scholarly journals ANG II-related myocardial damage: role of cardiac sympathetic catecholamines and β-receptor regulation

1998 ◽  
Vol 275 (2) ◽  
pp. H534-H541 ◽  
Author(s):  
Jeffrey R. Henegar ◽  
Dean D. Schwartz ◽  
Joseph S. Janicki
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Myocardial Damage ◽  
Sympathetic Neuron ◽  
Receptor Regulation ◽  
Ang Ii ◽  
Receptor Density ◽  
Β Receptor ◽  
Acute Nature

The objectives of this study were 1) to determine whether ANG II-induced myocardial damage (ANG Dam) is mediated via the β1-adrenergic receptor, 2) to elucidate whether adrenal medulla or cardiac sympathetic neuron catecholamines are responsible for ANG Dam, and 3) to determine whether the lack of damage after 3 days of elevated ANG II levels is due to β1-receptor downregulation. To this end, ANG II was administered to rats 1) that were treated with a β-receptor blocker, 2) after adrenal medullectomy and/or cardiac sympathectomy, and 3) for 3 or 8 days. ANG II caused both myocyte necrosis and coronary vascular damage after adrenal medullectomy but not after cardiac sympathectomy. There was a 38 and 55% decrease in β-receptor density after 3 and 8 days, respectively, of ANG II infusion, and an upregulation to control levels 5 days after a 3-day ANG II infusion was stopped. We conclude that cardiac sympathetic neuron catecholamines are responsible for ANG Dam and that the acute nature of this damage is associated with a downregulation of β1-adrenergic receptors.

β-Adrenergic regulation of Na+ uptake by larval zebrafish Danio rerio in acidic and ion-poor environments

2012 ◽  
Vol 303 (10) ◽  
pp. R1031-R1041 ◽  
Author(s):  
Yusuke Kumai ◽  
Mellissa A. R. Ward ◽  
Steve F. Perry
Keyword(s):  
Danio Rerio ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Acidic Water ◽  
Adrenergic Systems ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Adrenergic Receptor Agonist

The potential role of adrenergic systems in regulating Na+ uptake in zebrafish ( Danio rerio) larvae was investigated. Treatment with isoproterenol (a generic β-adrenergic receptor agonist) stimulated Na+ uptake, whereas treatment with phenylephrine (an α1-adrenergic receptor agonist) as well as clonidine (an α2-adrenergic receptor agonist) significantly reduced Na+ uptake, suggesting opposing roles of α- and β-adrenergic receptors in Na+ uptake regulation. The increase in Na+ uptake associated with exposure to acidic water (pH = 4.0) was attenuated in the presence of the nonselective β-receptor antagonist propranolol or the β1-receptor blocker atenolol; the β2-receptor antagonist ICI-118551 was without effect. The stimulation of Na+ uptake associated with ion-poor water (32-fold dilution of Ottawa tapwater) was unaffected by β-receptor blockade. Translational gene knockdown of β-receptors using antisense oligonucleotide morpholinos was used as a second method to assess the role of adrenergic systems in the regulation of Na+ uptake. Whereas β1- or β2B-receptor knockdown led to significant decreases in Na+ uptake during exposure to acidic water, only β2A-receptor morphants failed to increase Na+ uptake in response to ion-poor water. In support of the pharmacology and knockdown experiments that demonstrated an involvement of β-adrenergic systems in the control of Na+ uptake, we showed that the H+-ATPase-rich (HR) cell, a subtype of ionocyte known to be a site of Na+ uptake, is innervated and appears to express β-adrenergic receptors (propranolol binding sites) at 4 days postfertilization. These data indicate an important role of adrenergic systems in regulating Na+ uptake in developing zebrafish.

scholarly journals Role of beta-adrenergic receptor subtypes in pig uterus contractility with inflammation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Barbara Jana ◽  
Jarosław Całka
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Domestic Animals ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Beta Adrenergic Receptor ◽  
Pharmacological Modulation ◽  
Uterine Inflammation ◽  
Myometrial Contractility

