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At least 1,693 records · Page 94Linked to original sources
PubMed1993

Fetal catecholamine responses to vibroacoustic stimulation.

OBJECTIVE: The aim of this study was to determine whether fetal vibroacoustic stimulation caused a surge of catecholamines from the fetal sympathoadrenal system. STUDY DESIGN: A randomized, prospective, controlled trial was performed at The Queen Mother's Hospital, Glasgow. Circulating catecholamine levels in cord blood from a group of fetuses who received vibroacoustic stimulation 1 to 2 minutes before delivery by elective cesarean section (n = 25) were compared with those from a group of controls (n = 23) (Mann-Whitney U test). Fetal heart rate response to vibroacoustic stimulation was recorded in 10 additional pregnancies under identical experimental conditions. RESULTS: No differences were found in norepinephrine or epinephrine levels between the vibroacoustic stimulation group and the control group. A positive fetal heart rate response was observed in seven of 10 fetuses tested. Fetal norepinephrine levels were also found to be influenced by maternal blood pressure and administration of ephedrine. CONCLUSIONS: Under these conditions vibroacoustic stimulation does evoke the characteristic fetal heart rate response, but it does not induce a surge of catecholamines from the fetal sympathoadrenal system. Therefore it is unlikely that the immediate fetal heart rate response to vibroacoustic stimulation is induced by a surge in systemic catecholamines.

Acoustic Stimulation↗
PubMed2001

Catecholamine monoamine oxidase a metabolite in adrenergic neurons is cytotoxic in vivo.

3,4-Dihydroxyphenylglycolaldehyde is the monoamine oxidase-A metabolite of two catecholamine neurotransmitters, epinephrine and norepinephrine. This aldehyde metabolite and its synthesizing enzymes increase in cell bodies of catecholamine neurons in Alzheimer's disease. To test the hypothesis that 3,4-dihydroxyphenylglycolaldehyde, but not epinephrine or its major metabolite 4-hydroxy-3-methoxyphenylglycol, is a neurotoxin, we injected 3,4-dihydroxyphenylglycolaldehyde onto adrenergic neurons in the rostral ventrolateral medulla. Injections of epinephrine or 4-hydroxy-3-methoxyphenylglycol were made into the same area of controls. A dose response and time study were performed. Adrenergic neurons were identified by their content of the epinephrine synthesizing enzyme, phenylethanolamine N-methyltransferase, immunohistochemically. Apoptosis was evaluated by in situ terminal deoxynucleotidyl-transferase mediated dUTP nick end label staining. Injection of 3,4-dihydroxyphenylglycolaldehyde in amounts as low as 50 ng results in loss of adrenergic neurons and apoptosis after 18 h. The degree of neurotoxicity is dose and time dependent. Doses of 3,4-dihydroxyphenylglycolaldehyde 10-fold higher produce necrosis. Neither epinephrine nor 4-hydroxy-3-methoxyphenylglycol are toxic. A 2.5 microg injection of 3,4-dihydroxyphenylglycolaldehyde is toxic to cortical neurons but not glia. Active uptake of the catecholamine-derived aldehyde into differentiated PC-12 cells is demonstrated. Implications of these findings for catecholamine neuron death in neurodegenerative diseases are discussed.

Aldehydes↗
PubMed1997

Modulatory role of catecholamines in the transsynaptic expression of c-fos in the rat medial prefrontal cortex induced by disinhibition of the mediodorsal thalamus: a study employing microdialysis and immunohistochemistry.

We studied the interaction of catecholaminergic and thalamic afferents of the medial prefrontal cortex (PFC) by analyzing the effects of catecholamine depletion on thalamus-induced c-fos expression in the PFC of freely moving rats. Thalamic projections to the PFC were pharmacologically activated by perfusing the GABA-A receptor antagonist bicuculline (0.03 mM or 0.1 mM) through a dialysis probe implanted into the mediodorsal thalamic nucleus. Bicuculline perfusion induced Fos-like immunoreactivity in the thalamic projection areas, including the PFC, and in the thalamic nuclei surrounding the dialysis probe. 6-Hydroxydopamine lesions of the ventral tegmental area causing a 70-80% depletion of catecholamines in the PFC did not influence the increase in the number of Fos-like immunoreactive nuclei in the prefrontal cortex in response to thalamic stimulation. However, densitometric image analysis revealed that the intensity of Fos-like immunoreactivity in the PFC of lesioned rats perfused with 0.1 mM bicuculline was higher than in correspondingly treated controls. The behavioral activity to bicuculline perfusion, an increase of non-ambulatory activity (0.03 mM) followed by locomotion and rearing (0.1 mM), was not changed in 6-hydroxydopamine-lesioned rats. It is suggested that the thalamically induced c-fos response is directly mediated by excitatory, presumably glutamatergic, transmission and not indirectly by an activation of catecholaminergic afferents of the PFC. The increase in the intensity of Fos-like immunostaining in strongly stimulated, catecholamine-depleted rats suggests that catecholamines modulate the degree to which thalamic activity can activate the PFC of awake animals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2002

Plasma catecholamines in ethanol tolerance and withdrawal in mice.

