Beta-adrenergic Influence Research Articles

Toward a better noninvasive assessment of preejection period: A novel automatic algorithm for B-point detection and correction on thoracic impedance cardiogram.

Impedance cardiography is the most common clinically validated, noninvasive method for determining the timing of the opening of the aortic valve, an important event used for measuring preejection period, which reflects sympathetic beta-adrenergic influences on the heart. Automatic detection of the exact time of the opening of the aortic valve (B point on the impedance cardiogram) has proven to be challenging as its appearance varies between and within individuals and may manifest as a reversal, inflection, or rapid slope change of the thoracic impedance derivative's (dZ/dt) rapid rise. Here, a novel automatic algorithm is proposed for the detection of the B point by finding the main rapid rise of the dZ/dt signal, which is due to blood ejection. Several conditions based on zero crossings, minima, and maxima of the dZ/dt signal and its derivatives are considered to reject any unwanted noise and artifacts and select the true B-point location. The detected B-point locations are then corrected by modeling the B-point time data using forward and reverse autoregressive models. The proposed algorithm is validated against expert-detected B points and is compared with different conventional methods; it significantly outperforms them by at least 54% in mean error, 30% in mean absolute error, and 27% in standard deviation of error. This algorithm can be adopted in ambulatory studies requiring beat-to-beat evaluation of cardiac hemodynamic parameters over extended time periods where expert scoring is not feasible.

Heart rate response to post-learning stress predicts memory consolidation

Stressful experiences are often well remembered, an effect that has been explained by beta-adrenergic influences on memory consolidation. Here, we studied the impact of stress induced heart rate (HR) responses on memory consolidation in a post-learning stress paradigm. 206 male and female participants saw 52 happy and angry faces immediately before being exposed to the Cold Pressor Test or a non-stressful control procedure. Memory for the faces and their respective expression was tested twice, after 30min and on the next day. High HR responders (in comparison to low HR responders as well as to the non-stressful control group) showed enhanced recognition memory one day after learning. Our results show that beta-adrenergic activation elicited shortly after learning enhances memory consolidation and that the stress induced HR response is a predictor for this effect.

Exercise unmasks autonomic dysfunction in swine with a recent myocardial infarction

Severe congestive heart failure is associated with autonomic imbalance consisting of an increased sympathetic and decreased parasympathetic activity. In the present study, we investigated the influence of alterations in autonomic balance on cardiovascular function in 11 swine with left ventricular (LV) dysfunction produced by a 2- to 3-week-old myocardial infarction (MI). Swine underwent permanent occlusion of the left circumflex coronary artery resulting in MI of the lateral LV wall. Autonomic activity was studied 2-3 weeks later using blockers of muscarinic (atropine), alpha-adrenergic (phentolamine) and beta-adrenergic (propranolol) receptors. Under resting conditions, parasympathetic and sympathetic control of the heart and coronary circulation were similar in MI and normal swine. In contrast, during exercise of MI compared to normal swine, (i) there was a more pronounced gradual inhibition of parasympathetic control of heart rate with increasing exercise intensity; (ii) circulating catecholamines increased excessively, resulting in an increased beta-adrenergic influence on heart rate, while (iii) the beta-adrenergic influence on global left ventricular contractility was decreased, reflecting a blunted left ventricular beta-adrenergic responsiveness. Furthermore, (iv) an alpha-adrenergic vasoconstrictor influence was absent in the anterior LV wall of both MI and normal swine, while (v) the beta-adrenergic vasodilator influence in the coronary circulation was not different between normal and MI swine, which, in conjunction with the elevated catecholamine levels during exercise, suggests a diminished beta-adrenergic responsiveness of coronary resistance vessels within remote non-infarcted myocardium in MI swine. Swine with a recent MI display autonomic dysfunction, which is characterized by a more pronounced inhibition of parasympathetic influence and an exaggerated increase in sympathetic drive during exercise, as well as reduced myocardial and coronary vascular beta-adrenergic responsiveness.

