ATP-MgCl2 administration normalizes macrophage cAMP and beta-adrenergic receptors after hemorrhage and resuscitation

1994 ◽  
Vol 267 (1) ◽  
pp. G52-G58 ◽  
Author(s):  
P. Wang ◽  
S. M. Tait ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Receptor Binding ◽  
Kupffer Cells ◽  
Adrenergic Receptors ◽  
Binding Capacity ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Midline Laparotomy ◽  
Binding Characteristics ◽  
Beta Receptor ◽  
Camp Levels

Although ATP-MgCl2 attenuates the release of inflammatory cytokines and restores the defective macrophage (M phi) antigen presentation function after hemorrhage and resuscitation, it is not known whether administration of this agent after hemorrhage affects M phi adenosine 3',5'-cyclic monophosphate (cAMP) levels and beta-adrenergic receptors. To determine this, rats underwent a midline laparotomy (i.e., induction of trauma) and were then bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximum bleedout volume was returned in the form of Ringer lactate (RL). Animals were resuscitated with four times the volume of shed blood with RL, during and after which ATP-MgCl2 (50 mumol/kg) or saline was administered over 95 min. At 1.5 h postresuscitation (i.e., 10 min after completion of ATP-MgCl2 infusion), peritoneal M phi and Kupffer cells were isolated, and cAMP levels were measured by radioimmunoassay. beta-Receptor binding characteristics were also determined in isolated Kupffer cells. The results indicate that cAMP levels increased significantly in both peritoneal M phi and Kupffer cells after hemorrhage and resuscitation. Maximum binding capacity (Bmax) of beta-receptors increased in Kupffer cells, suggesting that the elevated cAMP may be due to the increased beta-receptor Bmax under such conditions. ATP-MgCl2 treatment, however, markedly decreased beta-receptor Bmax in Kupffer cells and cAMP in both peritoneal M phi and Kupffer cells, and the values were similar to shams. Thus normalization of M phi cAMP levels and beta-receptor binding capacity by ATP-MgCl2 may contribute to the immunoenhancing effects of this agent observed after trauma-hemorrhage and fluid resuscitation.

Downregulation of hepatic beta-adrenergic receptors after trauma and hemorrhagic shock

1995 ◽  
Vol 268 (5) ◽  
pp. G749-G753 ◽  
Author(s):  
S. M. Tait ◽  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Hemorrhagic Shock ◽  
Dissociation Constant ◽  
Adrenergic Receptors ◽  
Binding Capacity ◽  
Scatchard Analysis ◽  
Beta Adrenergic Receptors ◽  
Ringer Lactate ◽  
Beta Adrenergic ◽  
Midline Laparotomy ◽  
Maximal Binding

Although it is well known that sympathoadrenal activity increases under various adverse circulatory conditions, it is not known whether there are any alterations in hepatic plasma membrane beta-adrenergic receptors after trauma-hemorrhage and crystalloid resuscitation. To study this, rats underwent a 5-cm midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of the maximal bleedout (MB) volume was returned in the form of Ringer lactate. The animals were then resuscitated with four times the volume of MB in the form of Ringer lactate over 60 min. Hepatic plasma membranes were isolated using discontinuous Percoll gradient centrifugation. The maximal binding capacity and dissociation constant (i.e., 1/affinity) of [125I]iodopindolol binding to beta-adrenergic receptors were determined using a membrane filtration assay and Scatchard analysis. The results indicate that there was a significant decrease in the maximal binding capacity at the time of MB, which persisted despite crystalloid resuscitation after hemorrhage. However, there were no significant changes in the dissociation constant at any time point during this study. The downregulation of beta-adrenergic receptor binding capacity may be responsible for metabolic abnormalities observed after hemorrhagic shock.

