responses of the diabetic tissues were normal when the agonist was vasopressin or methoxamine, there would appear to be regionally selective changes in responsiveness to potassium chloride.

Adrenergic alpha-Agonists↗
PubMed1992

In vitro hyporeactivity to methoxamine in portal hypertensive rats: reversal by nitric oxide blockade.

The endothelial cell plays an important role in the local control of vascular smooth muscle tone. Portal hypertension is accompanied by systemic vasodilatation and a decreased response to vasoconstrictors, changes especially evident in the superior mesenteric arterial bed. To evaluate a possible effect of the locally released endothelium-derived relaxing factor nitric oxide (NO), we tested the effect of NO blockade in in vitro perfused superior mesenteric arterial beds of normal (sham) and portal hypertensive (PVL) rats, induced by partial portal vein ligation. A significant (n = 7/group; P = 0.02) hyporeactivity to the vasoconstrictive properties of the alpha-adrenoceptor agonist methoxamine (3 x 10(-6) to 3 x 10(-4) M) was prevented by blocking NO formation in PVL compared with sham rats, using the stereospecific biosynthesis antagonist N omega-nitro-L-arginine (10(-4) M, n = 7/group; NS for all methoxamine concentrations tested). This effect was reversed by the NO precursor L-arginine (10(-3) M, n = 5/group). In conclusion, these in vitro results in mesenteric vessels demonstrate that 1) portal hypertension is accompanied by a hyporeactivity to the vasopressor methoxamine and 2) locally released NO in this preparation is responsible for the decreased vasoconstrictive response.

Acetylcholine↗
PubMed1982

Hemodynamic responses to methoxamine in exercise-conditioned and aorta-constricted rats.

Hemodynamic responses to methoxamine hydrochloride (Vasoxyl) were determined in rats conditioned by a moderate treadmill exercise program and in rats subjected to 5 wk of abdominal aortic constriction. Rats of comparable age served as controls. Initial hemodynamic values for control rats were as follows: left ventricular pressure, 124 +/- 4 Torr and cardiac index, 145 +/- 8 ml . min-1 . kg-1. Although minor variations were noted, initial hemodynamic values for exercise-conditioned rats were within the normal range, and no left ventricular hypertrophy was present. Aorta-constricted rats exhibited a 50% increase in left ventricular weight and significant differences in left ventricular pressure (173 +/- 9 Torr) and cardiac index (117 +/- 10 ml . min-1 . kg-1). Sequentially increasing doses of methoxamine were infused to elevate myocardial preload and afterload. When compared with control rats, exercise-conditioned animals were better able to maintain cardiac index at comparable increases in either mean arterial or left ventricular end-diastolic pressures. In contrast, aorta-constricted rats demonstrated profound reductions in hemodynamic functions in response to methoxamine infusion. Directionally divergent hemodynamic results occur in exercise-conditioned and aorta-constricted animals when subjected to identical cardiovascular stresses.

Animals↗
PubMed1992

Effects of methoxamine on spontaneous uterine activity and blood flow of the rat uterus 'in vivo'.

The vascular (blood pressure, heart rate and peripheral blood flow) and uterine (spontaneous motility) responses to intravenous methoxamine were studied in anaesthetized rats pre-treated with diethylstilboestrol. Methoxamine produced an increase (0.5-2 mg/kg) or did not modify (0.01 and 3 mg/kg) spontaneous uterine motility. The alpha 1-agonist also induced a hypertensive effect (0.1-3 mg/kg) accompanied by bradycardia at the highest doses, and a decrease in blood flow significantly greater in intestinal than uterine tissues. These effects were abolished by prazosin. The uterine action of methoxamine in vivo appears to result from the balance between myometrial alpha 1-excitatory effect and vascular alpha 1-vasoconstriction which induced uterine inhibition. The oestrogens appear to protect the alpha 1-mediated vasoconstriction.

Animals↗
PubMed1978

Methoxamine-induced increase in afterload. Effect on left ventricular performance in chronic obstructive pulmonary disease.

