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The effects of graded elevations of intracranial pressure (ICP) on cardiac metabolism, blood flow and electrophysiology, and plasma catecholamines were studied in eight open-chest pigs. ICP was consecutively elevated from 15 +/- 3 mmHg in the control state to 40 +/- 4, 84 +/- 4 and 152 +/- 11 mmHg. Mean arterial blood pressure and heart rate were significantly increased at the two highest ICP levels. Cardiac oxygen uptake was also increased from 2.9 +/- 0.4 ml X min-1 to a maximum of 7.1 +/- 2.0 ml X min-1, and coronary sinus blood flow increased from 49 +/- 7 to 131 +/- 35 ml X min-1 at the highest ICP level. The transmyocardial blood flow distribution was unchanged, as determined by the microspheres technique. Arterial plasma catecholamine concentrations were significantly elevated at the two highest ICP levels, but noradrenaline overflow from the heart did not increase. The high arterial adrenaline concentrations (51 +/- 25 nmol X 1(-1) at the highest ICP level) may be responsible for the cardiac stimulation seen in these experiments. No signs of ischaemia, as judged by myocardial lactate production or the relative flow distribution to the endocardium were observed. Changes in the T-wave morphology appeared in the subendocardial ECG at all ICP levels, the changes being more prominent with increasing ICP levels. It is concluded that the increase in circulating catecholamine levels, adrenaline in particular, together with an elevation of afterload cause an increase of myocardial work, which may explain the T-wave changes in the ECG which are observed upon rapid elevation of intracranial pressure.

Sympathoadrenal and cardiovascular responses to tilting were studied in patients with pregnancy-induced hypertension and healthy control subjects during the last trimester of pregnancy and 8 to 12 weeks post partum. Blood volumes were lower in the patients with pregnancy-induced hypertension during pregnancy (0.065 versus 0.081 L/kg, p less than 0.01) but not post partum. Tilting induced significantly smaller increases in heart rate and arterial plasma norepinephrine concentrations and smaller changes in blood pressure during pregnancy as compared to after pregnancy in both groups. Forearm vascular resistance increased significantly in both groups after pregnancy but only in the patients with pregnancy-induced hypertension during pregnancy. The forearm vasoconstrictor response to tilting was, in fact, totally abolished in the third trimester of normal pregnancy. The hypertensive patients had higher arterial plasma epinephrine levels at rest and greater epinephrine and norepinephrine responses to tilting than the control subjects during pregnancy. Normal pregnancy appears to reduce the circulatory and sympathoadrenal responses to orthostatic stress, presumably because of volume expansion that allows venous return to be better maintained in the upright position. The less pronounced pregnancy-induced increase in blood volume in patients with pregnancy-induced hypertension appears to explain the increased sympathoadrenal and forearm vascular reactivity in this group during pregnancy.

The effect of renal nerve stimulation (RNS) on renal venous outflow and urinary excretion of endogenous norepinephrine, epinephrine, and dopamine was examined in anesthetized dogs. In the unstimulated denervated kidney, there was a negative venoarterial concentration difference for all catecholamines. Low-level RNS (LLRNS) caused small changes in renal hemodynamics and renal venous outflow of dopamine and increased norepinephrine outflow by 3.22 +/- 0.95 pmol X min-1 X g-1 (n = 5, P less than 0.05). High-level RNS (HLRNS) reduced renal blood flow by 50% and increased renal venous outflow of norepinephrine and dopamine by 9.58 +/- 0.67 and 0.46 +/- 0.05 pmol X min-1 X g-1, respectively (n = 27, P less than 0.01 for both). Renal uptake of epinephrine was unchanged by HLRNS. The urinary excretion of norepinephrine but not dopamine was increased to a similar degree following RNS at both levels. HLRNS caused a similar increase of the urinary norepinephrine excretion from the contralateral denervated and unstimulated kidney. This could be explained by the increase in arterial norepinephrine (from 0.74 +/- 0.08 to 1.20 +/- 0.14 nM, P less than 0.01) caused by HLRNS as shown by experiments with intravenous infusions of norepinephrine. The alpha-adrenoceptor antagonist phenoxybenzamine counteracted the hemodynamic response to HLRNS and enhanced the renal venous outflow and urinary excretion of norepinephrine and dopamine. Our results indicate that renal nerves release dopamine as well as norepinephrine and that urinary catecholamine excretion is a poor indicator of intrarenal catecholamine release.

