Regulation of atrial autonomic receptors in experimental cyanotic heart disease

1991 ◽  
Vol 261 (4) ◽  
pp. H1135-H1140 ◽  
Author(s):  
R. Doshi ◽  
E. Strandness ◽  
D. Bernstein
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Receptor Subtypes ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Beta 2 ◽  
The Right ◽  
Chronic Hypoxemia ◽  
Inotropic Responses

During chronic hypoxemia, left ventricular beta-adrenergic receptor density is decreased and a dissociation occurs between increased chronotropic and decreased inotropic responses to chronically elevated sympathetic tone. To determine whether this dissociation was related to alterations in autonomic receptor populations in the right atrium, we studied right atrial cholinergic and beta-adrenergic receptors in chronically hypoxemic newborn lambs and in normoxemic controls. Heart rate response was determined by infusing isoproterenol at 0.1 or 0.5 microgram.kg-1.min-1. Muscarinic receptors were quantified with [3H]quinuclidinyl benzilate and beta-adrenergic receptors with [125I]iodocyanopindolol. Competition with ICI 118,551 was used to determine beta 1- vs. beta 2-receptor subtypes. In the hypoxemic lambs, isoproterenol resulted in a lesser percentage increase in heart rate (hypoxemic, 46 +/- 6% vs. control, 89 +/- 17%, P less than 0.05); however, because baseline heart rate was higher in the hypoxemic lambs (213 +/- 7 vs. 177 +/- 12 beats/min, P less than 0.05), maximal heart rate responses were similar (310 +/- 7 vs. 326 +/- 6 beats/min, NS). There was no change in receptor density or affinity of either muscarinic or beta-adrenergic receptors and no change in the proportion of beta 1- vs. beta 2-receptor subtypes. Thus the dissociation between the chronotropic and inotropic responses to chronic hypoxemia may be in part secondary to a differential regulation of beta-adrenergic receptors between the left ventricle and the right atrium.

beta-Adrenergic receptors in the developing rabbit lung

1981 ◽  
Vol 240 (4) ◽  
pp. E351-E357 ◽  
Author(s):  
J. A. Whitsett ◽  
M. A. Manton ◽  
C. Darovec-Beckerman ◽  
K. G. Adams ◽  
J. J. Moore
Keyword(s):  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptors ◽  
Rabbit Lung ◽  
Beta Adrenergic ◽  
Beta 2

beta-Adrenergic receptors and catecholamine-sensitive adenylate cyclase were identified and partially characterized in membrane fractions of rabbit lungs from day 25 of gestation to adulthood with the beta-adrenergic antagonists (--)-[3H]dihydroalprenolol [(--)-[3H]DHA] and (--)-[125I]iodohydroxybenzylpindolol [(--)-[125I]HYP]. beta-Adrenergic receptor number (Bmax) increased 11.5-fold during this time period, increasing progressively during the latter days of gestation and the early neonatal period, from 37 +/- 10 fmol/mg protein at 25 days gestation to 425 +/- 51 fmol/mg in the adult rabbit lung (mean +/- SD). Receptor affinity for (--)-[3H]DHA (KD = 1.8 nM) or (--)-[125I]HYP (KD - 0.104 nM) and the proportion of beta 1- and beta 2-adrenergic receptor subtypes (60% beta 1 and 40% beta 2) did not change with advancing age. Basal adenylate cyclase activity in lung homogenates decreased significantly with increasing age, whereas the activity in the presence of catecholamine or NaF remained nearly constant. Catecholamines stimulated adenylate cyclase activity at all ages studied supporting a role of the maturation of beta-adrenergic receptors in the regulation of pulmonary function.

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.

Effect of exercise duration on density and coupling of beta-adrenergic receptors on human mononuclear cells

1989 ◽  
Vol 66 (3) ◽  
pp. 1494-1500 ◽  
Author(s):  
M. J. Frey ◽  
D. Mancini ◽  
D. Fischberg ◽  
J. R. Wilson ◽  
P. B. Molinoff
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Regulatory Protein ◽  
Nucleotide Binding ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Guanine Nucleotide ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Guanine Nucleotide Binding