With a radionuclide technique, left ventricular ejection fraction and stroke volume index were measured in the basal state and after the stress of a methoxamine-induced increase in afterload in 10 men with severe chronic obstructive pulmonary disease. The resting mean left ventricular ejection fraction was normal in all 10 patients. After an acute increase in resistance to left ventricular ejection with methoxamine, the left ventricular ejection fraction and the stroke volume index did not decrease significantly, even in the presence of cor pulmonale in 5 patients. Mean pulmonary capillary wedge pressure was normal before, and did not change significantly after, methoxamine infusion. The data suggest that latent left ventricular dysfunction is not present in this group of patients with severe chronic obstructive pulmonary disease.

Aged↗
PubMed1988

Age changes in secretory function of male and female rat parotid glands in response to methoxamine and pilocarpine.

Saliva secreted in response to methoxamine and pilocarpine was collected from the cannulated ducts of both parotid glands of male and female rats at weekly age intervals from three to 10 weeks, and at 3.5, 8, and 15 months of age. It was analyzed for the concentrations of protein, potassium, calcium, inorganic phosphate, and for amylase activity. The type of protein were determined electrophoretically, and an amino acid analysis of the total protein was also carried out. The wet weights of the glands increased substantially up to eight weeks of age, then reached almost plateau values, and finally tended to decrease at 15 months of age in both sexes. The salivary volumes secreted in response to methoxamine and pilocarpine were positively correlated with the parotid gland weights in both sexes. The concentrations of protein, potassium, and inorganic phosphate were inversely related to the salivary flow rates only at relatively low rates of flow. The amylase activity was positively correlated with the concentration of protein, independent of the nature of the stimulus, age, and sex. With methoxamine as a stimulus, the amylase activity was positively correlated with the concentration of calcium, independent of age and sex. The types of protein and amino acid concentrations were independent of the nature of the stimulus, age, and sex up to 15 months of age. However, in parotid saliva of several rats at 8 and 15 months of age, unusual proteins were observed electrophoretically, independent of the nature of the stimulus and sex.

Aging↗
PubMed1985

The role of calcium ion in methoxamine-induced amylase release from parotid glands of euthyroid and hypothyroid rats.

The change in responsiveness to alpha-adrenergic stimulation and to calcium ions in amylase release from parotid glands of hypothyroid rats was compared with that in euthyroid rats. Calcium depletion and addition of verapamil or W-7 in the medium caused a decrease in methoxamine-induced amylase release in both eu- and hypothyroid rats. Moreover, addition of calcium ions to Ca2+-free medium markedly increased the methoxamine-induced amylase release in proportion to its concentration in hypothyroid rats. These results suggest that calcium ions play an important role in methoxamine-induced amylase release from parotid glands of hypothyroid rats as well as those of the euthyroid ones.

Adrenergic alpha-Agonists↗
PubMed2000

Enhancement of vasoconstrictor responses to 5-HT but no to methoxamine by cooling in isolated dog lingual and mesenteric arteries.

The effect of temperature on submaximal vasoconstrictions to an intraluminal injection of serotonin (5-HT) and methoxamine was investigated in isolated and perfused canine lingual and mesenteric arteries, using the cannula insertion method. In both arteries cooling (from 37 degrees C to 27 degrees C) caused a remarkable enhancement of vasoconstriction to 5-HT, but did not to methoxamine. In lingual arteries, methoxamine-induced constrictions were strongly depressed, although those were slightly depressed in mesenteric arteries. It is assumed that 5-HT produces an important role to modulate vascular tonicity in low temperature conditions.

Adrenergic alpha-Agonists↗
PubMed2000

Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis.