To study if noradrenaline released from degenerating sympathetic nerves may contribute to metabolic stimulation and low blood flow in an experimental skin flap, we have determined noradrenaline levels in such skin flaps. Attempts to use radioenzymatic methodology for the determination of noradrenaline in rat skin extracts were unsuccessful due to interference with the assay. High performance liquid chromatography with electrochemical detection was, however, found to give accurate estimates of rat skin noradrenaline contents. Rat skin contained approximately 2.7 nmol (455 ng) noradrenaline per gram dry weight. Extensive depletion of skin flap noradrenaline, occurring mainly between 6 and 24 h postoperatively, was found. At 48 h nearly all sympathetic nerves in the skin flaps had degenerated as evidenced by noradrenaline levels of 0.13 nmol/g. The degeneration of sympathetic nerve endings appears to proceed from the sides towards the middle of the flap, indicating a segmental distribution of the nerves. Noradrenaline released from degenerating sympathetic nerves may adversely affect the survival of critical skin flaps by causing vasoconstriction and metabolic stimulation.

Effects of the vasodilator dipyridamole (Dip) on plasma adenosine levels, heart rate, blood pressure and skin microcirculation were studied in 13 healthy male volunteers. Venous plasma concentrations of adenosine, catecholamines, dipyridamole and theophylline were determined by HPLC. Skin capillary blood cell velocity (CBV) was measured by videophotometric capillaroscopy in the finger nailfold. The adenosine uptake inhibitor Dip (approximately 1-3 microM in plasma) increased plasma adenosine from 0.15 +/- 0.03 to 0.29 +/- 0.03 microM (p less than 0.01) and heart rate (HR) by 13 +/- 2 beats/min (p less than 0.01) and reduced diastolic blood pressure by 6 +/- 2 mmHg (p less than 0.05). Dip did not significantly affect the skin circulation since basal CBV, digital pulse amplitude (DAPA), skin temperature and post-occlusive reactive hyperemia were unchanged. Plasma catecholamine levels were also unaffected. The adenosine receptor antagonist theophylline (45-55 microM in plasma) did not influence basal plasma catecholamine or adenosine levels, HR, blood pressure or skin microcirculation. Following theophylline Dip caused similar elevations of plasma adenosine but no changes in HR or blood pressures. Our results support the hypotheses that Dip dilates blood vessels in man by elevating endogenous adenosine and that theophylline acts as an adenosine antagonist. Under basal conditions, the skin microcirculation appears to be regulated mainly by factors other than adenosine.

The parathyroid glands contain sympathetic nerve endings and the parathyroid cells are endowed with beta-adrenergic receptors. The physiological role of the sympathoadrenal system for the secretion of parathyroid hormone (PTH) has, however, not been clarified. Using the technique of lower body negative pressure (LBNP), which is an established method to achieve sympathetic nerve activation, it was found in 17 healthy subjects that the venous serum levels of PTH were reduced by 7% within 20 min [from 0.79 +/- 0.12 (SD) to 0.74 +/- 0.11 arbU/l, p less than 0.01, paired t test]. The reduction corresponds to 30% of the maximal suppressibility of PTH by induced hypercalcemia or following parathyroidectomy when studied with the same PTH assay and with the short time period involved. After cessation of LBNP the PTH levels returned to baseline within 20 min. There were no concomitant changes of the plasma ionized calcium concentrations. The findings are compatible with a role for the sympathetic nervous system in the physiologic regulation of the secretion of PTH.

Cardiovascular, sympathoadrenal, and subjective responses to mental stress induced by a color-word conflict test (CWT) were studied in 30 healthy males before and after intravenous administration of either placebo, beta 1-blockade by metoprolol (0.15 mg/kg), or nonselective beta-blockade by propranolol (0.15 mg/kg). CWT responses were reproducible. Mean arterial pressure increased by 20%. A mainly heart rate-dependent 65% increase in cardiac output (thermodilution) was associated with 25% decreases of both systemic (SVR) and calf vascular (CVR) resistances. Arterial plasma epinephrine (Epi) was doubled, and norepinephrine (NE) increased by 50%. Self-evaluated stress score correlated positively with changes in cardiac output and inversely with changes in SVR during CWT. Both metoprolol and propranolol halved heart rate responses; whereas increases in mean arterial pressure, Epi, and NE were uninfluenced. Metoprolol reduced the increase in stroke volume, and propranolol abolished it. SVR and CVR responses were attenuated by metoprolol and abolished by propranolol. The results suggest that mental stress accelerates the heart through neurogenic mechanisms and that peripheral vasodilatation is achieved through the concerted actions of reduced vasoconstrictor activity and elevated circulating Epi.