Beta-adrenergic influences on T wave alternans during pacing in patients with and without ventricular tachyarrhythmia

Beta-adrenergic influences on T wave alternans during pacing in patients with and without ventricular tachyarrhythmia

The effects of competition and competitiveness on cardiovascular activity

Cardiovascular activity was measured at resting baseline and in response to a car racing game, undertaken in competition or in cooperation with an experimenter, or individually. Competitiveness and win and goal orientations were assessed by questionnaire. Competition provoked increases in blood pressure and heart rate, and a significant shortening of the preejection period, an index of enhanced beta-adrenergic influences on the heart. The cooperation task was largely without effect, and although the solo task affected cardiovascular activity, it did so to a lesser extent and much less consistently than did the competition task. The three task conditions, then, were largely distinguishable by their capacity to activate beta-adrenergic processes. Participants high in competitiveness and desire to win showed higher blood pressure reactions and greater shortening of the preejection period to competition than those low in these characteristics.

Role of beta-adrenoceptor on renal interleukin-6 and tumor necrosis factor in spontaneously hypertensive rats

We have shown previously in the spontaneously hypertensive rat (SHR) kidney that interleukin-6 (IL-6) and tumor necrosis factor (TNF) mRNA levels were low under conditions of acute anaesthesia and surgical stress. The reasons for the suppression of IL-6 and TNF gene expression in the SHR were investigated by examining the influence of enhanced beta-adrenergic stimulation, high blood pressure, and renal function (renal blood flow, glomerular filtration rate, plasma creatinine levels) on renal IL-6 and TNF mRNAs. The experiments were performed by means of the following three studies; (1) SHR and Wistar rats at 4, 7, 9 week old were injected with lipopolysaccaride (LPS), and then a relationship between blood pressure levels and IL-6 and TNF mRNA levels were estimated, (2) isoproterenol and propranolol were administered into SHR and WKY rats, and the levels of IL-6 and TNF mRNA were compared, (3) under condition of anaesthesia and surgical stress, blood pressure and renal functions in SHR were measured, and then the relationships between these factors and IL-6 or TNF mRNA levels were analyzed. Renal IL-6 and TNF mRNAs in SHR remained low even though blood pressure increased with age and there was no significant correlation between IL-6 or TNF mRNA levels and values of blood pressure or renal function under anaesthesia and surgical stress. However, the inhibition of the IL-6 and TNF mRNAs in SHR was prevented by propranolol treatment. These results suggested that suppression of IL-6 and TNF mRNAs in the SHR kidney could be due to overactivity of beta-adrenergic influences which may importantly contribute to the development of hypertension.

Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa

In anorexia nervosa (AN), growth hormone (GH) hypersecretion and low insulin-like growth factor I (IGF-I) levels are present. It is unclear whether this is due to a peripheral GH resistance and a reduced IGF-I negative feedback on GH secretion or to a primary hypothalamic dysfunction. In AN, in contrast to normal subjects, cholinergic antagonists and agonists, whose action is somatostatin (SS)-mediated, have reduced and absent effects on the GH response to growth hormone-releasing hormone (GHRH). Since arginine, another substance acting via inhibition of SS, maintains its potentiating effect on GH secretion in AN, it has been hypothesized that somewhat specific alteration of the SS-mediated cholinergic influence may be present in this condition. To further clarify the neural control of AH secretion in AN, we evaluated the effects of beta-adrenergic agonists and antagonists, which are known to inhibit and increase, respectively, the GHRH-induced GH secretion in normal subjects. We studied the effect of atenolol (ATE), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-adrenergic agonist, on the GHRH-induced GH release in 10 patients with AN and in 10 normal age-matched women (NW). Basal GH levels were higher, whereas IGF-I were lower in AN than in NW. The GHRH-induced GH rise in AN was higher than that in NW. ATE significantly enhanced the GH response to GHRH in NW, but not in AN. The GH responses to GHRH after ATE pretreatment were similar in NW and in AN. The GH response to GHRH was inhibited by SALB in both NW and AN. The GH responses to GHRH after SALB pretreatment were similar in NW and AN. These data reveal an exaggerated somatotrope responsiveness to GHRH in AN that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairment of beta-adrenergic influence on GH secretion is present in anorexia nervosa.

