Effect Of Adrenergic Blockade Research Articles

‘Cold as ice’, why do old coronary arteries pay the price?

‘Cold as ice’, why do old coronary arteries pay the price?

Effect of adrenergic blockade on plasma adrenomedullin concentration during static handgrip in patients with heart failure

Our previous study showed that static handgrip caused increases in the plasma adrenomedullin (ADM) both in patients with heart failure (HF) and healthy subjects. The present study was designed to determine the role of the sympathetic nervous system in mediating plasma ADM changes during handgrip in patients with HF. Twelve male HF patients (II class NYHA) treated with carvedilol, a non-selective adrenergic blocker (TC) and 12 patients untreated with carvedilol (UC) performed two 3-min bouts of static handgrip at 30% of maximal voluntary contraction, alternately with each hand. At the end of both exercise bouts and in 5 min of the recovery period, plasma ADM and catecholamines were determined. In addition, heart rate, blood pressure and stroke volume (SV) were measured. The baseline plasma ADM, noradrenaline (NA) and adrenaline (A) levels were similar in the two groups of patients, while SV was higher (P<0.05) in TC than in UC. During exercise plasma ADM concentrations were lower (P<0.05) in TC than in UC, but the handgrip-induced increases in plasma ADM did not differ between the groups. Plasma ADM correlated with NA concentrations (r = 0.764) and with SV (r = -0.435) and increases in plasma ADM expressed as percentage of baseline values correlated with those of plasma NA (r = 0.499), diastolic BP (r = 0.550) and total peripheral resistance (r = 0.435). The study suggests that the sympathetic nervous system may be involved in the stimulation of ADM secretion during static exercise either directly or by changes in the haemodynamic response.

The effect of adrenergic blockade upon shock-induced lacticacidosis in sheep.

The effect of adrenergic blockade upon shock-induced lacticacidosis in sheep.

The effect of adrenergic blockade on blushing and facial flushing

The effect of adrenergic blockade on vascular responses in the forehead was assessed during stressful mental arithmetic, singing, and moderate exercise in 21 frequent blushers and 21 infrequent blushers. Adrenergic antagonists were introduced into a small site on the forehead by iontophoresis, and vascular responses were monitored bilaterally with laser Doppler flowmetry. Beta blockade prevented increases in blood flow in infrequent blushers during mental arithmetic and partially inhibited vasodilatation during singing, indicating minor participation of beta-adrenoceptors in blushing. Alpha blockade did not affect blushing but augmented vasodilatation during exercise. Despite higher ratings of self-consciousness in frequent than in infrequent blushers, vascular responses were similar in both groups. Thus, blushing propensity does not appear to be related to the density of alpha- or beta-adrenoceptors in facial vessels and may have a psychological basis.

Serum insulin/glucose ratio and urinary loss of insulin after trauma in young animals: effect of adrenergic blockade

Hyperglycemia and relative hypoinsulinemia are characteristic in the post-traumatic period. The altered insulin kinetics in this phase are dependent on many factors, which include stimulation of adrenoreceptors of pancreatic beta-cells and increased urinary clearance of insulin. Using the young rabbit as an experimental model, two series of experiments were designed. In study 1 (effect of trauma on serum insulin/glucose [I/G] ratio and urinary loss of insulin) two groups of animals (control and trauma) on parenteral nutrition were studied during 4 days. In study 2, in an acute 3-h period the effects of alpha- and beta-adrenoceptor blockers on insulin secretion were investigated. The animals were divided into four groups: control, trauma, trauma + phentolamine, and trauma + propranolol. In study 1 it was demonstrated that after trauma there was a decrease in I/G ratio and an increase in urinary loss of insulin, but no alteration in absolute levels of serum insulin. In study 2 we could demonstrate that treatment with adrenoceptor blockers did not prevent the lowering effect of trauma on I/G ratio. It is suggested that the diabetes-like state of the post-injury period is a complex phenomenon that is dependent on other important factors, as well as catecholamine inhibition of insulin secretion.

The effect of adrenergic blockade on glucose-induced thermogenesis

The effect of α, β, or combined sympathetic blockade on the increase in energy expenditure and concentrations of norepinephrine, glucose, and insulin following oral intake of 100 g of glucose was studied in lean subjects. Alpha blockade with intravenous (IV) phentolamine (n = 5) infusion increased oxygen consumption after glucose ingestion but no more than it increased the oxygen consumption when no glucose was given. Beta blockade with IV propranolol (n = 13) and combined α and β blockade (n = 6) did not affect basal metabolic rate or the increase in metabolic rate after glucose ingestion. Phentolamine or combined propranolol plus phentolamine administration markedly increased plasma norepinephrine concentrations. Basal glucose and insulin concentrations were not affected by any of the infused drugs. Glucose-stimulated insulin concentrations were unchanged by propranolol and combined blockade, whereas there was a trend ( P = 0.07) toward an increased response to glucose during phentolamine administration. These data do not support a role for the sympathetic nervous system in the increase in metabolic rate following glucose ingestion. The increase in metabolic rate during phentolamine administration can be attributed to β adrenergic stimulation.