Plasma levels of catecholamines (noradrenaline and adrenaline) as well as the ratio of the two catecholamines were measured in experimental mice during various stages of acute and chronic ethanol treatment. Acute intraperitoneal (i.p.) ethanol administration and acute per os (p.o.) ethanol ingestion resulted in a similar elevation of the plasma levels of both catecholamines. During the development of ethanol tolerance/dependence (ingestion of drinking water containing ethanol for 14 days), plasma catecholamine concentrations returned to the control levels. During subsequent ethanol withdrawal, a highly significant increase was observed in plasma noradrenaline. The withdrawal-associated elevation of plasma adrenaline was also significant; however, the rise in plasma noradrenaline during withdrawal appeared to be higher than that found for adrenaline. Thus, the ratio of plasma noradrenaline to adrenaline was higher during withdrawal, and this ratio also exhibited an association with the severity of ethanol withdrawal symptoms. Since plasma noradrenaline derives to a great extent from the sympathetic nervous system--and the alcohol withdrawal syndrome is characterized by symptoms of overactivity of this system--a positive correlation may exist between noradrenaline and the severity of withdrawal symptomatology.

Animals↗
PubMed2003

Seasonal variation in plasma catecholamines and adipose tissue lipolysis in adult female green sea turtles (Chelonia mydas).

We investigated three aspects of potential interrenal regulation of reproduction in female green sea turtles, Chelonia mydas. First, seasonal trends in plasma catecholamines were examined from female C. mydas at different stages of their reproductive cycles. Second, variation in catecholamine levels during a nesting season were analysed in relation to restraint time, and ecological variables such as nesting habitat, body size, and reproductive investment. Third, catecholamine and corticosterone (CORT) induced lipolysis was investigated with adipose tissue collected from gravid green turtles, using in vitro incubations. Plasma epinephrine (EPI) was lowest in non-vitellogenic (1.55 +/- 0.26 ng/ml) and post-breeding (1.57 +/- 0.22 ng/ml) females, and highest in courting females (2.87 +/- 0.28). Concentrations of norepinephrine (NE) and EPI were relatively constant throughout a nesting season, and not significantly related to restraint time, reproductive investment or nesting habitat. In vitro concentrations of CORT (>3 ng/ml) and NE (2 ng/ml) induced significant release of glycerol after 6h of incubation. Epinephrine tended to induce an antilipolytic affect at low concentrations (0.25 ng/ml) and a net lipolytic response at higher concentrations (>1 ng/ml). Our data suggest that EPI may play a role in regulating body condition during vitellogenesis, and maintaining energy stores during prolonged aphagia during courtship and nesting in female green sea turtles. Furthermore, we provide preliminary evidence that suggests that catecholamine production may be either down regulated or de-sensitised in gravid female C. mydas.

Adipose Tissue↗
PubMed1999

Lack of leptin suppression in response to hypersecretion of catecholamines in pheochromocytoma patients.

Leptin is a major regulator of body weight and energy balance and is subject to a variety of regulatory inputs. From several previous studies, catecholamines have been suggested to exert an inhibitory influence on leptin production in animals. In the present study, we analyzed leptin levels in relation to catecholamine hypersecretion in 27 human pheochromocytoma patients. A 10-fold increase in circulating norepinephrine (P < .0001) did not result in suppression of plasma leptin in the patients compared with normal controls (median and interquartile range, 4.3 ng/mL [2.4 to 6.8] v 2.2 ng/mL [1.9 to 3.0] in men and 18.6 [12.3 to 27.0] v 11.4 [10.1 to 15.9] in women). Correlation analysis indicated a significant association of leptin with epinephrine in normal subjects (r = -.81, P < .0001), but not in pheochromocytoma patients. Leptin was not related to norepinephrine in either group. In conclusion, our data suggest that a chronic elevation of catecholamines does not cause suppression of leptin secretion in patients with pheochromocytoma. This lack of effect may be attributable to the development of tolerance of adipose tissue leptin production to catecholamines.

