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PubMed1993

Plasma catecholamines and neonatal condition after induction of anaesthesia with propofol or thiopentone at caesarean section.

Increased maternal sympathetic nervous system activity may decrease placental perfusion and cause adverse neonatal effects. We have studied the catecholamine response and neonatal outcome in Chinese patients with uncomplicated, singleton pregnancies undergoing Caesarean section. Anaesthesia was induced with thiopentone 4 mg kg-1 (n = 32) or propofol 2 mg kg-1 (n = 30) followed by suxamethonium. Laryngoscopy was performed after 1 min and tracheal intubation completed by 2 min. Anaesthesia was continued with atracurium, nitrous oxide and isoflurane. Maternal venous blood samples were taken at 0, 1, 2, 3, 4 min and at delivery for assay of catecholamines. The increase from baseline values in mean arterial pressure after tracheal intubation was greater in the thiopentone group (29 (SD 15) mm Hg) compared with the propofol group (18 (14) mm Hg) (P < 0.01). The concentrations of noradrenaline and adrenaline increased in both groups after tracheal intubation. Maximum noradrenaline concentrations were greater in the thiopentone group (413 (177) pg ml-1) compared with the propofol group (333 (108) pg ml-1) (P < 0.05), but there were no differences between groups in adrenaline concentrations. Neonatal Apgar scores, neurobehavioural testing and umbilical catecholamine, blood-gas tension and oxygen content analysis were similar between groups. Propofol attenuated the hypertensive and catecholamine response associated with laryngoscopy and tracheal intubation but there was no improvement in neonatal outcome.

Adult↗
PubMed1998

Effect of clonidine on changes in plasma catecholamine concentrations and oxygen consumption caused by the cold pressor test.

This study was designed to investigate whether clonidine could attenuate the increase in oxygen consumption (VO2), arterial pressure (AP) and plasma catecholamines in response to the cold pressor test (CPT), an intense stimulation of the sympathetic nervous system. Six volunteers were given clonidine (2 micrograms kg-1 and 4 micrograms kg-1) and placebo i.m. in a random, double-blind, cross-over manner. Both clonidine doses decreased plasma catecholamine concentrations (P < 0.01), but only the higher dose of clonidine attenuated the CPT-induced absolute increase in plasma catecholamine concentration compared with the placebo group (P < 0.01). VO2 and AP decreased and were less after clonidine 4 micrograms kg-1 when compared with clonidine 2 micrograms kg-1 and placebo (P < 0.05) throughout the observation period. Thus, although clonidine 4 micrograms kg-1 attenuated the catecholamine response, the increases in VO2 and AP in response to CPT were similar in all groups.

Adrenergic alpha-Agonists↗
PubMed1991

Myocardial catecholamine concentrations in dilated cardiomyopathy and heart failure of different origins.

Myocardial catecholamine concentrations were determined in endomyocardial biopsies from patients with heart failure to assess if tissue catecholamine levels relate to the severity of myocardial damage or the aetiology of the underlying disease. Methodological studies revealed a good reproducibility of catecholamine determinations in biopsies; the variance between paired biopsies was below 17% when myocardial catecholamines were related to non-collagen protein (NCP). Myocardial norepinephrine (in pg micrograms-1 NCP) levels were comparable in patients with dilated cardiomyopathy (DCM, 5.3 +/- 3.4, n = 22) and in patients with coronary or valvular heart disease (5.6 +/- 4.7, n = 14). In both groups, a significant reduction of myocardial norepinephrine was found (controls 12.0 +/- 3.4, P less than 0.0006). In a subgroup of patients with heart failure and a LVEF less than 30% (3.9 +/- 3.5, n = 17) myocardial norepinephrine content was lower than in patients with heart failure and LVEF of 31-55% (6.6 +/- 3.4, n = 19) (both P less than 0.05 against controls: 12.0 +/- 3.4, n = 16). A correlation between myocardial norepinephrine and LVEF was found in DCM (P less than 0.001, r = 0.70). The loss of myocardial norepinephrine is a characteristic feature of heart failure. It is independent of the origin of failure, but correlates with the impairment of LV function.

Cardiomyopathy, Dilated↗
PubMed2004

Catecholamines potentiate LPS-induced expression of MMP-1 and MMP-9 in human monocytes and in the human monocytic cell line U937: possible implications for peri-operative plaque instability.