Sympathetic influence on cardiovascular responses to sustained head‐up tilt in humans

Sympathetic beta-adrenergic influences on cardiovascular responses to 50 degrees head-up tilt were evaluated with metoprolol (beta 1-blockade; 0.29 mg kg-1) and propranolol (beta 1 and beta 2-blockade; 0.28 mg kg-1) in eight males. A normotensive-tachycardic phase was followed by a hypotensive-bradycardic episode associated with presyncopal symptoms after 23 +/- 3 min (control, mean +/- SE). Head-up tilt made thoracic electrical impedance (3.0 +/- 1.0 omega), mean arterial pressure (MAP, 86 +/- 4-93 +/- 4 mmHg), heart rate (HR, 63 +/- 3-99 +/- 10 beats min-1) and total peripheral resistance (TPR, 15 +/- 1-28 +/- 4 mmHg min L-1) increase, while central venous oxygen saturation (74 +/- 2-58 +/- 4%), cardiac output (5.7 +/- 0.1-3.1 +/- 0.3 L min-1), stroke volume (95 +/- 6-41 +/- 5 mL) and pulse pressure (55 +/- 4-49 +/- 4 mmHg) decreased (P < 0.05). Central venous pressure decreased during head-up tilt (7 +/- 2-0 +/- 1 mmHg), but it remained stable during the sustained tilt. At the appearance of presyncopal symptoms MAP (49 +/- 3 mmHg), HR (66 +/- 4 beats min-1) and TPR (15 +/- 3 mmHg min L-1) decreased (P < 0.05). Neither metoprolol or propranolol changed tilt tolerance or cardiovascular variables, except for HR that remained at 57 +/- 2 (metoprolol) and 55 +/- 3 beats min-1 (propranolol), and MAP that remained at 87 +/- 5 mmHg during the first phase with metoprolol. In conclusion, sympathetic activation was crucial for the heart rate elevation during normotensive head-up tilt, but not for tilt tolerance or for the associated hypotension and bradycardia.

Accelerated myocardial relaxation in conscious dogs during acute cardiac tamponade.

Eight chronically instrumented conscious dogs were used to test the hypothesis that left ventricular (LV) relaxation is accelerated during cardiac tamponade. The time constant of LV transmural pressure fall was measured before and during intrapericardial (IP) saline infusion (baseline) with and without beta-adrenergic blockade (propranolol 1 mg/kg iv). Heart rate was controlled by atrial pacing. Increasing IP pressure caused a progressive linear decrease in stroke volume before and during beta-blockade in each animal. The time constant of LV transmural pressure fall also decreased continuously with an increase in IP pressure from 26 +/- 7 ms during baseline to 18 +/- 5 ms during severe cardiac tamponade (P < 0.01) before beta-blockade. However, after beta-blockade, the time constant of LV transmural pressure fall was constant over a wide range of IP pressures despite a continuous decrease in LV end-diastolic volume. The time constant of LV transmural pressure fall was not altered by vena caval occlusions that caused the same decrease in LV preload observed during cardiac tamponade. We concluded that despite decreased pump function, LV relaxation was accelerated progressively during graded cardiac tamponade, and this change was dependent not on changes in loading conditions but on an intact beta-adrenergic influence.

Cardiac autonomic mechanisms associated with borderline hypertension under varying behavioral demands: evidence for attenuated parasympathetic tone but not for enhanced beta-adrenergic activity.

Elevated blood pressure in psychophysiological studies of borderline hypertension is frequently attributed to the effects of increased sympathetic tone, and with few exceptions, the potential parasympathetic contributions have not been considered. Furthermore, of the investigations that have addressed vagal influences upon blood pressure, most have employed invasive pharmacological assessment of parasympathetic tone. In this study, cardiac parasympathetic and beta-adrenergic influences in borderline hypertension were evaluated noninvasively employing respiratory sinus arrhythmia as a vagal index and preejection period as a sympathetic index of cardiac functioning. Subjects were 30 borderline hypertensive and 23 normotensive males (age range, 24-45 years). The ECG, blood pressure, impedance cardiography, and respiration were measured during two baselines (initial and post-task), a memory-comparison reaction time task, the cold pressor, and CO2-rebreathing. Results indicated tonic differences between groups in all cardiovascular variables across tasks, with the exception of pre-ejection period, which showed no group effects at all. Hypertensives additionally manifested somewhat heightened systolic blood pressure reactivity and attenuated cardiac parasympathetic responsivity to specific tasks. Our findings provide no support for an exaggerated cardiac beta-adrenergic tonic level or reactivity in borderline hypertensives. On the other hand, the consistently lower magnitude of respiratory sinus arrhythmia in our hypertensives suggests that reduced parasympathetic control may be involved in the pathophysiology of hypertension.