Adrenergic blockade does not change ventilatory response to CO2 in awake resting goats.

Although adrenergic agonists increase resting ventilation and responsiveness to CO2, there are conflicting data about the effect of adrenergic blockade on ventilatory responses. In this study, we investigated the effect of alpha- or beta-adrenergic blockade on the response to hyperoxic CO2 rebreathing in awake goats. In 5 goats, studied before and after intravenous administration of phentolamine or propranolol, there was no difference (compared to control studies) in the mean slope, x-intercept, or ventilation at end-tidal PCO2 (PETCO2) = 70 torr for the CO2 response curves after either drug. When mean inspiratory flow rate (VT/Ti) was plotted against PETCO2, there was also no change in these measurements after propranolol. After phentolamine, there was a slight decrease in the slope and x-intercept, but no change in VT/Ti at PETCO2 = 70 torr. We conclude that acute administration of alpha- or beta-adrenergic blockers does not affect ventilatory response to CO2 inhalation in goats, and suggest that adrenergic activity is not an important modulating influence for CO2 responsiveness in this species.

The effect of adrenergic blockade on potassium concentrations in different conditions.

A moderate increase in serum potassium concentrations has been observed in several controlled clinical trials with beta-blockers. This increase cannot be explained by the retention of potassium in the organism, and is probably caused by the redistribution of potassium from intracellular to extracellular compartments. beta-adrenergic mechanisms seem to be concerned in the extrarenal handling of the potassium-load in man, presumably by inducing an increased uptake of potassium in muscular cells and liver cells. These beta-adrenergic mechanisms are probably of the beta 2-type. In theory there are several conditions in which it is important to have a defence against hyperkalaemia from exogenous or endogenous sources for example, during heavy physical exercise, after a potassium-rich meal, or after traumatic tissue damage. Available data indicate that non-selective beta-blockade increases serum potassium concentrations during and after heavy exercise and during coronary bypass. The clinical implications of these findings are unknown.

Effect of adrenergic blockade with bretylium and phentolamine on glomerular filtration rate in the rainbow trout, Salmo gairdneri Rich., adapting to saline water

1. In resting conscious trout, Salmo gairdneri, a gradual increase in external salinity (brackish water) resulted in an immediate decline of glomerular filtration rate and urine flow. 2. These renal responses were partly blocked by the administration of bretylium and phentolamine. 3. The presence of adrenergic nerve endings in the trout kidney and these pharmacological results together provide evidence of neural control of renal haemodynamics. 4. The action of vasoactive substances and innervation is discussed briefly in relation to their importance for normal renal function.

The effect of adrenergic blockade on the insulin release after intraduodenal glucose in man

The effect of adrenergic blockade on the insulin release after intraduodenal glucose in man

Effect of adrenergic blockade on dynamics of the pregnant primate uterus (Macaca mulatta)

Unanesthetized rhesus monkeys, conditioned to restraining chairs and monitored continuously by chronically implanted sensors, were used to explore the relationships between catecholamines and uterine dynamics during late gestation. Continuous intra-aortic infusion of phentolamine produced a dose-response decrease in uterine activity and blood flow. With alpha-adrenergic blockade the circadian (Fourier) variations of uterine activity were abolished and those of uterine blood flow were reversed. Placental blood flow (by the microsphere technique) was 86.1% of control values. Beta-adrenergic blockade (propranolol) accentuated the circadian variations of uterine dynamics. Vascular resistance to both the myometrium and the placentas was increased. The data indicate that the maternal placental vasculature is the primary site of uterine vascular resistance and is susceptible to adrenergic response. The data also suggest that the extrinsic resistance produced by the myometrium is of major importance in the distribution of uterine blood flow.

Effect of adrenergic blockade on autoregulation of the cerebral blood flow during orthostatic tests

The effect of phentolamine and anapriline on the cerebral blood flow autoregulation (CBFA) under the orthostatic test (OT) was studied in experiments on locally anesthetized rabbits. Cerebral blood flow (CBF) in the carotids, venous pressure in the cerebral vessels, perfusion pressure (PP) in the carotid arteries were measured, the resistance of cerebral vessels was calculated. OT was modeled by tilting a special table with the animal (with its head upwards or a special table with the animal (with its head upwards or downwards) by 40--80 degrees from the horizontal level. The results showed adrenergic block in most of OT cases to disturb CBFA; phentolamine promoted passive increase of CBF when PP was increased; on the contrary, anapriline promoted passive CBF reduction when PP was decreased.

Effect of adrenergic blockade on heart rate (HR) and blood pressure (BP) responses to exercise

Effect of adrenergic blockade on heart rate (HR) and blood pressure (BP) responses to exercise

Effect of adrenergic blockade on glucagon and growth hormone secretion in normal and diabetic children.