Thirty-four laboratories performed altogether 41 plasma catecholamine assays on each of four samples. Various radioenzymatic assays, high performance liquid chromatographic (HPLC) assays with electrochemical detection and fluorimetric assays were used. There was reasonable agreement that the levels of adrenaline and noradrenaline in a basal plasma pool were about 0.2 and 1.8 nM, respectively. The levels in a pool of plasma obtained after exercise were about 0.7 and 11 nM, respectively. The study, however, revealed a sometimes considerable variability between methods as well as between laboratories using the same method. Results from duplicate determinations of noradrenaline suggest frequent problems with intra-laboratory reproducibility. Results concerning the recoveries of 0.7 or 3.0 nM adrenaline or 2.0 nM noradrenaline (added to the basal plasma pool) showed a rather frequent need for improved precision. Fluorimetric assays gave unacceptable results. Plasma free dopamine measurements showed a basal level of 0.1-0.2 nM with most HPLC assays and a tendency towards higher levels and greater scatter with radioenzymatic methods. On the whole, reverse phase HPLC methods and an inhomogeneous group of single-isotope derivative radioenzymatic assays showed the largest variability. Less variability was found with the radioenzymatic assay of Peuler & Johnson (1977), provided that a few obviously erroneous results were excluded. The smallest variability was found with microparticulate cation exchange HPLC. It is concluded that plasma catecholamine assays would benefit from better standardization and a continuous quality control. Problems associated with validation of new assays, as well as modifications of old assays are discussed.

1 Seven women with hypertension of pregnancy were given the combined alpha- and beta-adrenoceptor blocking drug labetalol (50 mg i.v.) in their last trimester. Acute effects were studied for 3 h after administration. 2 Systolic and diastolic blood pressures were significantly reduced from 143 +/- 4 (s.e. mean) to 127 +/- 5 mmHg and from 101 +/- 2 to 88 +/- 2 mmHg, respectively. Maternal heart rate fell significantly from 77 +/- 5 to 68 +/- 3 beats/min. The changes remained during the 3 h of observation. Foetal heart rate was not affected. No side-effects were encountered. 3 Plasma noradrenaline increased significantly from 1.54 +/- 0.16 to a peak value of 2.37 +/- 0.41 nmol/l suggesting sympathetic activation following labetalol. Plasma adrenaline levels were essentially unchanged. Plasma glucose, insulin and C-peptide showed only minor changes. No major effects on lipid metabolism were seen except a significant fall of nonesterified fatty acids at 60 min. Plasma cyclic AMP increased significantly throughout the observation period, perhaps indicating beta-adrenoceptor agonist activity of labetalol. 4 The effectiveness of labetalol as an acute hypertensive agent together with apparent absence of metabolic disturbances and other side-effects makes it an interesting drug for the treatment of hypertension during pregnancy.

Responses to mental stress [a colour word test (CWT), orthostatic testing (ORT) and a cold pressor test (CPT) were studied in 33 subjects with essential hypertension (EHT), 16 subjects with borderline hypertension (BHT) and 17 age and sex-matched normotensive controls (NT). Venous plasma noradrenaline (NA) was similar in all groups. CWT induced marked circulatory responses and metabolic activation with minor increases in NA. Circulatory and NA responses to ORT and CPT were similar in all groups. CWT elevated diastolic blood pressure more in BHT and tended to elevate HR more in EHT and BHT than in NT. Plasma adrenaline (ADR) tended to be higher in BHT and increased during all provocations in EHT and BHT but not in NT. Early hypertension appears to be associated with enhanced cardiovascular and sympatho-adrenal reactivity (resembling a hypothalamic defence reaction) which is revealed by mental stress, rather than stimuli such as ORT or CPT. Venous plasma NA has limitations in defining neurogenic alterations in hypertension since it reflects poorly sympathetic activity in the organs responsible for pressor responses to emotional stimuli. Plasma ADR is more valuable in this respect.