Plaque destabilization leading to myocardial infarction is observed after surgery even if the intervention is of noncardiovascular nature. Mediators of peri- or postoperative stress responsible for such events could include catecholamines and lipopolysaccharide (LPS). Monocytes may be involved in destabilization of atherosclerotic plaques by production of matrix metalloproteinases (MMP). We examined whether catecholamines could affect the expression of MMPs in human monocytes/macrophages and whether catecholamines could modulate LPS-stimulated expression of particular MMPs in these cells. Epinephrine and norepinephrine up-regulated MMP-1 and potentiated LPS-induced expression of MMP-1 in peripheral blood monocytes and monocyte-derived macrophages. We further characterized this effect employing the monocytic cell line U937 and showed that catecholamines potentiate LPS-induced effects on MMP-1 and MMP-9 antigen and activity. mRNA levels of the respective MMPs also increased. These effects did not result from higher mRNA stability but rather from increased transcription possibly induced by enhanced DNA binding of AP-1 and were mediated by either beta1- or beta 2-receptors. If this mechanism is also effective in vivo, our findings might, at least in part, help to explain the observation that cardiac events are important causes of morbidity and mortality after noncardiac surgery and support the findings that peri-operative beta-blockade has been shown to reduce postoperative mortality from cardiac events.

Adrenergic beta-Antagonists↗
PubMed1991

Beneficial effect of upper thoracic epidural anesthesia in experimental hemorrhagic shock in dogs: influence of circulating catecholamines.

The question as to whether reduction of plasma catecholamine concentration contributes to the beneficial effects of upper thoracic epidural anesthesia on survival during hemorrhagic shock was examined. Twenty-six dogs were anesthetized with halothane and nitrous oxide, and blood was withdrawn to reduce the mean arterial blood pressure (MAP) to 40 mmHg. The 12 dogs in group A received both upper thoracic epidural anesthesia before the hemorrhage and intravenous infusion of epinephrine (450 ng.kg-1.min-1) and norepinephrine (150 ng.kg-1.min-1) during hemorrhage. The 14 dogs in group B received none of these. At 20 min after the start of the bleeding, plasma catecholamine concentrations were increased in both groups more than ten-fold. There were no significant intergroup differences with respect to these concentrations at any point during the experimental period. During the 100-min period of hemorrhage, 1 of the 12 animals in group A and 10 of the 14 in group B died. A significant difference in survival was seen between the two groups over the 100-min hypotensive period (P less than 0.01 by the generalized Wilcoxon test). These results suggest that the survival benefit of upper thoracic epidural anesthesia cannot be explained simply by differences in the level of catecholamines in the plasma, and that perhaps differences in the level of catecholamines at the nerve endings or other factors may be more important.

Anesthesia, Epidural↗
PubMed1994

Beneficial hemodynamic effects of prostaglandin E1 infusion in catecholamine-dependent heart failure: results of a prospective, randomized, controlled study.

OBJECTIVE: To study the hemodynamic effects of prostaglandin E1 (PGE1) administered in addition to a standard catecholamine infusion in patients with severe chronic heart failure. DESIGN: Prospective, placebo-controlled, randomized, single-blind study. SETTING: Intensive care unit at a university hospital. PATIENTS: Thirty patients with severe chronic heart failure, New York Heart Association functional class IV (28 men, two women, with a mean age of 54 +/- 2 yrs, mean left ventricular ejection fraction 10 +/- 0.6%). All patients received oral therapy with digitalis, furosemide (mean dose 300 +/- 46 mg/day), and enalapril (20 +/- 2.7 mg/day). INTERVENTIONS: Hemodynamic measurements using pulmonary artery flotation catheters were performed at baseline, > or = 24 hrs after standardized catecholamine infusion with dopamine (3 micrograms/kg/min) and dobutamine (5 micrograms/kg/min), as well as 48 hrs after randomization to infusion therapy with PGE1 (30 ng/kg/min) or a placebo. MEASUREMENTS AND MAIN RESULTS: The addition of PGE1 to an ongoing catecholamine infusion in 20 patients caused a 16 +/- 4% decrease in mean pulmonary arterial pressure (p < .001), a 22 +/- 5% decrease in pulmonary artery occlusion pressure (p < .0001), a 24 +/- 8% decrease in pulmonary vascular resistance index (p < .001), a 20 +/- 9% decrease in right atrial pressure (p < .01), a 14 +/- 3% decrease in mean arterial pressure (p < .001), and a 29 +/- 4% decrease in systemic vascular resistance index (p < .0001). These PGE1-induced decreases occurred without a change in heart rate. Stroke volume index increased with PGE1 therapy by 34 +/- 7% (p < .0001), and cardiac index increased by 34 +/- 6% (p < .0001). No hemodynamic changes were observed during combined infusion with catecholamines and placebo in ten patients. CONCLUSION: PGE1 improves the hemodynamic state in end-stage chronic heart failure patients already receiving a standard dose dopamine/dobutamine infusion.