Studies were conducted in four normal and six diabetic children to assess the role of adrenergic blockade on basal and arginine-stimulated growth hormone and glucagon secreation. Each subject had, on three separate occasions, infusion of arginine alone or in conjunction with alpha (phentolamine) or beta (propranolol) adrenergic blockade. Clinically, there was evidence of adequate blockade by each agent. Basal hormone growth levels were not significantly different in the two groups (1.3 +/- 0.2 to 2.1 +/- 1.0 ng/ml in normal subjects; 3.0 +/- 1.1 to 6.0 +/- 3.1 ng/ml in diabetics (mean +/- 1 SEM)) but the peak growth hormone after arginine was significantly greater in the diabetic children than control subjects (34.3 +/- 7.2 versus 12.3 +/- 3.1); in both groups alpha-blockade suppressed the growth hormone response, whereas beta-blockade had no significant effect. Basal glucagon concentrations were similar in both groups (147 +/- 31 to 214 +/- 21 pg/ml in normal subjects; 100 +/- 20 to 124 +/- 17 pg/ml in diabetics on three different occasions) despite the coexistent hyperglycemia of the diabetics. Neither basal nor maximally stimulated glucagon secretion was significantly affected by alpha or beta blockade in the juvenile diabetic or control children. The results suggest that sympathetic overactivity via alpha receptors may contribute to the hypersecretion of growth hormone in juvenile diabetes and that the alpha or beta adrenergic receptor alone does not appear to modulate basal or arginine stimulated glucagon secretion.

The effect of adrenergic blockade on the glucagon responses to starvation and hypoglycemia in man.

In an attempt to ascertain whether the sympathetic nervous system modulates glucagon release in man during starvation and hypoglycemia, the influence of alpha and beta adrenergic blockade on glucagon responses was studied in young, healthy men subjected to fasting and insulin-induced hypoglycemia. Six volunteers fasted for 84 h on three separate occasions. Plasma immunoreactive glucagon (IRG), measured initially at 12 h, climbed gradually from mean levels of 54 pg/ml to a zenith of 124 pg/ml at 48 h, with maintenance of these levels for the duration of the fast. The infusion of propranolol or phentolamine throughout the terminal 24 h of the second and third fasts failed to alter the pattern of IRG release. After an overnight fast, five volunteers received insulin intravenously, which evoked a mean rise in plasma IRG levels from 63 pg/ml to a maximum of 256 pg/ml at 30 min. The concurrent administration of propranolol or phentolamine did not modify the glucagon responses to insulin-induced hypoglycemia. These data suggest that the augmented glucagon release in man during starvation or after hypoglycemia is not significantly regulated by signals from the adrenergic nervous system.

Effect of adrenergic blockade and specific antithyroid therapy on electrocardiographic changes in hyperthyroidism.

Abstract:Considerable controversy still exists whether the cardiovascular manifestations of hyperthyroidism are due to the direct action of an increased amount of thyroid hormones on the heart or due to increased adrenergic activity of catecholamines. In this study, electrocardiograms (ECG) were rec

The effect of adrenergic blockade on exercise-induced hyperglucagonemia.

Rats subjected to forced swimming with a tail weight for 45 minutes exhibited a mean plasma glucagon level of 623 (SEM ± 80) pg/ml, significantly above the 102 (SEM ± 11) pg/ml average of resting control rats (p < 0.001). The administration of the α-adrenergic blocker phentolamine prior to exercise completely blocked exercise-induced hyperglucagonemia. Propranolol treatment, by contrast, failed to alter the rise in glucagon induced by exercise. Although differences in glucose concentration were present in the various groups and undoubtedly influenced the changes, they were not sufficient to account for the findings. It appears, therefore, that under the conditions of these experiments exercise-induced hyperglucagonemia in rats was mediated largely by α-adrenergic stimulation. (Endocrinology 94: 1254, 1974)

Adrenergic control mechanism for vasopressin-induced plasma growth hormone response

The effect of alpha adrenergic blockade with phentolamine on vasopressin-induced growth hormone elevations was tested in ten female volunteers. Only half of the subjects exhibited a plasma HGH rise following vasopressin administration. In the subjects who showed a plasma HGH response to vasopressin (“responders”), alpha adrenergic blockade inhibited the growth hormone response to approximately one-third of the response in the same subject without adrenergic blockade. This effect of adrenergic blockade could not be attributed to differences in blood glucose or plasma FFA. It is concluded that the stimulation of growth hormone secretion by vasopressin is mediated at least in part through catecholamines.

Effect of adrenergic blockade on the metabolic response to hemorrhagic shock

Effect of adrenergic blockade on the metabolic response to hemorrhagic shock

Effect of adrenergic blockade on hypoxia-induced pulmonary vasoconstriction in awake dogs.

Effect of adrenergic blockade on hypoxia-induced pulmonary vasoconstriction in awake dogs.