The interrelationships between psychosocial factors, several physiological variables and blood pressure (BP) were investigated in 88 young men (aged 26-32 years) in whom high, intermediate or low BP had been recorded at the age of 18 years. In the original high BP group, venous plasma noradrenaline was normal but adrenaline levels elevated. At the follow-up adrenaline correlated with systolic blood pressure (SBP), and this was also so after controlling for overweight and serum gamma-glutamyltranspeptidase [gamma-GT, a marker for alcohol consumption, which showed an independent association with diastolic blood pressure (DBP)]. Low assertiveness (low scores of verbal and indirect aggression) correlated with high BPs, even after controlling for other psychosocial variables. Several associations between psychosocial job variables and physiological variables were found. Among self-reported job variables, excessive 'demands' and 'bossing others' (but not 'decision latitude' or 'psychosocial conflict') were associated with high SBP. Habitual smoking of cigarettes was not associated with BP at rest, but influenced several associations between psychosocial and physiological variables. Men with high BP at rest and low plasma renin activity (PRA) reported more psychosocial problems at work and lower assertiveness than other groups.

Cardiovascular and neuroendocrine reactivity during arithmetic task performance were studied in 24 patients with borderline hypertension and normotensive controls. Personal control (self-paced versus externally paced performance) resulted in an attenuated blood pressure (BP) response to task performance in normotensives but not in borderline hypertensives. In response to self-paced work, systolic blood blood pressure (SBP) reactivity was significantly greater in borderline hypertensives, but the heart rate (HR) reactivity was similar in borderline hypertensives and normotensives under the different pacing conditions. Task difficulty (pace variation during external pacing) did not differentially affect reactivity in borderline hypertensives and normotensives. Venous plasma noradrenaline and adrenaline were unaffected by task performance. At rest after the task performance plasma noradrenaline was elevated in both normotensives and borderline hypertensives. The latter group also showed a persistent elevation of diastolic blood pressure after task performance, suggesting a prolonged vasoconstrictor response. The present findings indicate that, in terms of circulatory responses, borderline hypertensives may profit less than normotensives from personal control over environmental demands.

The development of sensitive detectors has allowed the use of high-performance liquid chromatography (HPLC) for measurements of catecholamines in extracts of plasma, urine, and tissue samples. Separation of the catecholamines may be effected by reversed phase chromatography or cation-exchange chromatography and quantitation by electrochemical detection (EC) or by fluorometry coupled with postcolumn derivatization according to the trihydroxyindole (THI) method. EC has a somewhat lower sensitivity than the THI method for norepinephrine (NE) and epinephrine (E). The THI method is insensitive to dopamine (DA). Basal plasma E levels of 0.1 nM (20 pg/ml) or less may be measured in sample volumes of 1-2 ml with EC. Sensitivity and reproducibility of an assay is not necessarily a guarantee of accuracy. It is argued that new methods and modifications of old methods should be validated against accepted methodology. This is rarely the case. Cation exchange HPLC with EC has been adequately validated, but only one of the reversed phase methods has been compared with radioenzymatic methodology. HPLC has the advantages of economy, speed, and more stimulating laboratory work, as compared with radioenzymatic methodology.

Hemorrhagic shock was induced in rats by bleeding to 35 mmHg for a period of 4 h. Plasma glucose increased rapidly following the onset of bleeding and reached twice the control value after 30 min. After 2 h hypotension the liver content of glycogen was depleted and subsequently the rats became hypoglycemic. The rise in plasma glucose was accompanied by a rise in plasma cyclic AMP, which was 10-fold after 1 h, but returned towards control values at the end of the hypotensive period. There were no corresponding changes in the cyclic AMP contents of liver, heart or adipose tissue. Blood lactate was increased 10-fold and the lactate/pyruvate ratio was more than doubled, suggesting an increased anaerobic metabolism. Plasma FFA levels fell significantly, while plasma glycerol was unchanged during the hypotensive period. In this hemorrhagic shock model there is an initial phase of glucose mobilization from the liver, which is accompanied by elevated plasma cyclic AMP. This phase is followed by a period of depressed levels of glucose as well as FFA and thus a lack of metabolizable substrates in plasma.