Adrenal Gland Neoplasms↗
PubMed2003

Stimulation of Staphylococcus epidermidis growth and biofilm formation by catecholamine inotropes.

BACKGROUND: Bacterial colonisation of indwelling medical devices by coagulase-negative staphylococci is a prevalent risk in intensive-care units. Factors determining biofilm formation and progression to catheter- related infection are incompletely understood. We postulated that administration of inotropic agents via indwelling intravenous catheters may stimulate growth and formation of biofilms by Staphylococcus epidermidis. METHODS: Inocula representing physiologically relevant infecting doses of S epidermidis were incubated in a minimum medium supplemented with fresh human plasma in the presence or absence of pharmacological concentrations of norepinephrine or dobutamine. Biofilm formation on polystyrene and medical-grade silicone was examined. After incubation, cultures were assessed for growth and formation of biofilms by colony counting and scanning electronmicroscopy. The production of exopolysaccharide, a major constituent of S epidermidis biofilms, was also assessed by use of immunofluorescence microscopy. FINDINGS: Incubation of S epidermidis with catecholamine inotropes in the presence of human plasma resulted in a significant increase in growth compared with control on both polystyrene and silicone surfaces, with pronounced increases in biofilm formation as visualised by scanning electronmicroscopy. Experiments with transferrin labelled with radioactive iron showed the ability of catecholamine inotropes to facilitate acquisition of iron by S epidermidis. Immunofluorescence microscopy revealed extensive exopolysaccharide production associated with S epidermidis biofilms. INTERPRETATION: The ability of catecholamine inotropic drugs to stimulate bacterial proliferation and biofilm formation may be an aetiological factor in the development of intravascular catheter colonisation and catheter-related infection. The removal of iron from transferrin for subsequent use by S epidermidis is a possible mechanism by which catecholamine inotropes stimulate bacterial growth as biofilms.

Adult↗
PubMed2002

Differential effect of catecholamines and MPP(+) on membrane permeability in brain mitochondria and cell viability in PC12 cells.

The present study examined the effect of dopamine, 6-hydroxydopamine (6-OHDA), and MPP(+) on the membrane permeability transition in brain mitochondria and on viability in PC12 cells. Dopamine and 6-hydroxydopamine induced the swelling and membrane potential change in mitochondria, which was inhibited by addition of antioxidant enzymes, SOD and catalase. In contrast, antioxidant enzymes did not reduce the effect of MPP(+) on mitochondrial swelling and membrane potential. Catecholamines enhanced the Ca(2+) uptake and release by mitochondria, and the addition of MPP(+) induced Ca(2+) release. Catecholamines induced a thiol oxidation in mitochondria that was decreased by antioxidant enzymes. MPP(+) showed a little effect on the cytochrome c release from mitochondria and did not induce thiol oxidation. Catecholamines and MPP(+) induced a cell death, including apoptosis, in PC12 cells that was inhibited by addition of antioxidant enzymes. The result suggests that the oxidation of dopamine and 6-hydroxydopamine could modulate the membrane permeability in brain mitochondria and induce PC12 cell death, which may be ascribed to oxidative stress. MPP(+) appears to exert a toxic effect on neuronal cells by the action, which is different from catecholamines.

1-Methyl-4-phenylpyridinium↗
PubMed1998

Stimulatory effect of lymphocyte-derived factor on catecholamine efflux from cultured bovine adrenal medullary cells.

The effects of lymphocytes and their conditioned medium on catecholamine efflux and uptake were examined in cultured bovine adrenal medullary cells. Co-culture of adrenal medullary cells with lymphocytes for 3 days caused an increase in appearance of catecholamines in the culture medium. Treatment of adrenal medullary cells with a conditioned medium prepared from lymphocytes also enhanced the appearance of catecholamines in culture medium in time- (8-48 h) and concentration-dependent manners. Heat treatment of the conditioned medium at 60 and 100 degrees C for 10 min reduced its stimulatory effect to 59 and 20% of control, respectively. After gel filtration on a Sephadex G-25 column or dialysis (<8 kDa molecular mass cutoff), the stimulatory activity of the conditioned medium was found in a high molecular fraction. The conditioned medium had little effect on the activity of lactate dehydrogenase in the medium of cultured adrenal medullary cells and on desipramine-sensitive [3H]norepinephrine uptake by the cells. These findings suggest that lymphocytes release a heat-sensitive factor(s) (molecular mass of more than 8 kDa) which increases efflux of catecholamines from cultured adrenal medullary cells.