Alprostadil↗
PubMed1984

The relationship between plasma catecholamines and severity of injury in man.

The relationship between plasma catecholamines and injury severity was investigated in order to determine: a) whether a correlation existed between the severity of injury as assessed by the Injury Severity Score (ISS), and circulating noradrenaline and adrenaline; and b) whether such measurements were of prognostic value. It was found that in the immediate postinjury period, both noradrenaline and adrenaline correlated positively with ISS over the range of injury studied (ISS = 0-54; r = 0.67, p less than 0.01). It appeared that part of the response might be attributed to psychological rather than physical factors; at lower levels of injury (ISS less than 9) these psychological factors were possibly responsible for the whole of the observed effect. In the subsequent recovery period (greater than 24 hr postinjury) no clear relationship between plasma catecholamines and injury severity was maintained. Studies on patients who died as a consequence of their injuries failed to confirm the previously suggested prognostic value of plasma catecholamine determinations in this later postinjury period. However, plasma noradrenaline levels in this group were significantly higher on admission than in the casualties who survived serious injury (p less than 0.05). It is concluded that plasma catecholamine concentrations, in combination with other indices of injury severity, may provide useful information on the response to injury in man, and aid in the assessment of its overall severity in physiologic terms.

Accidents, Traffic↗
PubMed1991

Effects of intoxication on the catecholamine response to multisystem injury.

In patients suffering isolated head trauma, we have previously shown that levels of circulating catecholamines obtained within 48 hours of trauma correlate with the severity of brain injury and predict outcome and that intoxication blunts this response. The effects of alcohol on the increase in catecholamines in systematically injured patients, however, have not been well defined. From 1983 to 1990, 78 patients (74% male; median age 30 years) with blunt head and multisystem injury, who also had alcohol levels measured within 5 hours of injury, were studied. Norepinephrine and epinephrine levels were assayed by a radioenzymatic technique. Injury severity was assessed by the admission Glasgow Coma Scale (GCS) score (4-15; median, 12), the Injury Severity Score (ISS) (13-50; median, 25) and the volume of blood products administered within the first 24 hours (0-14.4 L; median, 0.5 L). The impact of alcohol on the norepinephrine response to injury was analyzed using multiple linear regression models, including polynomial interaction terms. Norepinephrine levels significantly (p less than 0.0001) correlated with the GCS score and ISS. However, alcohol significantly lowered the norepinephrine response to decreasing GCS score (R = 0.49, p less than 0.002) and to increasing ISS (R = 0.51, p less than 0.0006). The blunting of the catecholamine response was most marked in those severely injured. The rise in norepinephrine concentrations seen with increasing volume of blood replacement was not affected by intoxication. An association between injury severity and epinephrine levels was also present, but not as consistently. Epinephrine concentrations rose with falling GCS score and with increasing ISS values, but unlike norepinephrine, there were no apparent effects of alcohol on changes in epinephrine levels. Thus, in patients suffering head and multisystem injury, catecholamine changes reflect the severity of injury using three different scalers. Furthermore, intoxication blunts only the norepinephrine component of this important biologic response.

Adolescent↗
PubMed1999

Heart rate variability and plasma catecholamines in patients during opioid detoxification.

It has been shown that rapid opioid detoxification is associated with increased sympathetic activity (SYMP) and plasma catecholamines. Heart rate (HR) variability may provide a noninvasive method of evaluating withdrawal and sympathetic activation caused by the reversal of opioid binding in patients who are opioid dependent. The purpose of this study was to evaluate the relationship between HR variability and plasma catecholamines during opioid detoxification. Patients were anesthetized with propofol, intubated, paralyzed with rocuronium infusion, and ventilated. The bispectral index (BIS) of the electroencephalogram was recorded with the patient awake as well as during propofol anesthesia. SYMP was determined by power spectral analysis of HR variability. Plasma epinephrine and norepinephrine were measured at baseline propofol anesthesia and during naltrexone treatment in eight opioid-dependent patients. Nonopioid-dependent controls (n = 7) were monitored during surgery without naltrexone treatment or measurement of plasma catecholamines. Compared with an awake status, propofol anesthesia significantly decreased the BIS and SYMP in both groups of patients. Controls showed no change from baseline anesthetized levels during surgery. Plasma norepinephrine and epinephrine as well as SYMP increased 300 to 400% (P < .05) during naltrexone treatment in opioid-dependent patients, and the time to peak increase in plasma norepinephrine correlated with the increase in SYMP (r = 0.89, P < .01). These results confirm that opioid detoxification increases plasma catecholamines and SYMP in a similar manner. HR rate variability may provide a low-cost real-time noninvasive method of evaluating the reversal of opioid binding in opioid-dependent patients.