Prolonged administration in vivo of alpha and beta adrenergic agonists decreases insulin binding to rat myocardial membranes in vitro by different mechanisms

Male Sprague Dawley rats were continuously treated in vivo for 6, 12 and 20 hours with a combination of an alpha- (beta-) adrenoreceptor agonist and a beta- (alpha-) adrenoreceptor antagonist in subcutaneously implanted depot tablets. Crude membranes prepared from myocardial cells exhibited a decreased maximum binding of [ 125I]-insulin after 20 hours irrespective of the treatment applied. Scatchard and non-linear regression analysis of the displacement curves assuming two non-cooperative binding sites revealed a downregulation of the high affinity receptors for about 85% and a concomitant 2.5-fold increased receptor affinity under beta-adrenergic influence. In contrast, alpha-adrenergic treatment did not affect the receptor number but decreased the high affinity by 70%. The low affinity binding sites were virtually unaffected by the different treatments. The phospholipid and cholesterol contents of the membranes were not significantly altered. The phospholipid/cholesterol ratios after 12 and 20 hours of alpha-adrenergic treatment, however, were decreased. We suggest that the decreased binding activity of insulin receptors on rat myocardial membranes after continuous in vivo treatment with alpha- and beta- adrenergic agonists is mediated by different mechanisms.

Heart rate variability in diabetic patients during orthostatic load — A spectral analytic approach

Spectral analysis of heart rate variability (HRV) was used to assess the autonomic nervous control of cardiac function during orthostatic load in insulin-dependent diabetic patients and healthy subjects. The diabetic patients were divided into three groups: diabetics without neuropathy (group 1), diabetics with peripheral neuropathy (group 2), and diabetics with peripheral and autonomic neuropathy (group 3). Resting mid-frequency (MF, 0.05-0.15 Hz) and respiration-related (RF, power around respiration rate) HRV were significantly lower in group 2 and 3 diabetics than in controls, indicating a reduced parasympathetic nervous system influence on the heart. Standing MF and RF spectral power data were significantly lower in all diabetic groups than in controls, suggesting marked alterations in the autonomic cardiovascular control during a mild physical load not only in symptomatic diabetics but also in patients with no signs and symptoms of neuropathy. The difference between supine and standing MF power, an estimate of beta-adrenergic influence on the heart, was significantly lower in all diabetic subject groups studied than in controls. This suggests a reduced sympathetic nervous system influence on the heart in diabetic patients. Our data suggest that computerized spectral analysis of HRV during orthostatic load seems to be a very sensitive method of evaluating of the autonomic nervous systems influence on the heart in patients suffering from diabetes mellitus.

Beta-adrenergic enhancement of angiotensin II-stimulated aldosterone secretion

Beta-adrenergic agonists have been shown to stimulate aldosterone secretion. Angiotensin II (AII) is one of the important stimuli of aldosterone secretion; conceivably beta-adrenergic influences affect the stimulatory potential of AII. Using cultured rat adrenal capsules, we found that 10 −7 M epinephrine and 10 −7 M isoproterenol enhanced 10 −7 M AII-stimulated aldosterone production. Propranolol (10 −7 M) completely inhibited the ability of epinephrine to augment the stimulatory actions of AII. In conclusion, beta-adrenergic agonists promote stimulation of aldosterone secretion by AII.

Race, borderline hypertension, and hemodynamic responses to behavioral stress before and after beta-adrenergic blockade.

Blood pressure (BP) and hemodynamic responses (cardiac output [CO] and total peripheral resistance [TPR]) to a competitive reaction-time task, previously shown to increase beta-adrenergic activity, were compared in 20 Black and 20 White young men, once following infusion of saline placebo and later repeated after infusion of the nonselective beta-antagonist, propranolol. Both racial groups included subjects with marginal systolic BP (SBP) elevations (n = 6 Whites, n = 5 Blacks) and subjects with normal BP (n = 14 Whites, n = 15 Blacks). Blacks with marginal SBP elevations showed greater diastolic BP increases during the stressor than their White counterparts, both before and after beta-blockade. Both Blacks and Whites with marginal SBP elevations showed greater CO increases during the task than normotensives prior to blockade. Independent of BP status, Black subjects consistently showed higher TPR responses to the task than Whites (lesser decreases before blockade and greater increases after blockade). Blacks also showed greater diminution than Whites after blockade in ionotropic myocardial responses (stroke volume, pre-ejection period, and CO) to the stressor. The possible contributions of alpha-adrenergic and beta-adrenergic influences to these racial group differences are discussed.