Adrenal Medulla↗
PubMed1990

Fully automated high-performance liquid chromatographic assay for the analysis of free catecholamines in urine.

A totally automated and reliable high-performance liquid chromatographic method is described for the routine determination of free catecholamines (norepinephrine, epinephrine and dopamine) in urine. The catecholamines were isolated from urine samples using small alumina columns. A standard automated method for pH adjustment of urine before the extraction step has been developed. The extraction was performed on an ASPEC (Automatic Sample Preparation with Extraction Columns, Gilson). The eluate was collected in a separate tube and then automatically injected into the chromatographic column. The catecholamines were separated by reversed-phase ion-pair liquid chromatography and quantified by fluorescence detection. No manual intervention was required during the extraction and separation procedure. One sample may be run every 15 min, ca. 96 samples in 24 h. Analytical recoveries for all three catecholamines are 63-87%, and the detection limits are 0.01, 0.01, and 0.03 microM for norepinephrine, epinephrine and dopamine, respectively, which is highly satisfactory for urine. Day-to-day coefficients of variation were less than 10%.

Autoanalysis↗
PubMed2002

Is electrical stimulation during administration of catecholamines required for the evaluation of success after ablation of atrioventricular node re-entrant tachycardias?

OBJECTIVES: The purpose of this study was to answer the question of whether stimulation after administration of catecholamines is mandatory for identifying unsuccessful ablations of atrioventricular node re-entrant tachycardia (AVNRT). BACKGROUND: The success of radiofrequency (RF) catheter ablation in AVNRT is confirmed in many centers by noninducibility of tachycardias during stimulation after the administration of catecholamines. METHODS: A total of 131 patients (81 women and 50 men; mean age 53.6 +/- 13.7 years [range 20 to 77]) were studied. Electrical stimulation was performed without and with the beta-adrenergic amine Orciprenaline (metaproterenol) before and after RF catheter ablation. RESULTS: In 100 patients (76.3%; confidence interval [CI] 68.1% to 83.3%) an AVNRT was inducible without administration of Orciprenaline. Thirty minutes after the initially successful ablation in 95 patients, tachycardia was inducible in none of these patients, not even after Orciprenaline administration. In the 31 patients (23.7%; CI 16.7% to 31.9%) in whom there was no tachycardia inducible before ablation, Orciprenaline was given, and the stimulation protocol was repeated. In only five patients (3.8%; CI 1.3% to 8.7%) was there still no tachycardia inducible. After an initially successful ablation in the 26 patients who had inducible tachycardias with Orciprenaline before ablation, no tachycardia could be re-induced. After Orciprenaline, the tachycardia was inducible again in only one patient. CONCLUSIONS: Only patients who require catecholamines for tachycardia induction before ablation need catecholamines for control of the success of the ablation of AVNRT.

Adrenergic beta-Agonists↗
PubMed1993

Plasma catecholamines--analytical challenges and physiological limitations.

Catecholamines in plasma may be measured to assess sympathoadrenal activity. Numerous assay methodologies have been published, illustrating the fact that there are many analytical problems. Different methodologies are discussed briefly. A plea for better validation, especially with regard to specificity (which should not be confused with sensitivity or reproducibility), is made. Plasma NA is a frequently used marker for sympathetic nerve activity in humans, but the data obtained are often misinterpreted due to lack of appreciation of the physiological determinants of the NA concentration measured. NA overflow from an organ gives a good reflection of nerve activity in that organ. However, sympathetic nerve activity is highly differentiated, particularly during stress, and conventional plasma NA levels (usually forearm venous samples) cannot be taken as an indication of 'sympathetic tone' in the whole individual. NA is rapidly removed from plasma, resulting in meaningless net veno-arterial concentration differences over organs unless its removal from arterial plasma is taken into account. In the forearm, for example, 40-50% of catecholamines are removed during one passage; about half of the NA in a venous sample is derived from the arm and half from the rest of the body. Therefore, conventional venous sampling overemphasizes local (mainly skeletal muscle) nerve activity. Whole-body sympathetic nerve activity may be monitored in arterial or mixed venous (i.e. pulmonary arterial) samples, which reflect NA overflow from all organs in the body. NA levels are determined both by overflow to plasma and clearance from plasma. NA turnover studies with 3H-NA infusions may be needed to assess clearance, but the simpler concentration measurements usually yield adequate information if the sampling site is relevant. NA overflow from an organ can be assessed (using 3H-NA or ADR as a marker for NA extraction in the organ) and provides valuable information on local sympathetic activity. Mental stress elicits marked circulatory responses, with mainly cardiorenal sympathetic activation and minor elevations of conventional venous plasma NA levels, thus illustrating the differentiated firing pattern of the sympathetic nerves. Circulating ADR is less important than neurogenic mechanisms in the responses to stress. Concentration-effect studies for infused catecholamines may be used for receptor sensitivity studies in vivo, but reflexogenic contributions to responses need to be determined. However, prejunctional mechanisms cannot be assessed without knowledge of the nerve activity present; for example, ADR infusion leads to increased nerve activity. When correctly sampled, measured and interpreted, plasma catecholamines can yield very valuable information on sympathoadrenal activity.

