Effects of salbutamol and BRL 37344 on diastolic arterial blood pressure, plasma glucose and plasma lactate in rabbits

Summary— The aim of this study was to investigate in rabbits the diastolic arterial blood pressure, plasma glucose and plasma lactate responses to salbutamol (a selective beta-2 adrenoceptor agonist) and BRL 37344 (a selective beta-3 adrenoceptor agonist) in comparison with CGP 12177 (a potent beta-1 and beta-2 adrenoceptor antagonist which also acts as a partial beta-3 agonist), isoprenaline (a non-selective beta-1, beta-2 and beta-3 adrenoceptor agonist) and adrenaline (a non-selective beta and alpha adrenoceptor agonist). All drugs were iv infused at the same dose: 0.3 μg/kg/min (30 min). In sodium pentobarbitone (40 mg/kg)-anasthetized animals none of these compounds altered diastolic arterial blood pressure. BRL 37344 (0.1, 0.3, 1 μg/kg/min) did not modify this parameter either. In conscious 24-h fasted rabbits, only adrenaline was able to increase plasma glucose levels. By contrast, under the same experimental conditions, salbutamol, isoprenaline and adrenaline, but not BRL 37344 or CGP 12177, induced a significant increase in plasma lactate levels. Finally, the salbutamol-mediated plasma lactate response was inhibited in the presence of clonidine (2 μg/kg/min, an alpha-2 adrenoceptor agonist), a drug considered to have opposite effects (stimulatory and inhibitory) on the adenylate cyclase system. In conclusion, these data suggest that only beta-2 adrenoceptor stimulation is able to increase plasma lactate levels, a response which is inhibited by alpha-2 adrenoceptor stimulation.     

Plasma adrenaline and noradrenaline during mental stress and isometric exercise in man. The role of arterial sampling

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during isometric exercise and during a mental stress test. In both conditions arterial plasma adrenaline increased significantly, whereas arterial plasma noradrenaline remained unchanged. During isometric exercise the increase in plasma adrenaline was greater in venous blood from the exercising arm than from the resting arm. The extraction of adrenaline in the forearm was greater in the resting than in the exercising arm. Venous plasma noradrenaline showed a rebound phenomenon after isometric exercise and tended to decrease during the mental stress test. The results indicate that it is preferable to measure arterial concentrations of adrenaline as an indicator of sympathoadrenal activity rather than venous concentrations since the extraction of adrenaline in forearm might not be constant. It is suggested that a selective increase in arterial plasma adrenaline as opposed to an increase in both plasma adrenaline and noradrenaline may indicate a selective increase in sympathoadrenal activity in visceral organs.     

Effect of acute selective beta-1-adrenoceptor blockade on hormonal and cardiovascular response to insulin-induced hypoglycaemia in insulin-dependent diabetic patients

The hormonal and cardiovascular responses to intravenous (i.v.) insulin were studied in 16 insulin-dependent normotensive diabetic patients after acute injection of selective beta-1-adrenoceptor blocking agents. The lowest blood glucose levels were not affected by beta-1-adrenoceptor blockade while the time for reaching nadir was significantly reduced. Plasma adrenaline levels increased significantly during selective beta-1-adrenoceptor blockade. Plasma noradrenaline, glucagon and human growth hormone levels, however, remained unaffected. The insulin-induced tachycardia was not prevented by the beta-1-blockade, and the mean arterial blood pressure was unchanged. The ability to recognize the symptoms of insulin-induced hypoglycaemia persisted in all patients, although less pronounced in nine of them. We suggest that selective beta-1-adrenergic blocking agents may be employed without risk in the treatment of hypertensive insulin-dependent diabetic patients.     

Studies on the effects of propranolol on plasma catecholamine levels in patients with essential hypertension

The influence of the beta receptor blocking agent propranolol on plasma catecholamine concentrations was studied in eight patients with essential hypertension. The study was of single blind crossover design. Propranolol given in oral doses ranging from 60 to 240 mg daily for a period of 3 weeks decreased blood pressure and heart rate. The beta-adrenergic blocking agent caused plasma catecholamine levels to increase both at rest and during bicycle exercise. Chromatographical analysis showed that concentrations of noradrenaline as well as of adrenaline rose during treatment with propranolol. However, dopamine-beta-hydroxylase activity in plasma was not altered. Furthermore, the urinary excretion of noradrenaline, adrenaline and 4-hydroxy-3-methoxy mandelic acid did not change during beta receptor blockade. The results are compatible with the assumption that antihypertensive doses of propranolol by decreasing cardiac output cause an activation of the sympatho-adrenal system.     