1. The effects of mental stress induced by a colour word conflict test (CWT; n = 9) or 3 h infusions of placebo or adrenaline (0.4 nmol min-1 kg-1; n = 9) on platelet function in vivo were studied in 16 healthy male volunteers. 2. Platelet function was assessed by a filtragometry technique, which reflects aggregability in vivo, and by measurements of the plasma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4). 3. Adrenaline and CWT induced marked cardiovascular responses as expected. Venous plasma adrenaline increased from 0.1-0.2 nmol/l at rest to 4.87 +/- 0.42 nmol/l during adrenaline infusion and to 0.46 +/- 0.10 nmol/l during CWT. 4. Filtragometry measurements were reproducible within individuals with coefficients of variation of 7.9% during placebo infusion and 5.4% for resting measurements between days. 5. Platelet aggregability, as measured by filtragometry, was similarly increased during both adrenaline infusion (P less than 0.05) and CWT (P less than 0.01). 6. The coefficients of variation for beta-TG and PF4 levels were 17.3% for log beta-TG and 27.9% for log PF4 between days, but could not be calculated for within-day variability. Both beta-TG (P less than 0.05) and PF4 (P less than 0.01) levels decreased time-dependently during placebo infusion, indicating that long resting periods (hours) are needed to attain basal levels. Artefactual results could not be identified by evaluating beta TG/PF4 ratios. 7. beta-TG and PF4 levels did not decrease time-dependently during adrenaline infusion. There were no significant changes of beta-TG or PF4 during CWT.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of circulating adrenaline on cardiovascular function were studied in 14 subjects with borderline hypertension (BHT) and in 14 matched normotensive controls. Adrenaline was infused in stepwise increasing doses (0.1, 0.2, 0.4, and 0.8 nM/kg/min, i.v.). Noninvasive measurements of cardiac function (M-mode echocardiography) and blood pressure and blood sampling for determinations of venous plasma noradrenaline, adrenaline, cyclic AMP, and potassium were performed. Systolic and diastolic blood pressure responses to adrenaline were similar in both groups. Cardiac output was increased in BHT at rest but the signs of an increased myocardial contractility disappeared during adrenaline infusion. The BHT group displayed elevated heart rates and systemic vascular resistances over the full range of adrenaline concentrations studied but the responsiveness was similar in both groups. The beta 2-adrenoceptor-mediated increases in plasma cyclic AMP and decreases in plasma potassium were similar in the BHT and control groups. The results suggest an increased arousal in BHT at rest. Furthermore, beta 2-adrenoceptor sensitivity appears to be unaltered in BHT.

Pre- and postjunctional effects of the alpha 1-selective adrenoceptor antagonist prazosin and the alpha 1- and alpha 2-selective adrenoceptor agonists methoxamine and 6-fluoronoradrenaline, respectively, were studied in skeletal muscle in situ. Prazosin reduced the vasoconstriction and enhanced the overflow of endogenous noradrenaline elicited by sympathetic nerve stimulation (1-4 Hz, 2 min); the threshold concentration was 10-100 times lower for postjunctional than for prejunctional alpha-adrenoceptor blockade. The enhancement of noradrenaline overflow by prazosin was not inversely frequency-dependent, as shown elsewhere for alpha 2-adrenoceptor antagonists. Thus, different mechanisms may be involved. Inhibition of prostaglandin synthesis by diclofenac did not alter the stimulation-evoked noradrenaline overflow, indicating a minor importance of prostaglandin-mediated transjunctional mechanisms in the modulation of noradrenaline overflow. Methoxamine and 6-fluoronoradrenaline elevated the basal vascular tone and, at higher concentrations, reduced the stimulation-evoked noradrenaline overflow. Methoxamine was 20 times more selective than 6-fluoronoradrenaline for postjunctional receptors. Our results are compatible with a pre- and postjunctional localization of alpha 2-adrenoceptors and a predominantly, but not exclusively, postjunctional localization of alpha 1-adrenoceptors. The postjunctional selectivity for prazosin was less marked than previously reported from in vitro studies. Hence, care should be taken when extrapolating in vitro findings to the more complex in vivo situation.

1. Seven latent hypertensive patients and seven matched controls were subjected to standardized mental stress and orthostatic provocation. 2. Mental stress increased blood pressure by approximately 25%, heart rate by 25 beats/min, plasma glycerol by 50% and plasma cyclic AMP by 25% in both groups. Plasma glucose and renin activity were unchanged. Plasma noradrenaline and adrenaline were essentially unchanged during stress. 3. There was an insignificant tendency towards higher noradrenaline levels in latent hypertensive subjects and two of these subjects displayed an exaggerated noradrenaline response to standing. 4. Our results indicate that the physiological responses to mental stress are caused by selective neuronal activation, rather than by generalized sympatho-adrenal activation. Latent hypertension does not seem to be associated with adrenergic hyperactivity or receptor supersensitivity, except possibly in individual cases.