Animals↗
PubMed2002

Influence of long-term changes in incubation temperature on catecholamine levels in plasma of chicken embryos (Gallus gallus f. domestica).

Catecholamine concentrations were determined from day 18 to 21 of incubation (D18, D21) in developing chicken embryos. The control group was continuously incubated at 37.5 degrees C. The eggs of the two other groups were incubated at 37.5 degrees C until day 14. In the cold group, temperature was decreased to 35.0 degrees C and in the warm group, incubation temperature was increased to 38.5 degrees C for the remainder of incubation. Plasma catecholamine concentrations were measured in eggs exposed to a change in incubation temperature for 4, 5, 6 and 7 days. Embryos in the warm group had dopamine (DA) and noradrenaline (NA) concentrations that were significantly higher than in the control group. On the contrary, eggs incubated at the cooler temperature had hormone levels that were significantly lower than in the control group. Adrenaline (A) levels in the two experimental treatments were significantly lower compared to control eggs. Temperature modulated the time needed for development. Chicken embryos are supposed to hatch on day 21. However, on day 20, NA concentration in the cold-incubated group was too low to fulfill its essential physiological function, whereas in the warm group, the NA concentration seems to be sufficient. Long-term exposure to altered incubation temperature affects the quantitative catecholamine concentration during development, but the relative proportion of each catecholamine remained constant.

Animals↗
PubMed2001

Tolcapone increases plasma catecholamine levels in patients with Parkinson's disease.

Tolcapone is a catechol-ortho-methyl-tranferase (COMT) inhibitor that increases the L-DOPA half-life and the duration of effect in Parkinson's disease. We investigated the effect of tolcapone on the plasma catecholamine levels. We measured plasma catecholamines 2h after the first daily dose of L-DOPA or L-DOPA+tolcapone while resting and 2 and 10min after standing. We also measured the pharmacokinetics of L-DOPA and 3-OM-DOPA and the clinical response to the medication for 6h after the early morning dose. The levels of dopamine, norepinephrine, adrenaline and total catecholamines significantly increased and 3-OM-DOPA decreased with tolcapone. We did not observe significant changes in the plasma L-DOPA levels at the doses of tolcapone used in this study. Tolcapone side effects included worsening of dyskinesia and psychosis, diarrhea and elevation of liver enzymes. Twenty-four-hour ambulatory recording of arterial blood pressure and heart rate did not reveal cardiovascular side effects in patients treated with tolcapone for less than 1year. Since adrenergic stimulation may increase the hepatotoxic potential of commonly used drugs, usually thought of as safe for the liver, we postulate that some of the already reported life threatening complications of tolcapone could be related to excessive adrenergic stimulation by high catecholamine levels caused by inhibition of COMT activity.

Journal Article↗
PubMed2003

Intraoperative catecholamine release in brain-dead organ donors is not suppressed by administration of fentanyl.

BACKGROUND AND OBJECTIVE: Endogenous catecholamines are released in brain-dead organ donors following painful stimulation during retrieval surgery, and might be harmful to harvested organs. Our hypothesis was that inhibition of pain by fentanyl would inhibit such catecholamine release. METHODS: We tested 17 brain-dead organ donors in a randomized, placebo-controlled, double-blinded study. Blood samples for determination of epinephrine and norepinephrine concentrations were obtained before and 10 min after in take of either fentanyl 7 microg kg(-1) or an equivalent volume of placebo. Further points of measurement were taken after skin incision and sternotomy. Mean arterial pressure and heart rate at these points were recorded. RESULTS: Catecholamine concentrations rose following painful stimuli. No differences in haemodynamics, between the fentanyl and the placebo group were detectable. Epinephrine concentrations, but not those of norepinephrine, were higher in the fentanyl group, reaching significance following sternotomy. CONCLUSION: We conclude that the use of fentanyl (7 microg kg(-1)) was not effective in suppressing the catecholamine release, following painful surgical stimulation in brain-dead organ donors.