The effect of maximal exercise on lymphocyte beta-adrenergic receptors was examined in 26 normal subjects. Exercise increased O2 consumption (Vo2) from 5 +/- 1 to 50 +/- 4 ml.min-1.kg-1, plasma norepinephrine level from 188 +/- 28 to 2,682 +/- 160 pg/ml, and plasma epinephrine level from 94 +/- 72 to 857 +/- 180 pg/ml. The density of beta-adrenergic receptors on lymphocytes obtained at rest was 31 +/- 3.7 fmol/mg protein; exercise increased the density of receptors by 86 +/- 33% (range 0–257%) to 58.3 +/- 1.5 fmol/mg protein but did not alter the affinity of the receptor for [125I]iodopindolol or the coupling of the receptor to the guanine nucleotide-binding regulatory protein. The density of beta-adrenergic receptors increased progressively throughout exercise and paralleled the increase in heart rate. The magnitude of the change in the density of beta-adrenergic receptors did not correlate with the magnitude of the increase in heart rate, Vo2, or plasma levels of catecholamines. The density of receptors was still elevated 15 min after completion of exercise but fell below base line 1 h after peak exercise to 18.2 +/- 6.7 fmol/mg protein (P less than 0.05 vs. base-line levels). These results demonstrate that exhaustive exercise results in a progressive increase in the number of beta-adrenergic receptors on lymphocyte membranes, followed by a reduction in the density of receptors during the recovery phase of exercise. Despite a significant increase in the level of plasma catecholamines, the receptor remains coupled to the guanine nucleotide-binding regulatory protein.

Beta-adrenergic receptors predict heart rate reactivity to a psychosocial stressor.

1990 ◽  
Vol 52 (6) ◽  
pp. 621-623 ◽  
Author(s):  
P J Mills ◽  
J E Dimsdale ◽  
M G Ziegler ◽  
C C Berry ◽  
R D Bain
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Beta Adrenergic Receptors ◽  
Psychosocial Stressor ◽  
Heart Rate Reactivity ◽  
Beta Adrenergic

scholarly journals Thyroid-hormone modulation of the number of β-adrenergic receptors in rat fat-cell membranes

1978 ◽  
Vol 176 (3) ◽  
pp. 1007-1010 ◽  
Author(s):  
Y Giudicelli
Keyword(s):  
Thyroid Hormone ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Hormone Modulation ◽  
Β Adrenergic Receptors

Adipocytes from thyroidectomized rats contain 3 times less [3H]dihydroalprenolol-binding sites (beta-adrenergic receptors) than adipocytes from euthyroid animals. This alteration is not solely due to cell-size differences, but also to a thyroidectomy-induced defect in beta-adrenergic receptor density per adipocyte surface area, a defect that is furthermore corrected by tri-iodothyronine treatment.

Effect of age and hypoxia on beta-adrenergic receptors in rat heart

1991 ◽  
Vol 71 (6) ◽  
pp. 2094-2098 ◽  
Author(s):  
S. L. Mader ◽  
C. L. Downing ◽  
E. Van Lunteren
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Left Ventricular ◽  
Hypoxic Exposure ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Young Rats ◽  
Age Related

Previous reports suggest that hypoxia downregulates cardiac beta-adrenergic receptors from young rats. Because aging alters response to stress, we hypothesized an age-related alteration in the response to hypoxia. Male Fischer-344 rats, aged 3 and 20 mo, were divided into control and hypoxic groups. The hypoxic rats were exposed to hypobaric hypoxia (0.5 atm) for 3 wk. After hypoxic exposure, body weight decreased, hematocrit increased, right ventricular weight increased, and left ventricular weight decreased in all animals. beta-Adrenergic receptor density declined after hypoxic exposure in the young but not in the older animals, a change that was confined to the left ventricle. beta-Adrenergic receptor density in the right ventricle was significantly lower in the older animals than in the young animals. Plasma catecholamines (norepinephrine, epinephrine) drawn after the animals were killed (stress levels) decreased in young rats and increased in old rats after the exposure to hypoxia. Hypoxia is a useful physiological stress that elucidates age-related changes in cardiac beta-adrenergic receptor and catecholamine regulation that have not previously been described.

Characterization of beta-adrenergic receptors in cultured bovine tracheal gland cells

1989 ◽  
Vol 256 (2) ◽  
pp. C310-C314 ◽  
Author(s):  
J. M. Madison ◽  
C. B. Basbaum ◽  
J. K. Brown ◽  
W. E. Finkbeiner
Keyword(s):  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Rank Order ◽  
Beta Adrenergic Receptors ◽  
Binding Studies ◽  
Beta Adrenergic ◽  
High Affinity ◽  
Gland Cells ◽  
Beta 2