Effect of propranolol on ventricular repolarization and refractoriness: role of beta-blockade versus direct membrane effects.

The purpose of this study was to define the role of beta-adrenergic blockade and direct membrane effects in the ability of dl-propranolol to alter ventricular repolarization and refractoriness in the intact heart. The effective refractory period (ERP) and the local Q-T interval were measured at an epicardial site in the left ventricle in 14 open-chest dogs anesthetized with alpha-chloralose. Beta-adrenergic influences were eliminated in seven dogs (group 1) by stellate transection and nadolol (0.5 mg/kg IV), and enhanced in seven dogs (group 2) by stellate transection and stimulation of the left ansae subclavia. Each dog received an initial beta-blocking dose of propranolol (0.5 mg/kg) followed by a second, cumulative dose of 5.0 mg/kg. In group 1 dogs, there was no significant change in either the ERP or local Q-T interval in response to the first dose of propranolol. In group 2 dogs, left stellate stimulation significantly shortened the ERP (20 +/- 2 msec) and the local Q-T interval (17 +/- 4 msec). The first dose of propranolol prolonged these parameters to values not different from prestimulation control values. There was no change in the H-V interval, QRS complex duration, or diastolic threshold (DT) in either group after the initial propranolol dose. The second dose of propranolol significantly shortened the ERP (5 +/- 1 msec) and the local Q-T interval (11 +/- 2 msec) in both groups. This dose also significantly increased the DT, H-V interval, and QRS complex duration.(ABSTRACT TRUNCATED AT 250 WORDS)

β-Adrenergic Stimulation of Growth Hormone (GH) Releasein Vivo, and Subsequent Inhibition of GHReleasing Factor-Induced GH Secretion*

In vivo and in vitro studies of beta-adrenergic influences on GH secretion have produced apparently conflicting data in which the in vivo effect seems to be inhibitory and the in vitro effect to be stimulatory. The present studies were designed to observe the in vivo effect of isoproterenol (ISO), a beta-adrenergic agonist, on 1) GH release during a brief interval after intraatrial infusion, and 2) GH release in response to GRF infused 10 min after ISO. ISO was found to stimulate GH release in both intact and hypothalamus-lesioned animals within 2 min after infusion, but GH returned to control levels within 10 min. ISO also profoundly inhibited the release of GH in response to GRF. Pretreatment of animals with somatostatin (SRIF) antiserum prevented the inhibitory action of ISO on GRF-induced GH release. No change in peripheral levels of SRIF was detected. Also, there was no suppression of GRF-induced GH release by ISO when the treatments were applied in vitro to dispersed perifused pituitary cells. These data show that beta-adrenergic systems can stimulate a rapid but brief release of GH in vivo, and that the subsequent inhibitory action on GRF-induced GH release might be by means of SRIF release.

Neuropharmacological modulation of swimming activity and life span in a digenean parasite, Cercaria caribbea LXXI cable

1. 1. Exogenously applied neuropharmacological agents profoundly affected the swimming behaviour and survivorship of Cercaria caribbea LXXI. 2. 2. Propranolol (1.1–40 μM), haloperidol (0.66–0.133 mM) and physostigmine (0.08–2.5 mM) were the most potent reducers of population half-life (T 50). 3. 3. Some drugs (e.g. reserpine) produced apparent osmotic disturbances leading to shortened life span. 4. 4. Serotonin had the greatest excitatory effect on swimming and on the electrical activity, increasing the amplitude and frequency of spike discharge. Physostigmine most effectively reduced both parameters. 5. 5. Neuromuscular control of swimming may involve central excitatory nicotinic (cholinergic) and beta adrenergic influences, inhibitory muscarinic (cholinergic) and dopaminergic influences; and local excitatory muscarinic and serotonergic influences.