Plasma concentrations of adrenaline,noradrenaline and dopamine during forearm dynamic exercise

Summary. In six healthy volunteers plasma concentrations of adrenaline, noradrenaline and dopamine were measured at rest and during dynamic forearm exercise at submaximal and maximal intensities. Arterial and venous concentrations of adrenaline and noradrenaline increased with forearm exercise at all workloads. Dopamine concentrations did not change. The increases in adrenaline and noradrenaline were almost linearly related to the increase in heart rate with no levelling off at maximal exercise intensities. It is concluded that dynamic exercise with the forearm muscle group causes a small but significant activation of the sympatho-adrenal system as reflected by increases in plasma concentrations of adrenaline and noradrenaline.     

Selective beta-1 receptor blockade with oral practolol in man. A dose-related phenomenon.

The purpose of this study was to test the hypothesis that oral administration of a low dose of practolol in man produces selective beta-1 receptor blockade, whereas oral administration of a high dose blocks both beta-1 and beta-2 receptors. Normal men were studied 2-4 h after a single oral dose of practolol (1.5 or 12 mg/kg) and after placebo. Effects on beta-1 receptors were studied by measuring heart rate responses to exercise. Effects on beta-2 receptors were tested by measuring forearm vascular responses to brachial arterial infusions of isoproterenol. Neither dose of practolol altered base-line heart rate, forearm vascular resistance, and arterial pressure, Both low and high doses significantly attenuated heart rate responses to exercise. Forearm vasodilator responses to isoproterenol were attenuated by the high dose, but not the low dose, of practolol. Serum concentrations of practolol 2 h after administration of the drug and at the time of the studies of forearm vascular responses averaged 0.5+/-0.1 (SE) and 5.9+/-1.0 mug/ml for low and high doses of practolol, respectively. The results indicate that the phenomenon of selective beta-1 receptor blockade in man is related to the dose and serum concentration of practolol selectively block beta-1 receptors; a high dose and serum concentrations block both beta-1 and beta-2 receptors.     

Beta adrenoceptor subtype binding activity in plasma and beta blockade by propranolol and beta-1 selective bisoprolol in humans. Evaluation with Schild-plots

In the present study we investigated whether the beta adrenoceptor subtype binding activity in plasma samples can predict selective and nonselective beta blockade in humans. From the right shifts of isoprenaline dose-response curves 0 to 84 hr after administration of propranolol and the beta-1 selective bisoprolol, in vivo beta blockade was assessed. In an in vitro radioreceptor assay with membrane preparations of beta-1 or beta-2 adrenoceptors, plasma samples were assayed for subtype selective blocking activity. After propranolol administration, in vitro beta-1 and beta-2 adrenoceptor occupancy declined from initially 97% to less than 10% within 48 hr. An isoprenaline dose ratio (DR)-1 of 1 coincided with a 50% occupancy of the beta-1 or the beta-2 subtype in vitro. In Schild-plots using plasma concentrations (radioreceptor assay) and the isoprenaline DR-1 for heart rate, diastolic blood pressure and inotropy (QS2C), slopes of unity were observed. After bisoprolol administration, in vitro beta-1 occupancy shifted from initially 95% to less than 10% within 72 hr. For the beta-2 subtype, an occupancy of greater than 10% was detectable only within the first 12 hr. An isoprenaline DR-1 of 1 coincided with a 50% occupancy of beta-1 adrenoceptors. The bisoprolol Schild-plots yielded a slope of unity for inotropy, but less than unity for the heart rate and diastolic blood pressure. From an extended analysis of subtype selective antagonism in Schild-plots, the fractions of the beta-2 adrenoceptor subtype participating in the isoprenaline response were calculated: heart rate 0.45 +/- 0.12 and diastolic blood pressure 0.23 +/- 0.13. It is concluded that in vitro receptor occupancy can predict beta blockade in humans for propranolol. Beta adrenoceptor subtype-mediated effects in humans can be evaluated with a selective antagonist and a refined analysis of Schild-plot data.     