Adult↗
PubMed2004

Cardiovascular responses to catecholamines and interactions with endothelin-1 and adenine nucleosides in the pericardium of the dog heart.

The pericardial fluid may accumulate endogenous regulatory agents, such as catecholamines, endothelin or adenine nucleosides. However, very little information is available on the cardiovascular effects of intrapericardial (i.p.) catecholamines and their interaction with the endogenous endothelins and adenine nucleosides. The cardiovascular effects of increasing doses of i.p.- administered dopamine boluses (0.06-8 micromol/kg, n = 8) were studied in the in situ canine heart: systemic blood pressure, heart rate and left ventricular dP/dt were recorded, and pericardial infusate samples were obtained to measure the changes in endothelin-1 (ET-1), adenosine and inosine levels (enzyme-linked immunosorbent assay and high-performance liquid chromatography methods, respectively). The responses to i.p. dopamine were compared with the effects of i.p. norepinephrine boluses (0.004-0.5 micromol/kg, n = 8). Dopamine elicited dose-dependent increases of heart rate (P < 0.01), and the highest dose of dopamine resulted in significant elevation in dP/dt and blood pressure (P < 0.01) with a nearly twofold increase of i.p. ET-1 (from 14.3 +/- 0.1 pg/mL to 26.1 +/- 0.1 pg/mL, P < 0.02) and a more than threefold augmentation of i.p. adenosine (from 2.9 +/- 0.5 microM to 11.1 +/- 3.0 microM, P < 0.05), but not of inosine levels. Similar responses were obtained with i.p. norepinephrine. The results confirm that i.p. catecholamines exert significant hemodynamic effects and modulate ET-1 and adenosine release from the heart. However, the pattern of catecholamine actions initiated from the pericardium may characteristically differ from that of intravascular ones.

Adenosine↗
PubMed1992

Growth stimulation by catecholamines in plant tissue/organ cultures.

Addition of catecholamines at micromolar concentrations caused a dramatic stimulation of growth of tobacco (Nicotiana tabacum) thin cell layers (TCLs) and Acmella oppositifolia "hairy" root cultures. A threefold increase in the rate of ethylene evolution was observed in the catecholamine-treated explants. Aminooxyacetic acid and silver thiosulfate, inhibitors of ethylene biosynthesis and action, respectively, reduced the growth-promoting effect of dopamine. However, these compounds alone could also inhibit the growth of the TCL explants. When ethylene in the culture vessel was depleted by trapping with mercuric perchlorate, dopamine-stimulated growth was still obtained, suggesting that ethylene does not mediate the dopamine effect. Dopamine potentiated the growth of TCLs grown in Murashige and Skoog medium supplemented with indoleacetic acid (IAA) and kinetin. When IAA was replaced by 2,4-dichlorophenoxyacetic acid, dopamine addition showed no growth-promoting effect. Instead, 2,4-dichlorophenoxyacetic acid stimulated the growth of TCL explants to the same extent as that obtained with IAA plus dopamine. Because synthetic auxins do not appear to be substrates for IAA oxidizing enzymes, we hypothesized that catecholamines exert their effect by preventing IAA oxidation. Consistent with this explanation, dopamine (25 micromolar) inhibited IAA oxidase activity by 60 to 100% in crude enzyme extracts from tobacco roots and etiolated corn coleoptiles, but had no effect on peroxidase activity in the same extracts. Furthermore, addition of dopamine to TCL cultures resulted in a fourfold reduction in the oxidative degradation of [1-(14)C]IAA fed to the explants. Because the growth enhancement by catecholamines is observed in both IAA-requiring and IAA-independent cultures, we suggest that these aromatic amines may have a role in the regulation of IAA levels in vivo.

Journal Article↗
PubMed1995

Catecholamines in human keratinocyte differentiation.