Potentiation of surfactant release in fetal lung by thyroid hormone action

1984 ◽  
Vol 56 (6) ◽  
pp. 1621-1626 ◽  
Author(s):  
D. K. Das ◽  
J. Ayromlooi ◽  
D. Bandyopadhyay ◽  
S. Bandyopadhyay ◽  
A. Neogi ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Adrenergic Receptors ◽  
Actinomycin D ◽  
Binding Capacity ◽  
Fetal Lung ◽  
Lavage Fluid ◽  
Beta Adrenergic Receptors ◽  
Lung Maturation ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist

Thyroid hormone has been shown to accelerate fetal lung development, but the mechanisms by which this hormone acts are yet unknown. Since this hormone may act indirectly by potentiating the action of endogenous catecholamines, we studied this mechanism by measuring beta-adrenergic receptors in fetal lung. Fetal rabbits at 27 days of gestation were treated with triiodothyronine (T3), 100 micrograms/100 g, in the presence and absence of propranolol, 200 micrograms/100 g, or actinomycin D, 20 micrograms/100 g. Fetuses were killed by decapitation either after 4 or 24 h of T3 treatment. The beta-adrenergic antagonist l-[3H]dihydroalprenolol was used to directly estimate the number and affinity of beta-adrenergic receptor in lung membranes. T3 increased the number of beta-adrenergic receptors in fetal lung, but the affinity of binding did not change. The enhancement of binding capacity after 4 h of T3 treatment was not inhibited by actinomycin D. However, 24-h T3-mediated stimulation was partially blocked by actinomycin D. In addition, T3 stimulated the catecholamine content, adenylate cyclase activity, and adenosine 3′,5′-cyclic monophosphate content of lung. T3 increased the lecithin-to-sphingomyelin ratio, phosphatidylglycerol, and disaturated phosphatidylcholine content of the pulmonary lavage fluid. These parameters were completely inhibited by propranolol after 4 h and partially inhibited by actinomycin D after 24 h. Thus thyroid hormone enhances lung maturation by increasing the number of beta-adrenergic receptors in fetal lung.

Burn-induced alterations in cardiac beta-adrenergic receptors

1992 ◽  
Vol 262 (5) ◽  
pp. H1585-H1591 ◽  
Author(s):  
T. M. Kaufman ◽  
J. W. Horton
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Adrenergic Receptors ◽  
Burn Injury ◽  
Binding Capacity ◽  
Total Body Surface Area ◽  
Scatchard Analysis ◽  
Beta Adrenergic Receptors ◽  
Binding Studies ◽  
Beta Adrenergic

Previous studies in our laboratory have demonstrated that burn injury (45% total body surface area, 3rd-degree scald burn) diminishes contractile and relaxation function in the isolated perfused guinea pig heart. The mechanisms responsible for the burn-mediated dysfunction are not well understood. Therefore the purpose of this study was to examine the inotropic response to isoproterenol, a beta-adrenergic agonist, and burn-induced alterations in beta-adrenergic receptors (beta-AR) in adult guinea pig hearts. Isoproterenol dose-response curves were generated in isolated perfused hearts from sham-burned and burned guinea pigs. In addition, binding studies were performed using [125I]iodocyanopindolol on hearts from sham-burned and burned guinea pigs. Both the functional response and sensitivity to isoproterenol were significantly diminished 24 h after burn injury. beta-AR density (binding capacity, Bmax) and affinity were determined by Scatchard analysis. Agonist competition curves were performed in the presence or absence of 0.1 mM 5'-guanylyl imidodiphosphate. There was no difference in Bmax in membranes from sham-burned and burned hearts; however, the affinity of beta-AR was significantly decreased after burn injury compared with sham burn [dissociation constant = 32.5 +/- 1.9 (mean +/- SE), n = 10, vs. 26.7 +/- 1.7 pM, n = 10, P = 0.039]. Furthermore, the fraction of receptors in a high-affinity state (those functionally coupled to Gs protein) was significantly decreased after burn injury compared with sham burn (41.2 +/- 4.7%, n = 9, vs. 54 +/- 2%, n = 9, P = 0.023).(ABSTRACT TRUNCATED AT 250 WORDS)

Initial externalization followed by internalization of beta-adrenergic receptors in rat heart during sepsis

1996 ◽  
Vol 270 (1) ◽  
pp. R254-R263 ◽  
Author(s):  
C. Tang ◽  
M. S. Liu
Keyword(s):  
Rat Heart ◽  
Adrenergic Receptors ◽  
Binding Capacity ◽  
Photoaffinity Labeling ◽  
Cecal Ligation ◽  
Beta Adrenergic Receptors ◽  
Binding Studies ◽  
Beta Adrenergic ◽  
Rat Hearts ◽  
Early Sepsis