Beta-adrenoceptor responsiveness was studied both in vivo and in vitro in patients with exercise-induced asthma (EIA), asthmatic patients without EIA (NEIA), and control subjects. All subjects were age- and sex-matched and without medication at least one week prior to the tests. In vivo, beta-adrenoceptor responsiveness was evaluated by plasma concentration-effect studies for intravenously infused isoprenaline (0.02-0.1 micrograms X kg-1 X min-1). Mainly beta 2-adrenoceptor mediated responses to isoprenaline, ie, decreases in diastolic blood pressure and increases in plasma cyclic AMP, were reduced in EIA patients but not in NEIA patients. Heart rate and plasma glycerol responses to isoprenaline did not differ between the groups. In vitro, the beta 2-adrenoceptor mediated accumulation of cyclic AMP in lymphocytes stimulated by isoprenaline was attenuated (p less than 0.05) in EIA patients, whereas the beta 2-adrenoceptor responsiveness of lymphocytes from NEIA patients was normal. Thus, beta 2-adrenoceptor mediated responses were reduced both in vivo and in vitro in EIA patients, but not in NEIA patients. This finding that beta 2-adrenoceptor responsiveness was reduced only in a subgroup of asthmatic patients could explain some of the controversies in the literature concerning beta-adrenoceptor function in asthma.

The renal venous outflow of dopamine and noradrenaline were studied in the canine kidney in situ in connection with renal nerve stimulation (RNS). RNS (0.5-4 Hz) caused frequency-dependent increases in the outflow of both catecholamines, which could be detected already at 0.5 Hz. The ratio dopamine/noradrenaline in renal venous plasma (approximately 0.15) was not influenced by varying the RNS parameters but was significantly enhanced (to about 0.25) by pretreatment with guanethidine according to a procedure previously used to demonstrate renal dopaminergic vasodilation. The unstimulated kidney removed conjugated dopamine (which represents 98-99% of the total dopamine in plasma). During RNS the conjugated dopamine outflow to renal venous blood increased, but measurements of conjugated dopamine were less reliable than measurements of free dopamine to assess dopamine release from the kidney. When studying the renal nerve contributions to the renal venous outflow of dopamine and noradrenaline more accurate estimates may be obtained by correcting for the removal of catecholamines delivered to the kidney in arterial plasma. Such corrections were performed with endogenous adrenaline or radiolabelled noradrenaline. The two methods of correction yielded similar results and showed that RNS reduced catecholamine extraction in the kidney. The high ratio of dopamine/noradrenaline in kidney tissue (with a preferential distribution of dopamine to the cortex) and the dopamine outflow to renal venous plasma during RNS support the existence of specific dopaminergic nerves in the dog kidney.

The maturity of beta-adrenoceptors in newborn infants was studied in relation to the catecholamine surge during labor. Umbilical blood was collected at birth from 12 infants delivered vaginally and 13 infants delivered by elective cesarean section. Granulocytes and lymphocytes were isolated. Receptor numbers and binding affinity were determined in the granulocytes by incubation with 125I-iodohydroxybenzylpindolol. Receptor responsiveness was tested by assessing isoproterenol-induced cyclic AMP accumulation in lymphocytes. Significantly higher plasma noradrenaline, adrenaline, and dopamine concentrations were found in infants born vaginally (108; 8.9; 0.9 nmol/liter, liter, respectively, median values) as compared with those delivered by cesarean section (11.0; 2.4; 0.2 nmol/liter). No significant differences in beta-adrenoceptor binding sites (receptor number: 39.2 +/- 2.6 versus 44.7 +/- 5.9 fmol/mg protein and binding affinity: 66.6 +/- 7.8 versus 65.0 +/- 6.2 pM) or responsiveness (maximal isoprenaline induced cAMP formation 52.4 +/- 10.3 versus 40.6 +/- 8.9 pmol/10(6) cells) were found between the two groups of infants. Lymphocyte beta-adrenoceptor sensitivity was similar to that found in adults. The beta-adrenoceptors on whole blood cells seem to be mature at birth and have the same responsiveness as in adults. The higher catecholamine surge during vaginal delivery as compared to elective cesarean section does not seem to affect beta-adrenoceptor function. Our results do not support the idea that reduced beta-adrenoceptor function is the cause of the previously observed inappropriately small cardiovascular and metabolic responses to the exceptionally high plasma catecholamine concentrations at birth.