Human keratinocytes have the capacity to synthesize catecholamines from L-tyrosine, which in turn is produced from L-phenylalanine via phenylalanine hydroxylase. This enzyme activity is controlled by the supply of the essential cofactor/electron donor (6R)5,6,7,8 tetrahydrobiopterin (6-BH4). Undifferentiated keratinocytes express high levels of the rate-limiting enzymes for the de novo synthesis of 6-BH4, i.e., GTP-cyclohydrolase-1, and for its recycling, i.e., 4a-hydroxytetrahydrobiopterin dehydratase. As a consequence of 6-BH4 synthesis, phenylalanine hydroxylase is activated, yielding L-tyrosine, which in the presence of excess 6-BH4 turns on the biosynthesis of catecholamines via the rate-limiting enzyme tyrosine hydroxylase. Therefore, undifferentiated keratinocytes contain high levels of the catecholamine system yielding sufficient levels of norepinephrine and epinephrine, required for the induction of beta-2-adrenoceptors. Stimulation of beta-2-adrenoceptors by epinephrine causes a rise in intracellular calcium via extracellular influx. This event corresponds with keratinocyte differentiation. In differentiated keratinocytes, all enzyme activities involved in 6-BH4, L-tyrosine, and epinephrine biosynthesis are decreased, resulting in significantly lower levels of epinephrine and a concomitant decrease in the expression of beta-2-adrenoceptors. These data strongly suggest a connection between catecholamine biosynthesis, beta-2-adrenoceptor expression, calcium flux, and the differentiation of keratinocytes in human epidermis.

Biopterins↗
PubMed1989

Pre-operative assessment of anxiety and measurement of arterial plasma catecholamine concentrations. The effect of oral beta-adrenergic blockade with metoprolol.

A double-blind study of 40 patients who underwent elective hysterectomy was conducted to evaluate the role of arterial plasma catecholamine concentrations as an objective index of anxiety, and to assess the effect of pre-operative oral treatment with a beta-adrenoceptor blocking drug. The patients were premedicated with diazepam and either metoprolol or placebo 2-3 hours before surgery. The effect on anxiety was evaluated by the anaesthetist and by visual analogue scoring by the patients. Using pooled data, a significant decrease in both adrenaline and noradrenaline concentrations was demonstrated after premedication, but no difference was found between the groups. In general, patients were less anxious after premedication, but patients who received metoprolol had greater relief of anxiety (p = 0.0007). A significant change in perceived anxiety was found in patients who received metoprolol, but there was no significant change in the placebo group. The correlation between the observers' assessment and the patients' visual analogue scores was poor, but some correlation was found between the assessed relief of anxiety and the changes in visual analogue score. We could not demonstrate any correlations between anxiety and catecholamine concentrations, between relief of anxiety and changes in catecholamine concentrations, or haemodynamics and catecholamine concentrations.

Anxiety↗
PubMed1993

Effects of nifedipine and Bay-K-8644 on the release of catecholamines from the dog adrenal gland in response to splanchnic nerve stimulation.

1. The effects of nifedipine and Bay-K-8644 on the release of adrenal catecholamines were examined in anaesthetized dogs. 2. Splanchnic nerve stimulation (SNS) at 1 and 3 Hz produced frequency-dependent increases in adrenaline (ADR) and noradrenaline (NA) output determined from adrenal venous blood. 3. Neither nifedipine (10 and 30 micrograms/kg, i.v.) nor Bay-K-8644 (10 and 30 micrograms/kg, i.v.) modified the SNS-induced increases in catecholamine output. Basal catecholamine output tended to be increased and decreased by nifedipine and Bay-K-8644, respectively. 4. Nifedipine produced significant decreases in arterial pressure and renal blood flow rate. Bay-K-8644 produced a significant increase in arterial pressure associated with a decrease in renal blood flow rate. 5. These results suggest that dihydropyridine-sensitive calcium channels do not play a major role in adrenal catecholamine release evoked by SNS.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1993

Methoxyverapamil reduction of nicotine-induced catecholamine release involves inhibition of nicotinic acetylcholine receptor currents.