Adult↗
PubMed1982

Increased plasma catecholamines in patients with Friedreich's ataxia.

We studied free plasma catecholamines in 23 patients with Friedreich's ataxia, having a mean age of 22 +/- 9.6 (SD) years. Conjugated catecholamines were also studied in 10 patients. Mean plasma norepinephrine and epinephrine were significantly higher than controls both in the supine and standing positions. In total 15 out of 23 patients (65%) had increase free and/or conjugated plasma catecholamines. The increased in plasma catecholamines was more marked in patients with severe neuromotor impairment. Among the patients with left ventricular concentric hypertrophy (wall thickness greater than 12 mm), only 3 had no demonstrable sympathetic hyperfunction. Since the high local concentrations of norepinephrine at the site of release from sympathetic nerve terminals may serve as a trigger for the hypertrophic response of the myocardial cell, it is suggested that early pharmacological intervention could prevent or limit the cardiomyopathic process or its clinical consequences.

Adolescent↗
PubMed2000

Urinary catecholamine levels and incidence of dentofacial injuries in children: a 2-year prospective study.

Urinary catecholamines have been used to measure emotionally stressful states which may have an impact on dentofacial injuries. This prospective study investigated the hypothesis that urinary catecholamines such as epinephrine, norepinephrine and dopamine do not affect significantly the incidence of dentofacial injuries in children. As a test of this hypothesis 204 children, males and females, aged 8 to 10 years, were included in the study. After a first examination, each subject was re-examined, at one-year intervals, over a period of two years. Dentofacial injuries were recorded by a clinical examination and a questionnaire. Three 24-h urine samples, with an interval of one year between each, were collected and analyzed by the high performance liquid chromatography technique to assay the catecholamine content. Socio-economic factors were recorded by a questionnaire. Using the panel of data collected, the logistic multiple regression model was employed to test whether the incidence of dentofacial injuries was affected by the studied variables. The 95% probability level was used. Specificity and sensitivity as well as the positive and negative predictive rates were computed. The results showed that epinephrine had a significant correlation with the incidence of dentofacial injuries. Other factors found to have a significant impact were child's age and gender. The values of sensitivity and specificity were 81% and 69% respectively, while the positive and negative predictive rates were 68% and 82% respectively. The data, therefore, provided evidence that emotionally stressful states measured by the urinary catecholamines were prominent etiologic factors of dentofacial injury.

Accidents↗
PubMed1983

Effect of phenoxybenzamine on cardiovascular and plasma catecholamine responses to clonidine.

To determine whether the alpha-adrenergic antagonist phenoxybenzamine would alter cardiovascular or plasma catecholamine response to the alpha-adrenergic agonist clonidine, six patients with pheochromocytomas and eight with labile hypertension were studied. Clonidine, 0.3 mg, was given with and without 48 hr pretreatment with 30 mg/day phenoxybenzamine. The response to 10 mg diazepam was also observed in seven of the subjects who had labile hypertension. In the hypertensive patients, clonidine alone induced a fall in supine blood pressure from 137 +/- 21/91 +/- 14 to 109 +/- 18/76 +/- 17 mm Hg and, with phenoxybenzamine, clonidine reduced blood pressure from 141 +/- 22/89 +/- 10 to 107 +/- 21/72 +/- 11 mm Hg. Plasma norepinephrine fell from 179 +/- 60 to 107 +/- 79 pg/ml without phenoxybenzamine and from 229 +/- 159 to 95 +/- 46 pg/ml with phenoxybenzamine in hypertensive subjects. Responses with phenoxybenzamine did not differ from those without phenoxybenzamine and diazepam induced no cardiovascular or plasma catecholamine changes. Clonidine did not lower plasma catecholamines in patients with a pheochromocytoma in the presence or in the absence of phenoxybenzamine. Blood pressure tended to decline after clonidine in pheochromocytoma patients not taking phenoxybenzamine, but it was not reduced by clonidine when these patients were taking phenoxybenzamine. Phenoxybenzamine does not inhibit reduction in blood pressure and plasma catecholamines induced by clonidine in patients with essential hypertension or interfere with the clonidine suppression test in patients with pheochromocytomas.

Blood Pressure↗