Forearm vasoconstrictor response in uncomplicated type 1 diabetes mellitus

BACKGROUND: According to the 'haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM). MATERIALS AND METHODS: In 15 DM patients (DM duration 6.3 +/- 3.8 year; HbA1c 7.9 +/- 1.3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular alpha- and beta-adrenergic receptor blockade. RESULTS: At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (DeltaFVR: 12 +/- 4 vs. 19 +/- 3 arbitrary units, P < 0.05). The responses of plasma NA and heart rate variability did not differ. CONCLUSIONS: Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness.     

Plasma adrenaline and noradrenaline during orthostasis in man: the importance of arterial sampling

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during supine rest and after 30 min standing in normotensive, healthy 50-year-old men (n = 16). After 30 min standing, venous noradrenaline had increased from 1.61 +/- 0.11 to 4.22 +/- 0.30 nmol/l and arterial from 1.43 +/- 0.06 to 2.93 +/- 0.15 nmol/l. Orthostasis induced a seven-fold increment in the forearm arterial-venous difference of noradrenaline from -0.18 +/- 0.08 to -1.29 +/- 0.25 nmol/l (p less than 0.001). Orthostasis more than doubled the forearm arterial-venous difference of adrenaline from 0.15 +/- 0.03 to 0.31 +/- 0.05 nmol/l (p less than 0.001) since arterial adrenaline increased from 0.31 +/- 0.03 to 0.53 +/- 0.05 nmol/l and venous from 0.16 +/- 0.02 to 0.22 +/- 0.02 nmol/l. Arterial adrenaline correlated significantly with venous in the supine (r = 0.64, p less than 0.01) but not in the standing position (r = 0.34, NS). The results indicate that arterial concentrations of adrenaline are a much better indicator of sympatho-adrenal activity during orthostasis than peripheral venous concentrations. For noradrenaline, measurements of arterial concentrations during the orthostatic manoeuvre seem to provide information about the total noradrenergic sympathetic reactivity, while the corresponding measurements in peripheral venous blood represent the forearm locally.     

Reduced plasma noradrenaline during angiotensin II-induced acute hypertension in man

1. Plasma noradrenaline and adrenaline concentrations were measured in ten subjects before, during and after intravenous infusion of angiotensin II (ANG II) in order to determine the sympathoadrenal response of ANG II challenge in man. In five subjects ganglionic blockade was additionally performed by intravenous infusion of trimethaphan. 2. During ANG II infusion mean arterial blood pressure increased by 30% (P < 0.001), and plasma noradrenaline decreased by 25% (P < 0.001). Plasma adrenaline decreased less. 3. During ganglionic blockade plasma noradrenaline decreased significantly (P < 0.005) and similarly to the decrease obtained with ANG II infusion. 4. The results indicate that a decrease in sympathoadrenal activity occurs during ANG II-induced acute hypertension in man. This may be elicited by the arterial baroreflex, which seems to dominate any direct sympathoadrenergic facilitating effect of ANG II.     

Effects of euglycaemic and hypoglycaemic hyperinsulinaemia on sympathetic and parasympathetic regulation of haemodynamics in healthy subjects

The effects of hypoglycaemia during hyperinsulinaemia, occurring under various pathophysiological conditions, on the cardiovascular regulatory system and vasculature are largely unknown. The aim of the present study was to investigate regulatory and haemodynamic responses to acute hyperinsulinaemia and consequent hypoglycaemia in 18 healthy subjects. Blood sampling and 5 min ECG and blood pressure recordings were performed at baseline and during the euglycaemic and hypoglycaemic phases of a hyperinsulinaemic clamp. Heart rate variability (HRV) and blood pressure variability (BPV) were assessed by using power spectral analysis, and baroreflex sensitivity (BRS) was assessed using the cross-spectral method. Stroke volume was assessed from the non-invasive blood pressure signal by the arterial pulse contour method. Euglycaemic hyperinsulinaemia did not change plasma catecholamine concentrations, HRV, BPV, BRS, heart rate, blood pressure, stroke volume, cardiac output or peripheral resistance. However, hyperinsulinaemic hypoglycaemia resulted in an 11.7-fold increase in the plasma adrenaline concentration (from 0.19+/-0.03 to 1.68+/-0.32 nmol/l; P <0.001), and a modest 1.3-fold increase in the plasma noradrenaline concentration (from 1.74+/-0.22 to 2.02+/-0.19 nmol/l; P <0.05) compared with baseline. Furthermore, we observed significant decreases in diastolic blood pressure (from 68+/-3 to 60+/-3 mmHg; P <0.05) and peripheral resistance (from 24.1+/-1.2 to 18.5+/-1.1 mmHg.min(-1) x l(-1); P <0.01). Stroke volume and cardiac output increased markedly from the euglycaemic to the hypoglycaemic period only ( P <0.01 for both). Hypoglycaemia did not influence HRV, BPV or BRS. Our findings indicate that hyperinsulinaemic hypoglycaemia is characterized by a significant increase in the plasma adrenaline concentration and by decreases in peripheral resistance and blood pressure. Counter-regulation during hyperinsulinaemic hypoglycaemia involves selective adrenomedullary sympathetic activation, and does not influence cardiac parasympathetic regulation or baroreflex control of heart rate.     