AbstractUterine inflammation is a very common and serious condition in domestic animals. To development and progression of this pathology often lead disturbances in myometrial contractility. Participation of β1-, β2- and β3-adrenergic receptors (ARs) in noradrenaline (NA)-influenced contractility of the pig inflamed uterus was studied. The gilts of SAL- and E.coli-treated groups were administered saline or E.coli suspension into the uterine horns, respectively. Laparotomy was only done in the CON group. Compared to the period before NA administration, this neurotransmitter reduced the tension, amplitude and frequency in uterine strips of the CON and SAL groups. In the E.coli group, NA decreased the amplitude and frequency, and these parameters were lower than in other groups. In the CON, SAL and E.coli groups, β1- and β3-ARs antagonists in more cases did not significantly change and partly eliminated NA inhibitory effect on amplitude and frequency, as compared to NA action alone. In turn, β2-ARs antagonist completely abolished NA relaxatory effect on these parameters in three groups. Summarizing, NA decreases the contractile amplitude and frequency of pig inflamed uterus via all β-ARs subtypes, however, β2-ARs have the greatest importance. Given this, pharmacological modulation of particular β-ARs subtypes can be used to increase inflamed uterus contractility.

Increased alpha 1-adrenergic vascular sensitivity during development of hypertension in conscious dogs

1993 ◽  
Vol 264 (4) ◽  
pp. H1259-H1268 ◽  
Author(s):  
N. Uemura ◽  
D. E. Vatner ◽  
Y. T. Shen ◽  
J. Wang ◽  
S. F. Vatner
Keyword(s):  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Aortic Tissue ◽  
Ang Ii ◽  
Receptor Density ◽  
Adrenergic Stimulation ◽  
Before And After ◽  
Vascular Responsiveness

The goal of this study was to determine whether enhanced vascular responsiveness during the development of perinephritic hypertension is selective or nonspecific. The effects of graded infusions of norepinephrine (NE), phenylephrine (PE), angiotensin II (ANG II), and vasopressin (VP) were examined on mean arterial pressure, total peripheral resistance (TPR), and aortic pressure-diameter relationships in conscious dogs. NE increased TPR significantly greater (P < 0.01) in hypertension than normotension, as did PE infusion, whereas ANG II and VP increased TPR similarly before and after hypertension. Analysis of aortic pressure-diameter relationships also demonstrated significant (P < 0.05) shifts in response to NE and PE, but not ANG II and VP, during the development of hypertension. In normotensive dogs, low doses of ANG II infusion also enhanced the vasoconstrictor response not only to NE and PE but also to VP. In contrast to what was observed in hypertension, in the presence of ANG II infusion after ganglionic blockade, enhanced responses to PE and NE were no longer observed. The alpha 1-adrenergic receptor density in membrane preparations from aortic tissue, as determined by [3H]prazosin binding, was higher (P < 0.05) in hypertensive dogs than control dogs. Thus the vascular responsiveness in the aorta and resistance vessels is enhanced to alpha 1-adrenergic stimulation, but not to all vasoconstrictors, during developing perinephritic hypertension. The mechanism appears to involve increased alpha 1-adrenergic receptor density.

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.

scholarly journals Noradrenergic control of central oxytocin release during lactation in rats

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Additional Experiment ◽  
Adrenergic Agonist ◽  
Magnocellular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Oxytocin Release ◽  
Stimulation Of

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.

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).

scholarly journals Heat and α1-adrenergic responsiveness in human skeletal muscle feed arteries: the role of nitric oxide

2012 ◽  
Vol 113 (11) ◽  
pp. 1690-1698 ◽  
Author(s):  
Stephen J. Ives ◽  
Robert H. I. Andtbacka ◽  
Sun Hyung Kwon ◽  
Yan-Ting Shiu ◽  
Ting Ruan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Human Skeletal Muscle ◽  
Bovine Endothelial Cells ◽  
No Bioavailability ◽  
Feed Arteries ◽  
Skeletal Muscle Feed Arteries