We characterized the beta-adrenergic receptors that mediate secretory responses to isoproterenol in cultured bovine tracheal submucosal gland cells. Previous studies have shown that these cells have morphological and biochemical features characteristic of serous cells. Isoproterenol, epinephrine, and norepinephrine each stimulated the secretion of 35SO4-labeled macromolecules from these cultured serous cells with a rank order of potency (isoproterenol greater than epinephrine greater than norepinephrine) consistent with the presence of beta 2-adrenergic receptors. These functional studies were supported by radioligand-binding studies using [I125]-iodocyanopindolol (125I-CYP) to identify beta-adrenergic receptors. 125I-CYP binding to membrane particulates prepared from cultured serous cells was saturable and of high affinity (equilibrium dissociation constant 20 +/- 3 pM; mean +/- SE, n = 6) and was antagonized stereoselectively by propranolol. Adrenergic agonists competed for 125I-CYP-binding sites with a rank order of potency characteristic of the beta 2-adrenergic receptor subtype. A specific beta 2-adrenergic receptor antagonist, ICI 118.551, competed for a single class of 125I-CYP-binding sites with high affinity (inhibition constant 1.8 +/- 0.3 nM, n = 3). We concluded that the secretory response of cultured tracheal gland cells to isoproterenol is a response mediated by beta-adrenergic receptors of the beta 2 subtype.

Evidence that beta 2-receptors mediate action of catecholamines on endolymphatic sac DC potential

1991 ◽  
Vol 260 (5) ◽  
pp. R911-R915 ◽  
Author(s):  
N. Mori ◽  
N. Uozumi
Keyword(s):  
Direct Current ◽  
Adrenergic Receptors ◽  
Endolymphatic Sac ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Selective Antagonist ◽  
Dc Potential ◽  
Beta 2 ◽  
Current Potential

Our recent study has revealed that catecholamines depress the endolymphatic sac direct current potential (ESP) by the beta-adrenergic action [Mori et al., Am. J. Physiol. 259 (regulatory Integrative Comp. Physiol. 28): R921-R924, 1990]. Beta-Adrenergic receptors have been subclassified into beta 1- and beta 2-receptors. Using beta 1-selective (dobutamine) and beta 2-selective (salbutamol) agonists and a beta 1-selective antagonist (atenolol), we determined the subtype of beta-adrenergic receptors that mediate the action of catecholamines on the ESP. Salbutamol depressed the ESP to a larger degree than dobutamine [34.0 +/- 2.6 (n = 7) vs. 13.0 +/- 2.0% (n = 8)] with a much lower dose (100 vs. 1,000 micrograms/kg). Atenolol failed to block the action of salbutamol on the ESP at a dose of 1 mg/kg, whereas propranolol inhibited it at the same dose. The results indicate that beta 2-receptors mediate the action of catecholamines on the ESP.

Refined membrane preparations mask ischemic fall in myocardial beta-receptor density

1989 ◽  
Vol 257 (3) ◽  
pp. H1032-H1036
Author(s):  
A. A. Wolff ◽  
D. K. Hines ◽  
J. S. Karliner
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Coronary Occlusion ◽  
Acute Ischemia ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Use Of Data ◽  
H2 Receptors ◽  
Myocardial Membrane

Most of the previous studies of ischemic myocardial beta-adrenergic receptors have employed membrane preparations in which the initial pellet from the myocardial homogenate spun at a low speed was discarded. We studied changes in beta-adrenergic receptor density ([125I]-iodocyanopindolol; Bmax) during 30 min of coronary occlusion in surgically anesthetized open-chest rabbits using just such a pellet [homogenized heart spun at 1,000 g (1,000-g pellet)], as well as a second pellet from the supernatant of the first pellet [spun at 40,000 g (40,000-g pellet)]. Bmax fell during acute ischemia in the 1,000-g pellet [46.8 +/- 6.1 vs. 21.6 +/- 2.4 (SE) fmol/mg protein; P less than 0.01; n = 7] but did not change in the 40,000-g pellet [46.8 +/- 6.5 vs. 47.9 +/- 2.6 (SE) fmol/mg protein; P = NS; n = 6]. The 1,000-g pellet contained 70.0 +/- 8.1% of the beta-adrenergic receptors measured between the two preparations (P less than 0.05; n = 8) and all of the histamine H2-receptors; therefore, to minimize receptor loss and other potential artifacts, unspun myocardial homogenate was studied. An ischemic decrease in Bmax was still observed [32.9 +/- 2.0 vs. 20.9 +/- 4.1 (SE) fmol/mg protein; P less than 0.05; n = 5]. These results support the use of data from cruder myocardial membrane preparations (e.g., 1,000-g pellet or unspun homogenate), which may be of greater pathophysiological relevance than data derived from a standard more-refined preparation (40,000-g pellet).

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