Plasma catecholamine responses to change of posture in alcoholics during withdrawal and after continued abstinence from alcohol

Plasma catecholamine, blood pressure and heart rate responses to standing were measured in ten alcoholics during withdrawal, ten alcoholics after 2-7 weeks of abstinence from alcohol, six abstinent alcoholics with orthostatic hypotension and ten normal control subjects. Withdrawing alcoholics had supine and standing heart rates and plasma noradrenaline and adrenaline concentrations that were higher than in abstinent alcoholics or control subjects. Supine blood pressures were also higher in withdrawing alcoholics than in abstinent alcoholics or control subjects, but on standing blood pressures in withdrawing alcoholics fell, four patients having a fall of more than 30/5 mmHg. Abstinent alcoholics without orthostatic hypotension had higher basal and standing concentrations of noradrenaline than control subjects but normal heart rates and adrenaline concentrations. Abstinent alcoholics with orthostatic hypotension showed a wide range of basal plasma noradrenaline concentrations and were found to have variable plasma noradrenaline responses to standing, three subjects having normal responses and three subjects having no or little increase in plasma noradrenaline on standing. It is concluded that alcohol withdrawal is associated with increased sympathetic nervous activity, as reflected by raised supine and standing plasma concentrations of catecholamines, and that even after 2-7 weeks of abstinence from alcohol plasma noradrenaline concentrations may be higher than in control subjects. Despite increased sympathetic nervous responses to standing, alcoholics during withdrawal have impaired blood pressure control and some may exhibit orthostatic hypotension. Orthostatic hypotension may also be observed in alcoholics during continuing abstinence from alcohol; in some of these patients failure of reflex noradrenaline release in response to standing may contribute to orthostatic hypotension.     

Changes in plasma catecholamines in response to reflex modulation of sympathetic vasoconstrictor tone by cardiopulmonary receptors

The effects of selective deactivation and stimulation of cardiopulmonary receptors on plasma noradrenaline (radioenzymatic method) were studied in nine normotensive subjects by reducing and increasing central venous pressure for 20 min via lower body suction and leg-raising manoeuvres that did not alter arterial blood pressure and heart rate. Deactivation of cardiopulmonary receptors was accompanied by a rise in plasma noradrenaline that achieved a peak within 5 min (91.8 +/- 22%, mean +/- SE) and was then sustained. Stimulation of cardiopulmonary receptors was accompanied by a fall in plasma noradrenaline (-16.6 +/- 3.4%) that levelled off at the second minute and was then sustained. On average the increase and the reduction in plasma noradrenaline had a time course and a magnitude similar to the increase (80.5 +/- 10.5%) and the reduction (-28.4 +/- 5%) in forearm vascular resistance (derived from plethysmographic flow measurement) concomitantly caused by cardiopulmonary receptors. Furthermore, analysis of individual data showed that changes in plasma noradrenaline and forearm vascular resistance were linked by a positive relationship (r = 0.64). Thus the cardiopulmonary receptor reflex can produce rapid, marked and sustained changes in both plasma noradrenaline and forearm vasomotor tone. This is in sharp contrast with the previously observed inability of the carotid baroreflex to alter both these humoral and haemodynamic variables. Taken together these findings support the hypothesis that sympathetic tone to skeletal muscle is an important determinant of the concentration of plasma noradrenaline in blood.     