Increased local temperature exerts a sympatholytic effect on human skeletal muscle feed arteries. We hypothesized that this attenuated α1-adrenergic receptor responsiveness may be due to a temperature-induced increase in nitric oxide (NO) bioavailability, thereby reducing the impact of the α1-adrenergic receptor agonist phenylephrine (PE). Thirteen human skeletal muscle feed arteries were harvested, and wire myography was used to generate PE concentration-response curves at 37°C and 39°C, with and without the NO synthase (NOS) inhibitor NG-monomethyl-l-arginine (l-NMMA). A subset of arteries ( n = 4) were exposed to 37°C or 39°C, and the protein content of endothelial NOS (eNOS) and α1-adrenergic receptors was determined by Western blot analysis. Additionally, cultured bovine endothelial cells were exposed to static or shear stress conditions at 37°C and 39°C and assayed for eNOS activation (phosphorylation at Ser1177), eNOS expression, and NO metabolites [nitrate + nitrite (NOx)]. Maximal PE-induced vasocontraction (PEmax) was lower at 39°C than at 37°C [39 ± 10 vs. 84 ± 30% maximal response to 100 mM KCl (KClmax)]. NO blockade restored vasocontraction at 39°C to that achieved at 37°C (80 ± 26% KClmax). Western blot analysis of the feed arteries revealed that heating increased eNOS protein, but not α1-adrenergic receptors. Heating of bovine endothelial cells resulted in greater shear stress-induced eNOS activation and NOx production. Together, these data reveal for the first time that, in human skeletal muscle feed arteries, NO blockade can restore the heat-attenuated α1-adrenergic receptor-mediated vasocontraction and implicate endothelium-derived NO bioavailability as a major contributor to heat-induced sympatholysis. Consequently, these findings highlight the important role of vasodilators in modulating the vascular response to vasoconstrictors.

Role of angiotensin II and alpha-adrenergic receptors during estrogen-induced vasodilation in ewes

1992 ◽  
Vol 263 (5) ◽  
pp. E837-E843 ◽  
Author(s):  
L. E. Davis ◽  
R. R. Magness ◽  
C. R. Rosenfeld
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Perfusion Pressure ◽  
Cardiovascular Effects ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Renin Angiotensin ◽  
Alpha Adrenergic Receptors ◽  
Adrenergic Systems

Estradiol-17 beta (E2 beta) produces uterine and systemic vasodilation in nonpregnant ewes without altering mean arterial pressure (MAP). Mechanisms responsible for maintaining MAP and thus uterine blood flow (UBF) may include activation of the renin-angiotensin and/or adrenergic systems. We therefore investigated the effects of systemic blockade of angiotensin II (ANG II) and/or alpha-adrenergic receptors in nonpregnant, castrated ewes, using saralasin (Sar) and/or phentolamine (Phen) in the presence or absence of intravenous E2 beta (1.0 microgram/kg). In nonestrogenized ewes neither antagonist alone had substantial cardiovascular effects; however, Sar + Phen decreased systemic vascular resistance (SVR) 20 +/- 7.4% (SE) and increased heart rate (HR) 50 +/- 19% (P < 0.01); MAP and UBF were unaffected. Following E2 beta treatment SVR fell 17 +/- 2.4% (P < 0.01), UBF increased more than fourfold, and MAP was unchanged. Compared with E2 beta alone, Phen + E2 beta decreased SVR 42 +/- 4.7%, and MAP fell 11 +/- 1.8% (P < 0.05) despite 40–50% increases in HR and cardiac output (P < 0.05). Responses to Sar + E2 beta were similar to E2 beta alone, except for a fall in MAP, whereas responses to Sar + Phen + E2 beta resembled those of Phen + E2 beta. E2 beta-induced uterine vasodilation was unaltered by Sar and/or Phen. During E2 beta-induced vasodilation, MAP is maintained by enhanced activation of the alpha-adrenergic and renin-angiotensin systems; however, uterine vascular responses to E2 beta are independent of both systems and perfusion pressure.

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