Increase In Adrenergic Activity Research Articles

Postprandial cardiorespiratory responses and the regulation of digestion-associated tachycardia in Nile tilapia (Oreochromis niloticus).

Cardiorespiratory adjustments that occur after feeding are essential to supply the demands of digestion in vertebrates. The well-documented postprandial tachycardia is triggered by an increase in adrenergic activity and by non-adrenergic non-cholinergic (NANC) factors in mammals and crocodilians, while it is linked to a withdrawal of vagal drive and NANC factors in non-crocodilian ectotherms-except for fish, in which the sole investigation available indicated no participation of NANC factors. On the other hand, postprandial ventilatory adjustments vary widely among air-breathing vertebrates, with different species exhibiting hyperventilation, hypoventilation, or even no changes at all. Regarding fish, which live in an environment with low oxygen capacitance that requires great ventilatory effort for oxygen uptake, data on the ventilatory consequences of feeding are also scarce. Thus, the present study sought to investigate the postprandial cardiorespiratory adjustments and the mediation of digestion-associated tachycardia in the unimodal water-breathing teleost Oreochromis niloticus. Heart rate (fH), cardiac autonomic tones, ventilation rate (fV), ventilation amplitude, total ventilation and fH/fV variability were assessed both in fasting and digesting animals under untreated condition, as well as after muscarinic cholinergic blockade with atropine and double autonomic blockade with atropine and propranolol. The results revealed that digestion was associated with marked tachycardia in O. niloticus, determined by a reduction in cardiac parasympathetic activity and by circulating NANC factors-the first time such positive chronotropes were detected in digesting fish. Unexpectedly, postprandial ventilatory alterations were not observed, although digestion triggered mechanisms that were presumed to increase oxygen uptake, such as cardiorespiratory synchrony.

The Effects of Feeding on Cardiac Control of the Broad-Nosed Caiman (Caiman latirostris): The Role of the Autonomic Nervous System and NANC Factors.

The metabolic increment that occurs after feeding demands cardiovascular adjustments to be maintained, as increased heart rate (fH ) and cardiac output. In mammals, postprandial tachycardia seems to be triggered by an increase in adrenergic activity and by nonadrenergic noncholinergic (NANC) factors, while in ectothermic vertebrates, this adjustment seems to be linked to a withdrawal of vagal drive as well as to NANC factors. Because the factors behind postprandial tachycardia have not yet been investigated in crocodilians, the present study sought to evaluate the postprandial tachycardia mediators in the broad-nosed caiman. To this end, fasting and digesting animals were instrumented with intraperitoneal cannula and subcutaneous electrocardiogram electrodes (for the measurement of fH , cardiac autonomic tones, and total fH variability, as well as for a power spectral analysis of fH ). Data were then collected with the animals in an untreated state, as well as after muscarinic cholinergic blockade with atropine (2.5mgkg-1 ) and after double autonomic blockade with atropine and propranolol (5.0 mg kg-1 ). Fasting animals' fH was ∼18 bpm, a value which increased to ∼30 bpm during digestion. After the double autonomic blockade, fasting animals exhibited an fH of ∼15 bpm, while digesting animals' fH was ∼23 bpm. This result is evidence of the presence of NANC factors with positive chronotropic effects acting during digestion. The calculated autonomic tones showed that, after feeding, the adrenergic tone increased while the cholinergic tone remained unchanged. Finally, fH variability analyses revealed that this adrenergic increase is primarily derived from circulating catecholamines.

Antiarrhythmic vs. pro-arrhythmic effects depending on the intensity of adrenergic stimulation in a canine anthopleurin-A model of type-3 long QT syndrome

The effects of adrenergic activity and beta-blockade were studied in a canine experimental model of type-3 long QT syndrome (LQT3) induced by application of anthopleurin-A. Boluses of epinephrine at 0.5 and/or 1.0 microg/kg were administered before and after propranolol, 0.3 mg/kg, and the distribution of the ventricular repolarization and the development of polymorphic ventricular tachyarrhythmia (VA) were assessed. Using needle electrodes, transmural unipolar electrograms were recorded across the left ventricle (LV) and right ventricle (RV). Activation-recovery interval (ARI) was measured in each electrogram to estimate local repolarization during RV pacing at the cycle length of 750 ms after the creation of complete atrioventricular block. Before propranolol, epinephrine, 0.5 microg/kg, did not induce VA in any experiment. However, a dose of 1.0 microg/kg induced polymorphic VA following multiple premature ventricular complex (PVC) in four of six experiments. Epinephrine, 0.5 microg/kg, shortened ARI at all sites and lessened LV transmural ARI dispersion. Neither ARI nor its dispersion could be determined after 1.0 microg/kg of epinephrine because of the induction of PVC, polymorphic VA, or both. Propranolol (i) prevented epinephrine-induced PVC and polymorphic VA in all experiments, (ii) slightly prolonged ARI at all sites, along with a decrease in LV transmural ARI dispersion, and (iii) reversed the epinephrine-induced shortening of ARI. In this LQT3 model, an increase in adrenergic activity by epinephrine had dose-dependent, opposite effects on ventricular electrical stability. Since beta-adrenergic blockade suppressed epinephrine-induced PVC and polymorphic VA, it might be considered for supplemental therapy to suppress VA in patients presenting with LQT3.