The mechanism by which the putative Ca2+ channel blocker methoxyverapamil (D600) inhibits nicotine-induced catecholamine release was investigated in bovine adrenal chromaffin cells and in neurons from paravertebral sympathetic ganglia of chick embryos. We found D600 to prevent catecholamine release evoked by 30 s applications of nicotine with a significantly higher potency than the release induced either by 30 s K+ depolarizations or by electrical field stimulation of sympathetic neurons. Like the use-dependent action of D600 upon Ca2+ channels, the magnitude of inhibition of the K(+)-evoked secretion depended on the duration of stimulation (10 s to 5 min). Data on catecholamine release were supplemented by patch-clamp recordings. We found whole-cell currents in chromaffin cells evoked by (extrapolated) 0.5 s applications of nicotine to be significantly more sensitive to D600 than Ca2+ currents induced by a 0.5 s depolarization from -80 to 0 mV. In both instances, the potency of D600 depended on the duration of the (nicotinic and depolarizing) stimuli. Our data suggest that D600 inhibits nicotine-induced catecholamine release by reducing nicotinic acetylcholine receptor currents rather than voltage-gated Ca2+ currents. Hence, in chromaffin cells as well as in sympathetic neuronal preparations, D600 does not appear to be a suitable tool to investigate the part voltage-activated Ca2+ currents play in cellular events induced by nicotine.

Adrenal Medulla↗
PubMed1991

Catecholamines and blood glucose control in type 1 diabetes.

To evaluate the influence of blood glucose control on serum catecholamine levels (which reflect both plasma and platelet levels), six healthy non-diabetic subjects, seven well-controlled Type 1 diabetic patients, and six poorly controlled Type 1 diabetic patients were studied before (baseline) and after standardized exercise. A significant correlation was found between serum noradrenaline and HbA1 at baseline (r = 0.53, p less than 0.025) and after exercise (r = 0.71, p less than 0.001). Similar results were found for serum adrenaline (r = 0.68, p less than 0.005 and r = 0.61, p less than 0.005, respectively) and consequently total serum catecholamine content (r = 0.65, p less than 0.005 and r = 0.75, p less than 0.001, respectively). However, no relationship was found between serum catecholamine levels and actual blood glucose levels, age, body mass index or insulin dose. A moderate correlation was found between systolic blood pressure and serum levels of noradrenaline and total catecholamines after exercise (r = 0.48 and r = 0.48, both p less than 0.025).

Adult↗
PubMed1980

Transport of catecholamines by native and reconstituted rat heart synaptic vesicles.

Highly purified "heavy" synaptic vesicles were isolated from rat heart by differential centrifugation. Because of the high intravesicular concentrations of proteins, catecholamine, and ATP, resealed vesicle ghosts were prepared and used to study the detailed kinetics of catecholamine transport. ATP stimulated the uptake of l-norepinephrine and was saturable with a Km for l-norepinephrine at 3.3 microM and 1.8 mM for ATP. The ghosts also accumulated 5-hydroxytryptamine and l-epinephrine via an ATP-dependent mechanism. Uptake was stereospecific for the l-form. A functional catecholamine transporter could be solubilized by the detergent octyl-glucoside and incorporated into phospholipid vesicles, which, after detergent removal, generated proteoliposomes that accumulated l-norepinephrine. Reserpine- and l-propranolol-sensitive accumulation against a concentration gradient is achieved by artificially creating a pH gradient across the membrane, and lends further support to the idea that at least the initial phase of catecholamine transport is driven by the trans-membrane pH gradient created by the proton-translocating ATPase.

Adenosine Triphosphate↗
PubMed1992

Synapsin II phosphorylation and catecholamine release in bovine adrenal chromaffin cells: additive effects of histamine and nicotine.

Primary cultures of bovine adrenal medullary chromaffin cells can be stimulated with nicotine, which mimics the cholinergic stimulus from the splanchnic nerve. Histamine also stimulates catecholamine release in a time- and dose-dependent manner. We have previously shown that nicotine stimulates incorporation of 32Pi into the vesicle-associated phosphoprotein synapsin II. We report here that histamine, too, stimulates an increase in 32Pi incorporation into synapsin II, which is blocked by the H1-histamine receptor-specific antagonist pyrilamine. The time course of histamine-stimulated synapsin II phosphorylation closely paralleled that of histamine-stimulated catecholamine release. Interestingly, histamine and nicotine produced an additive increase in both catecholamine release and synapsin II phosphorylation, suggesting that these two secretogogues stimulate the phenomena via independent mechanisms. When we investigated the dependence of these two agonists on extracellular calcium, we found that nicotine-stimulated release and synapsin II phosphorylation were reduced to basal levels at low calcium concentrations. However, the histamine-stimulated effects remained significantly elevated. This suggests that calcium arising from two separate pools can stimulate catecholamine release and synapsin II phosphorylation in bovine chromaffin cells. Taken together, these data support the hypothesis that synapsin II phosphorylation is a component of the secretory response from these cells.

Adrenal Glands↗