We determined the acute effects of methoxamine, a specific alpha1-selective adrenoceptor agonist, on the left ventricular-arterial coupling in streptozotocin (STZ)-diabetic rats, using the end-systolic pressure-stroke volume relationships. Rats given STZ 65 mg x kg(-1) iv (n = 8) were compared with untreated age-matched controls (n = 8). A high-fidelity pressure sensor and an electromagnetic flow probe measured left ventricular (LV) pressure and ascending aortic flow, respectively. Both LV end-systolic elastance E(LV,ES) and effective arterial elastance Ea were estimated from the pressure-ejected volume loop. The optimal afterload Q(load) determined by the ratio of Ea to E(LV,ES) was used to measure the optimality of energy transmission from the left ventricle to the arterial system. In comparison with controls, diabetic rats had decreased LV end-systolic elastance E(LV,ES), at 513 +/- 30 vs. 613 +/- 29 mmHg x mL(-1), decreased effective arterial elastance Ea, at 296 +/- 20 vs. 572 +/- 48 mmHg x mL(-1), and decreased optimal afterload Q(load), at 0.938 +/- 0.007 vs. 0.985 +/- 0.009. Methoxamine administration to STZ-diabetic rats significantly increased LV end-systolic elastance E(LV,ES), from 513 +/- 30 to 602 +/- 38 mmHg x mL(-1), and effective arterial elastance Ea, from 296 +/- 20 to 371 +/- 28 mmHg x mL(-1), but did not change optimal afterload Q(load). We conclude that diabetes worsens not only the contractile function of the left ventricle, but also the matching condition for the left ventricular-arterial coupling. In STZ-diabetic rats, administration of methoxamine improves the contractile status of the ventricle and arteries, but not the optimality of energy transmission from the left ventricle to the arterial system.

Adrenergic alpha-Agonists↗
PubMed1987

Influence of methoxamine, 5-hydroxytryptamine and physically induced low pH on thermal sensitivity and thermotolerance.

The influence of pH on split-dose hyperthermic response of non-resistant and thermotolerant Ehrlich tumors was studied. Vasoactive agents, methoxamine and 5-hydroxytryptamine (5-HT) and, mechanical interruption of the tumor blood flow by wire technique were applied in combination with hyperthermia at 72-hour intervals, where an increased thermal response was observed in Ehrlich tumor. A potential influence in suppressing the induction of thermotolerance (hyperthermia at 24-hour intervals) was evident in the case of 5-HT and methoxamine. These vasoactive agents and the wire technique showed a selective effect in reducing the tumor microcirculation as well as lowering its pH. However, unlike the wire technique, the pH was rather low in the postheating period in the case of 5-HT and methoxamine. Poor tumor vascularization induced by vasoactive agents or physical means would demonstrate a poor nutritional condition with a low pH, whereby an increase in thermal response would be obvious and may be expected to have maximal influence either in the decay or in delaying the induction of thermotolerance. A low tumor pH particularly during the postheating period may have some role against the development of thermotolerance.

Animals↗
PubMed1983

Interaction of methoxamine with compensatory vasodilation distal to coronary stenoses.

The interaction of alpha 1-receptor mediated vasoconstriction with the compensatory vasodilation distal to coronary stenoses was examined in 9 open-chest dogs. Stenoses on proximal circumflex artery were produced by a circumferential wire snare; an intermediate stenosis was defined by reduction of the reactive hyperemia repayment to 70%, a critical stenosis by prevention of any repayment following a 15-s occlusion. Methoxamine (Vasoxine), 500 micrograms, was infused via a small catheter distal to the stenosis under a constant coronary perfusion pressure of 80 mmHg and a constant heart rate of 160 bpm. The vasoconstrictive response to methoxamine correlated with the degree of reactive hyperemia repayment after 15 s occlusion (r = 0.74) and the preexisting level of poststenotic resistance (r = 0.62). At increasing peripheral coronary pressure distal to the stenosis the resistance of the stenosis was reduced (r = -0.84). Thus, alpha 1-adrenergic vasoconstriction is less marked with increasing compensatory vasodilation distal to coronary stenosis. The severity of the stenosis is reduced at increased intraluminal pressure, probably by distention of its luminal area. Methoxamine might induce a redistribution of coronary blood flow towards ischemic regions and reduce ischemic injury.

Animals↗
PubMed1982

Nitroglycerin combined with methoxamine in experimental coronary occlusions.

The effect of nitroglycerin, methoxamine, and the combination of both drugs were studied in anaesthetized dogs, during the acute phase of experimental myocardial infarction. Different haemodynamic and electrophysiological parameters were measured during the first three minutes of occluding the left descending coronary artery, while each drug or the combination were being infused. After stopping infusions, new occlusions were performed periodically in order to assess the persistence of drug effects. Nitroglycerin alone provoked hypotension and reduced the development of the ischaemic area, while methoxamine did not modify the measured variables. A long-lasting favourable effect on the ischaemic area was recorded when methoxamine prevented hypotension induced by nitroglycerin.