Oesophageal pressure during an earthquake

Stress can alter gastrointestinal motility; in particular, oesophageal motility may be altered by stress, although most studies have investigated only the body of the oesophagus and the upper oesophageal sphincter. Almost all studies have been done in a controlled setting. We had the opportunity to observe the behaviour of the lower oesophageal sphincter during a natural stress. On Oct 3, 1997, while doing a manometric examination in a 62-year-old woman complaining of non-obstructive dysphagia, in Perugia in Umbria, Italy, there was an earthquake. The epicentre was in the Colfiorito area, about 35 miles from the city, and the magnitude of the earthquake was 5·2o on the Richter scale and 7o–8o on the Mercalli scale. We were half way through the manometry when the seismic event struck. Sphincter pressure immediately dropped from about 20 mm Hg to about 5 mm Hg. The examination was stopped, and when repeated 3 days later average sphincter pressure was within the normal range (21 mm Hg) and the oesophagus showed no abnormalities. It appears that, unlike in the oesophageal body or at the upper oesophageal sphincter, where the responses to stress are usually excitatory, the effects of stress on the lower sphincter is to inhibit tone. This inhibition might be due to a sudden increase in adrenergic activity, which has been suggested as one cause of the increased incidence of sudden cardiac deaths triggered by an earthquake. As previously noted, these observations exemplify the tradition in medical science of extracting information from a catastrophe.

Cocaína y corazón

The marked increase in cocaine consumption observed in recent decades, has led to the identification of previously unknown multiple medical problems. Cardiovascular complications related to cocaine abuse include myocardial ischemia and infarction, myocarditis, cardiomyopathy, rhythm disturbances and sudden death, endocarditis, pneumopericardium and left ventricular hypertrophy. Although the mechanisms involved in cocaine-related cardiac diseases are multiple, many cardiac complications in these patients are caused in part or totally by an increase in adrenergic activity due to the blockade of catecholamine reuptake induced by the drug.

Sustained Increase in Adrenergic Activity in Gerbil Striatum Following Transient Ischemia

We investigated the changes in striatal monoaminergic functions, focusing on the release and metabolism, in a cerebral ischemic model induced by a 5-min bilateral occlusion of the carotid arteries (BOCA) and reperfusion in anesthetized gerbils. In the microdialysis study, the striatal extracellular level of dopamine (DA) markedly increased (144-fold) immediately after BOCA. Although norepinephrine (NE) and 5-hydroxytryptamine (5-HT) could not be detected in the dialysates throughout the baseline period, they increased to detectable levels after BOCA. On the contrary, the tissue contents of NE and 5-HT decreased or tended to decrease up to 4 hr following reperfusion. Striatal DA contents did not show any changes in the early period after ischemia-reperfusion and slightly increased at 4 hr or later. Tissue contents of 3-methoxytyramine (3-MT), a metabolite of DA by catechol-O-methyltransferase (COMT), increased 0 and 5 min after reperfusion. Normethanephrine (NMN), which is a metabolite of NE by COMT, also increased not only 5 min after but also up to 4 hr after ischemia-reperfusion, indicating a sustained increase in NE release. These results suggested that the neuronal activity of NE, which is supposed to exert a protective effect on ischemic damage, was enhanced for a longer period than that of DA after transient ischemia.

The control of cardiac chronotropic function in hypobaric hypoxia.