Cigarette smoke-induced elevation of plasma neuropeptide Y levels in man

Summary. The purpose of the present study was to evaluate whether neuropeptide Y, which coexists with noradrenaline in sympathetic nerves, may be released upon cigarette smoking. Therefore, previously non-smoking adults inhaled smoke from one cigarette once every minute during 10 min, and the effects on blood pressure, heart rate and plasma levels of noradrenaline and neuropeptide Y were analysed. A prompt rise of systolic blood pressure and heart rate (by 25 mmHg and 30 beats min^-1, respectively) was observed upon smoking. Systemic plasma levels of noradrenaline and neuropeptide Y were significantly elevated after 3 and 5 min of smoking, respectively, and reached maximal values (neuropeptide Y from 32±4 to 49± 7pmoll^-1, and noradrenaline from 0.72±0.16 to 1.8±0.44 nmol 1^-1) 2–5 min after the smoking period. It is concluded that smoking in man is associated with increased plasma levels of both noradrenaline and neuropeptide Y, suggesting release of these agents. Since neuropeptide Y is a potent vasoconstrictor, the present data suggest that this peptide may contribute to the smoke-induced cardiovascular response.     

Cardiovascular effects of two xanthines and the relation to adenosine antagonism

We hypothesize that the hemodynamic effects of xanthine derivatives depend on their ability to antagonize the vasodilating effects of endogenous adenosine. In a randomized, double-blind, and placebo-controlled study of 10 normotensive volunteers caffeine, a xanthine with in vitro adenosine antagonistic properties, increased mean arterial pressure by 5.6 +/- 0.9 mm Hg and lowered heart rate by 5.3 +/- 1.1 beats/min. After administration of enprofylline, a xanthine without adenosine antagonism, forearm vascular resistance decreased by 5.6 +/- 3.4 IU, heart rate increased by 10.6 +/- 2.6 beats/min, and plasma adrenaline, plasma noradrenaline, and renin activity increased by 178 +/- 86%, 14 +/- 8%, and 36 +/- 13%, respectively. Adenosine infusion alone induced a dose-related increase in pulse pressure and heart rate, and it increased plasma adrenaline and noradrenaline by 186 +/- 77% and 132 +/- 55%, respectively. This response to adenosine was reduced by pretreatment with caffeine but not enprofyline. Thus opposite circulatory responses to caffeine and enprofylline occurred, with signs of vasoconstriction and vasodilation, respectively. In addition, caffeine, but not enprofylline, reduced the cardiovascular response to exogenous adenosine.     

Sympathetic reflex control of subcutaneous blood flow in patients with congestive heart failure

Central and local regulation of forearm subcutaneous vascular resistance (FSVR) during postural changes were studied in congestive heart failure (CHF). Blood flow was measured by the local 133Xe-washout technique. Nine patients with severe CHF (baseline angiographic ejection fraction, 23 +/- 2%, mean +/- SEM; cardiac index, 2.2 +/- 0.2 litres min-1 m-2; increased left ventricular pressures and dimensions) were compared with seven control subjects who had normal cardiac performance. Baseline FSVR and plasma concentrations of noradrenaline and adrenaline were substantially higher in patients with CHF than control subjects. However, the patients, like control subjects, increased FSVR by 46 +/- 3% in response to increase in local venous transmural pressure and disclosed a normal response to decrease in forearm perfusion pressure. Both responses to changes in vascular transmural pressure were preserved after either proximal nervous blockade or local beta-receptor blockade. Central sympathetic stimulation was induced with use of 45 degrees upright tilt. Control subjects developed vasoconstriction (FSVR increased by 59 +/- 5%), which was completely abolished after proximal nerve blockade. Patients with CHF developed vasodilatation (FSVR decreased by 24 +/- 8%), which was not only abolished but reversed after proximal nerve blockade (FSVR increased by 22 +/- 7%), probably owing to the increased humoral vasoconstrictor activity. The paradoxical vasodilator response to central sympathetic stimulation in these patients was reversed after local beta-receptor blockade (FSVR increased by 19 +/- 9%). The local vasoconstrictor reflex responsiveness and intrinsic vascular reactivity were not affected by the augmented baseline sympathetic vasoconstrictor activity in patients with CHF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of low dose adrenaline and noradrenaline infusions on airway calibre in asthmatic patients