Animals↗
PubMed1977

Low cortisol and growth hormone secretion in response to methoxamine administration in obese subjects.

To investigate the hypothalamic responsiveness in obesity, changes in the levels of plasma cortisol and growth hormone (GH) were studied in 11 obese and six normal-weight subjects after hypothalamic alpha-adrenergic stimulation with methoxamine, 20 mg i.v. To allow for dose/body weight differences, five additional obese subjects received 30 mg methoxamine. Plasma GH, cortisol, insulin, free fatty acid and glucose levels were determined during the 3-h infusion of methoxamine. The responses of cortisol and GH were reduced in the obese subjects as compared with the normal-weight subjects. No significant changes in plasma glucose, free fatty acids or insulin were observed in any of the groups. The reduced responses of plasma cortisol ang GH in the obese subjects are considered to be an expression of hypothalamic underresponsiveness, since the stimuli for the secretion of these hormones are at least partially controlled by an alpha-adrenergic mechanism.

Adult↗
PubMed2001

Effect of methoxamine on maximum urethral pressure in women with genuine stress incontinence: a placebo-controlled, double-blind crossover study.

The aim of the study was to evaluate the potential role for a selective alpha1-adrenoceptor agonist in the treatment of urinary stress incontinence. A randomised, double-blind, placebo-controlled, crossover study design was employed. Half log incremental doses of intravenous methoxamine or placebo (saline) were administered to a group of women with genuine stress incontinence while measuring maximum urethral pressure (MUP), blood pressure, heart rate, and symptomatic side effects. Methoxamine evoked non-significant increases in MUP and diastolic blood pressure but caused a significant rise in systolic blood pressure and significant fall in heart rate at maximum dosage. Systemic side effects including piloerection, headache, and cold extremities were experienced in all subjects. The results indicate that the clinical usefulness of direct, peripherally acting sub-type-selective alpha1-adrenoceptor agonists in the medical treatment of stress incontinence may be limited by associated piloerection and cardiovascular side effects.

Adrenergic alpha-Agonists↗
PubMed1976

Pre- and post-junctional supersensitivity: differentiation by intraventricular infusions of norepinephrine and methoxamine.

Intraventricular infusions of methoxamine, an adrenergic agonist that has a relatively low affinity for the presynaptic uptake mechanism, produces a significant dose-dependent increase in locomotor activity comparable to the increase elicited by infusion of equimolar doses of norepinephrine (NE). The behavioral responsiveness to infusion of both NE and methoxamine was more than doubled 3 weeks after pretreatment with 6-hydroxydopamine (6-OHDA). These results indicate that the increased responsiveness to NE induced by 6-OHDA is due to enhanced postsynaptic receptor sensitivity rather than to a loss of presynaptic uptake inactivation.

Animals↗
PubMed1977

Responses of the flexor reflex to LSD, tryptamine, 5-hydroxytryptophan, methoxamine, and d-amphetamine in acute and chronic spinal rats.

The flexor reflex of acute (40-48 h after mid-thoracic spinal transection) and chronic (at least 2 months after transection) spinal rats was evoked by tetanic electrical stimulation of both hindfeet and recorded on a polygraph using a transducer connected to the left hindfoot. The flexor reflex in the chronic spinal rat was more responsive to electrical stimulation and to the actions of drugs studied than was the flexor reflex in the acute spinal rat. In chronic spinal rats, d-amphetamine, methoxamine, LSD, tryptamine, and 5-hydroxytryptophan (5-HTP) facilitated the flexor reflex and induced spontaneous movements. These facilitative effects were seen in acute spinal rats only when much larger i.p. doses of amphetamine, methoxamine, and LSD were used. Small i.v. doses of tryptamine also produced the facilitation. The facilitation caused by LSD and tryptamine, but not 5-HTP, in chronic spinal rats was antagonized by cyproheptadine. These observations suggest that chronic spinal rats were more sensitive to the drugs than acute spinal rats and support the hypothesis that the mode of action of LSD is similar to that of tryptamine but different from that of 5-HTP since cyproheptadine antagonized the facilitative effects of LSD and tryptamine but not those of 5-HTP.

5-Hydroxytryptophan↗