Altitude hypoxia induces an increase in adrenergic activity in humans. However, a decrease in maximal heart rate is observed after a few days of exposure to altitudes above 3500 m, as well as a decrease in chronotropic response to isoproterenol infusion. This phenomenon has been linked to a desensitization of beta-adrenoceptors (beta AR), and/or an increase in parasympathetic activity. A decrease in the density of beta AR in chronic hypoxia has been found in rat left ventricle and in human lymphocytes, without modification of the affinity of beta AR for an agonist or antagonist, and a decreased adenylate cyclase activity in the right ventricle. In the same conditions, the density of adenosine A1 receptors is decreased by 46% in rat myocardium, without alteration in the coupling between hormone, receptor and Gi protein. The density of muscarinic receptors is increased by 40%, with an increase in the affinity for an agonist, suggesting an augmented parasympathetic effect. Hypoxia probably acts on all the receptors involved in the modulation of cardiac chronotropic activity; the combined effects of chronic hypoxia on these receptors tend to a beneficial limitation of myocardial oxygen consumption, especially during heavy exercise.

Effects of beta-blocking drugs in alcohol withdrawal: a double-blind comparative study with propranolol and diazepam

Alcohol withdrawal is associated with a decrease in γ-aminobutyric acid neurotransmission. This explains the efficacy of benzodiazepines. However, an increase in adrenergic activity may also play a part in alcohol withdrawal symptoms, suggesting a potential efficacy of beta-blocking drugs. A double-blind comparative study of propranolol and diazepam was carried out in 28 patients suffering from moderate uncomplicated alcohol withdrawal. Patients were treated for 15 days with either 75 mg of propranolol or 30 mg of diazepam. The results show that both drugs at the dosages used are equipotent in reducing physical withdrawal symptoms and anxiety symptoms. This suggests that most likely the central as well as the peripheral effects determine the clinical usefulness of propranolol in the management of alcohol withdrawal. However, propranolol is ineffective in preventing major motor seizures, suggesting that different neurobiological mechanisms underlie the alcohol withdrawal symptoms. beta-blocking drugs / propranolol / alcohol withdrawal

Return of plasma norepinephrine to normal after resolution of congestive heart failure in congenital heart disease

Plasma norepinephrine is elevated in both adult and pediatric patients with congestive heart failure (CHF), and the degree of elevation corresponds to the severity of the CHF. 1–4 It is not known whether this abnormal increase in adrenergic activity is reversible with the resolution of CHF.

Central adrenergic activity in the mediobasal hypothalamus is temporally related to surge outputs of gonadotrophins in oestrogen-stimulated infant female rats.

In the mediobasal hypothalamus (MBH) of pro-oestrous rats or acutely ovariectomized oestrogen-treated adults a marked but short-lived increase in adrenergic activity occurs at 16.00 h, 2 h before the oestrogen-dependent surge of gonadotrophins at 18.00 h. In this study oestrogen-stimulated (noon on day 1) 22-day-old female rats were used which are known to produce surge levels of prolactin at 18.00 h on day 2 and surges of both prolactin and LH at 18.00 h on day 3; although similar treatment of 18-day-old animals or oil-treated 22-day-old rats failed to produce these effects. Radioenzymatic assays of adrenaline concentrations and of the activity of its synthesizing enzyme (phenylethanolamine-N-methyl transferase; PNMT, EC 2.1.1.28) in the MBH of oestrogen-treated 22-day-old rats showed significant (P less than 0.05-0.01) increases in both parameters at 16.00 h (i.e. 2 h before surge levels of gonadotrophins) on days 2 and 3 when compared with other times of day. Such effects were not seen in oil-treated 22-day-old animals or in oestrogen-treated 16-day-old rats. Noradrenaline and dopamine concentrations in the MBH of oestrogen-treated 22-day-old rats remained at baseline levels on days 2 and 3 with the exception of noradrenaline at 17.00 h on day 3 when levels appeared higher (P less than 0.05) than at either 15.00 or 16.00 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in concentrations and rate of decline of adrenaline in the medial preoptic area and mediobasal hypothalamus of acutely ovariectomized steroid-treated rats.