Autonomic control of ventricular tachycardia: Direct effects of beta-adrenergic blockade in 24 hour old canine myocardial infarction

The purpose of this study was to determine whether alpha- or beta-adrenergic influences directly modulate the rate of spontaneous ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Chloralose-anesthetized, open chest dogs (n = 41) with ventricular tachycardia were studied. The left anterior descending artery was cannulated distally. Neither intracoronary saline solution nor phenylephrine (0.3 to 12 micrograms) changed the rate of ventricular tachycardia; however, isoproterenol (0.01 to 10 micrograms) produced dose-dependent increases in the rate. In six dogs, metoprolol, 5 mg given intravenously, slowed ventricular tachycardia from 174 +/- 10 (mean +/- SE) to 140 +/- 17 beats/min (p less than 0.05). This was accompanied by decreases in mean arterial pressure from 106 +/- 7 to 95 +/- 8 mm Hg, cardiac output from 2.6 +/- 0.3 to 1.6 +/- 0.3 liters/min and prolongation of atrioventricular conduction from 134 +/- 10 to 189 +/- 29 ms (all p less than 0.05) during atrial pacing at a cycle length of 300 ms. In 10 dogs, metoprolol (0.5 mg) given intracoronary, a dose that shifted the isoproterenol dose-response curve to the right, slowed ventricular tachycardia from 174 +/- 7.2 to 140 +/- 9.7 beats/min (p less than 0.05) without hemodynamic changes. Additional metoprolol (4.5 mg) given intravenously produced hemodynamic alterations, but ventricular tachycardia did not slow further. Therefore, beta- but not alpha-adrenergic influences control the rate of ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Furthermore, beta-adrenergic blockade slows ventricular tachycardia solely by a direct electrophysiologic effect on the tachycardia foci and not indirectly as a result of hemodynamic effects.

Long-term adrenergic β-action decreases and α-action enhances Corticosterone levels in rats

A 20 h hyperadrenalinemia in rats was produced by subcutaneously implanted A-retard tablets with an output rate of 1.8 micrograms/min/250 g. This caused a moderate (6 h, 20 h) to expressed (12 h) rise in Corticosterone. Concomitant beta-blockade leads to equal (12 h, 20 h) or even more expressed (6 h) enhancement of plasma corticosterone, while A + alpha-blockade lowers those levels significantly against A or A + Prop treated animals. At 6 and 20 h they are even significantly lower than control values. We therefore conclude that enhanced alpha-adrenergic influence increases and beta-adrenergic influence decreases plasma Corticosterone levels in rats.

Beta adrenergic influence on oesophageal peristalsis in man.

The effects of the beta-1 adrenergic agonist prenalterol and the beta-2 adrenergic agonist terbutaline on oesophageal peristalsis were studied in nine healthy volunteers with pressures recorded in the proximal, middle, and distal oesophagus. Two doses of the agonists were given after pretreatment with placebo, propranolol, or metoprolol in a double blind randomised fashion. Terbutaline 0.25 +/- 0.25 mg iv decreased peristaltic pressure in middle oesophagus from 8.1 +/- 1.1 to 5.1 +/- 0.8 kPa (p less than 0.01) and in the distal oesophagus from 9.5 +/- 1.0 to 4.7 +/- 0.6 kPa (p less than 0.001). Peristaltic velocity was decreased in the distal oesophagus after terbutaline from 3.3 +/- 0.2 cm/sec to 2.9 +/- 0.2 cm/sec (p less than 0.05). Prenalterol 1 mg iv was followed by a decrease of peristaltic pressure in the middle oesophagus from 10.2 +/- 1.3 to 7.7 +/- 1.1 kPa (p less than 0.01) and a decrease of peristaltic velocity in upper oesophagus from 3.6 +/- 0.2 to 3.3 +/- 0.1 cm/sec (p less than 0.05) while no significant changes were seen in the distal oesophagus. Pretreatment with the beta-1 blocker metoprolol 15 mg iv blocked the effects of prenalterol 1 mg iv but not the effects of terbutaline. Propranolol 10 mg iv blocked the effects of terbutaline on peristaltic pressure. After metoprolol infusion mean distal peristaltic amplitude was 11.9 +/- 0.8 kPa compared with 8.5 +/- 1.2 kPa after placebo (p less than 0.01). It is concluded that both beta-1 and beta-2 adrenoceptor stimulation significantly decrease oesophageal peristaltic pressure in man. The body of the oesophagus seems to be under beta adrenergic inhibitory influence under physiological conditions.