Airway, cardiovascular and metabolic responses were measured in six asthmatic patients with stable asthma during separate adrenaline, noradrenaline and control infusions. Four incremental infusion rates (4, 10, 25 and 62.5 ng min-1 kg-1) produced circulating catecholamine concentrations within the physiological range. Specific airways conductance and maximal expiratory flow rates measured from complete and partial flow-volume curves increased significantly (P less than 0.05) during adrenaline infusion, in a dose-response manner. No changes in specific airways conductance or maximal expiratory flow rates were seen during the noradrenaline or control infusion. The highest adrenaline infusion rate caused a rise in systolic blood pressure (P less than 0.05) and plasma glucose (P less than 0.05) and a fall in plasma potassium (P less than 0.05). Noradrenaline infusion caused a slight increase in diastolic blood pressure (P less than 0.05) but no metabolic changes. No cardiovascular or metabolic changes occurred during the control infusion. Infused adrenaline, producing circulating concentrations within the physiological range, caused dose-related bronchodilatation in asthmatic patients. Circulating noradrenaline does not appear to have a role in the control of basal airway tone in asthmatic patients.     

Reproducibility of haemodynamic and plasma catecholamine responses to isometric exercise and mental arithmetic in normo- and hyper-tensive subjects

1. To determine the reproducibility of a mental arithmetic stress test and a handgrip exercise test, we studied the responses of blood pressure, heart rate, forearm blood flow and plasma catecholamines on two occasions, with an interval of at least 1 week, in 24 normotensive and 22 hypertensive subjects. 2. The SE of a single observation of the percentage changes of blood pressure ranged from 3.9 to 9.3% in normotensive subjects and from 3.9 to 7.4% in hypertensive subjects in both tests. For heart rate, these values were 4.9-12.3% in the normotensive subjects and 4.8-5.7% in the hypertensive subjects. However, there was a wide individual scatter of these haemodynamic responses during both tests. The forearm blood flow, only measured during mental arithmetic, had an SE of a single observation of 33.7%. 3. In 10 normotensive subjects the SE of a single observation of the change in plasma noradrenaline was 0.16 nmol/l during handgrip exercise and 0.09 nmol/l during mental arithmetic. The corresponding values for plasma adrenaline were 0.04 and 0.05 nmol/l. 4. In conclusion, although both tests showed a rather low SE of a single observation for the blood pressure and heart rate responses in normo- and hyper-tensive subjects, there was a considerable individual variability. If related to the mean forearm blood flow responses, the SE of a single observation of the forearm blood flow response was of similar magnitude. The limited intra-individual reproducibility of both tests should be borne in mind when interpreting pharmacological intervention studies or studies evaluating sympathoadrenal reactivity in cardiovascular disorders.     

Haemodynamic and metabolic effects of combined adrenergic α- and β-receptor blockade with labetalol in the exercising human forearm

At rest supine acute intravenous administration of the combined adrenergic alpha- and beta-receptor blocking compound labetalol (1 mg/kg body weight) to young, healthy, male subjects, produced a clear-cut fall in arterial blood pressure. During dynamic forearm exercise, forearm blood flow decreased by 17.2%, and calculated vascular resistance increased by 11.3% after labetalol. Forearm oxygen uptake decreased (14.6%), suggesting an increased mechanical efficiency. Lactate release from the exercising forearm decreased (17.6%), probably because of the beta-receptor blockade. Forearm uptake of glucose and free fatty acids remained unchanged. Arterial blood glucose concentration attained a higher level after labetalol. Arterial plasma concentration of FFA was reduced during exercise and post-exercise probably because beta-receptor mediated lipolysis was antagonized.     

Arterial and venous plasma catecholamines during submaximal steady-state exercise

Arterial and venous plasma catecholamine responses to 15 min of cycling at 60% of maximal oxygen uptake were examined 11 times during exercise and recovery in nine young men. Intra-arterial blood pressure, heart rate and oxygen uptake were recorded continuously. All variables increased significantly during the initial 4 min, after which oxygen uptake, diastolic blood pressure and arterial plasma adrenaline showed no further increase. Heart rate and plasma noradrenaline, however, continued to increase, although significantly more slowly, and were closely correlated (r = 0·81, 95% CI 0·71–0·87), as were systolic blood pressure and heart rate (r = 0·78, 95% CI 0·71–0·87). Venous plasma adrenaline showed a steady increase during the whole exercise period and thus a different response pattern from arterial plasma adrenaline. In conclusion, arterial plasma catecholamines respond to steady-state exercise by a two-phase pattern paralleling the changes in arterial blood pressure and heart rate. Venous sampling does not reveal this association.