Changes in the distribution of beta-adrenergic receptors in two subcellular fractions, the sarcolemma and the light vesicle, of rat heart during sepsis were studied, using [3H]dihydroalprenolol ([3H]DHA) binding and photoaffinity labeling with [125I]iodocyanopindolol ([125I]ICYP). Sepsis was induced by cecal ligation and puncture (CLP). Septic rat hearts exhibit an initial hypercardiodynamic (9 h after CLP; early sepsis) and a subsequent hypocardiodynamic (18 h after CLP; late sepsis) state. [3H]DHA-binding studies show that, during early sepsis, the maximum binding capacity (Bmax) was increased by 35% in sarcolemma but was decreased by 25% in light vesicles, whereas during late sepsis, the Bmax was decreased by 39% in sarcolemma but was increased by 30% in light vesicles. Photoaffinity labeling studies show that the incorporation of [125I]ICYP into 64,000-Da peptide during early sepsis was increased by 32% in sarcolemma but was decreased by 27% in light vesicles, whereas during late sepsis, the incorporation was decreased by 30% in sarcolemma but was increased by 35% in light vesicles. These data indicate that beta-adrenergic receptors in the rat heart were externalized from light vesicles to sarcolemma during the hyperdynamic phase but were internalized from surface membranes to intracellular sites during the hypodynamic phase of sepsis. Because beta-adrenergic receptors mediate adrenergic control of cardiac muscle contraction, a biphasic intracellular redistribution of beta-adrenergic receptors in the heart may contribute to the development of the initial hypercardiodynamic and subsequent hypocardiodynamic states during sepsis.

Molecular and functional identification of beta-adrenergic receptors in distal convoluted tubule cells

1997 ◽  
Vol 272 (6) ◽  
pp. F712-F720 ◽  
Author(s):  
F. A. Gesek ◽  
K. E. White
Keyword(s):  
Adrenergic Receptors ◽  
Receptor Activation ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptors ◽  
Functional Responses ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Beta 2 ◽  
Camp Formation

Renal nerve stimulation or circulating catecholamines activate the beta-adrenergic receptors that mediate direct effects on tubular transport. Three subtypes of beta-adrenergic receptors have been characterized: beta 1, beta 2, and beta 3. beta-Adrenergic-receptor effects on Na+ and Ca2+ transport in distal convoluted tubules (DCT) have not been established. The focus of this study was to 1) identify the subtypes of beta-adrenergic receptors in DCT cells and 2) examine functional responses to beta-receptor activation on adenosine 3',5'-cyclic monophosphate (cAMP) formation and Na+ and Ca2+ entry. To determine the subtypes of beta-receptors present, RNA isolated from immortalized mouse DCT cells was reverse transcribed, and the cDNA was amplified using primers designed to reported sequences for beta 1-, beta 2-, and beta 3-receptor subtypes. Products of the appropriate sizes were obtained with beta 1- and beta 2-primers. No product was observed with primers to the beta 3 sequence. Receptor products were confirmed by sequencing and are identical to reported mouse beta 1- and beta 2-receptor sequence. Receptor binding of[3H]dihydroalprenolol was 123 +/- 13 fmol/mg protein, and a 3:1 ratio of beta 1- to beta 2-receptors was observed with DCT cell membranes. Isoproterenol, a beta-receptor agonist, increased cAMP formation 8.5-fold. Pretreatment with the antagonist propranolol abolished agonist-induced cAMP accumulation. Isoproterenol significantly increased 22Na+ uptake to 345 +/- 23 compared with a basal rate of 256 +/- 12 nmol.min-1.mg protein-1 and was blocked with propranolol and beta 1- and beta 2-selective antagonists. Isoproterenol had no effect on 45Ca2+ entry into DCT cells. In summary, DCT cells express three times more beta 1- than beta 2-receptors and express no detectable beta 3-adrenergic receptors. beta-Receptors couple to adenylyl cyclase, and activation of beta-adrenergic receptors increases Na+ but not Ca2+ entry in DCT cells.

Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors

1992 ◽  
Vol 127 (6) ◽  
pp. 526-530 ◽  
Author(s):  
A Mayerhofer ◽  
RW Steger ◽  
G Gow ◽  
A Bartke
Keyword(s):  
Receptor Antagonist ◽  
Golden Hamster ◽  
Adrenergic Receptors ◽  
Synergistic Effects ◽  
Beta Adrenergic Receptors ◽  
Stimulatory Action ◽  
Beta Adrenergic ◽  
Testosterone Production ◽  
Beta Receptor

Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.

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