The presence of adrenaline within the central nervous system appears to be essential for the occurrence of an oestrogen-stimulated surge of LH in both pro-oestrous and ovariectomized rats. Previous measurements of adrenergic activity based on the rate of decline of adrenaline (RDA) 2 h after injection of a synthesis inhibitor (SKF 64139) suggested that adrenergic activity increases in both the medial preoptic area (MPOA) and the mediobasal hypothalamus (MBH) at the start of the LH surge (15.00-17.00 h). The purpose of the present studies was to see whether oestrogen and progesterone affected this increase in adrenergic activity at the sites of the cell bodies (MPOA) and axon terminals (MBH) of the gonadotrophin-releasing hormone-synthesizing neurone. Rats ovariectomized at dioestrus showed a reduction in both plasma LH concentrations and RDA (P less than 0.01) in the MBH between 15.00 and 17.00 h on the day of expected pro-oestrus. Oestrogen replacement at operation restored LH levels and the RDA to values found in intact rats. Injection of an antioestrogen (Cl-628), with or without oestrogen, also reduced plasma LH levels and the RDA (P less than 0.01) in the MBH. Removal or replacement of oestrogen apparently had little effect on the RDA in the MPOA. In ovariectomized oestrogen-primed rats an injection of progesterone on the morning of expected pro-oestrus advanced and enhanced not only the LH surge but also the RDA in the MBH (P less than 0.001). Moreover, concentrations of adrenaline in the MBH (but not the MPOA) decreased (P less than 0.001) consistently over a 2-h period following injection of progesterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium and blood pressure regulation in normal and hypertensive subjects.

To elucidate the mechanisms involved in calcium-mediated blood pressure (BP) control, plasma norepinephrine (NE), epinephrine, renin activity, and angiotensin II (AII) levels and the cardiovascular pressor responsiveness to NE and AII were assessed before and during acute mild hypercalcemia or short-term calcium (Ca) inhibition with nifedipine in 20 normal and five borderline hypertensive subjects. In normal subjects, systolic BP and plasma NE and epinephrine concentrations were increased significantly (p less than 0.05) during an acute rise in serum Ca of 3.1 mg/dl (intermediate rate Ca infusion, 0.05 mg/kg/min for 3 hours), but not following an increase of 1 mg/dl (low rate Ca infusion, 0.034 mg/kg/min for 2 hours). In the borderline hypertensive group, low-rate Ca infusion elevating serum Ca by 1 mg/dl was associated with a slight increase in systolic BP (p less than 0.05) and plasma catecholamines. In both groups, the pressor responses to infused NE and AII, and plasma renin and AII levels, were unchanged during mild to moderate hypercalcemia. Nifedipine given for 2 weeks (average dose, 48 mg/d) reduced BP significantly (p less than 0.05) in the borderline hypertensive subjects only and NE pressor responses in both groups (p less than 0.025), but had no significant effect on plasma catecholamines, renin, or AII levels. These findings suggest that the adrenergic BP control mechanism may be more dependent on clinical variations in calcium metabolism than the angiotensin BP regulatory mechanism. Acute hypercalcemia may increase BP at least in part by causing an increase in adrenergic activity without an equivalent decrease in cardiovascular reactivity. Calcium inhibition with nifedipine may modify noradrenergic BP control by lowering the NE pressor reactivity without causing an equivalent increase in adrenergic activity.

Amniotic fluid catecholamines and metabolites in intrauterine growth retardation

Simultaneous determinations of amniotic fluid levels of the catecholamines dopamine (DA), norepinephrine (NE), and epinephrine (E), and the intraneuronal metabolites of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and NE, 3,4-dihydroxyphenylglycol (DOPEG), were made, by radioenzymatic assay, in pregnancies resulting in growth-retarded (n = 14) normal (n = 63) infants. Significant elevations in the mean concentrations of (p < 0.000005), E (p > 0.0005), and DOPEG(p < 0.000001) as well as a significant decrease in the mean concentration of DOPAC (p < 0.000001) were found in pregnancies resulting in growth-retarded infants as compared to pregnancies resulting in normal infants. Amniotic fluid DOPES levels were found to be the most discriminative. As amniotic fluid catecholamines are predominantly of fetal origin, these findings suggest that an increase in adrenergic activity and a decrease in dopaminergic activity occur in intrauterine growth retardation as a response to chronic stress. (Am. J. Obstet. Gynecol. 141:608, 1981.)

Idiopathic edema: II. Pathogenesis of edema in patients with hypoalbuminemia

Patients with idiopathic edema, previously shown to have a significantly subnormal total circulating albumin level and a significantly subnormal plasma volume, were found to have abnormally large amounts of the neurohumoral transmitter norepinephrine in the urine, an abnormally high plasma renin activity when supine which increased still further when they assumed the upright posture, and hypersecretion of aldosterone. The subnormal plasma volume and the increase in adrenergic activity apparently produced thereby, presumably increased plasma renin activity and, in turn, the secretion of aldosterone. An increase in adrenergic discharge to the kidney and an increase in circulating aldosterone can both increase the reabsorption of sodium by the renal tubules and could therefore be the basis for the excessive sodium retention and edema which is characteristic of these patients.