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Journal articles on the topic 'Cardiac receptors'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

SAXENA, P. "Cardiac serotonin receptors." Journal of Molecular and Cellular Cardiology 18 (1986): 60. http://dx.doi.org/10.1016/s0022-2828(86)80659-9.

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2

Yang, Ronghua, and Bruce T. Liang. "Cardiac P2X 4 Receptors." Circulation Research 111, no. 4 (August 3, 2012): 397–401. http://dx.doi.org/10.1161/circresaha.112.265959.

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3

ANGUS, J. "Cardiac receptors — An overview." Journal of Molecular and Cellular Cardiology 18 (1986): 1. http://dx.doi.org/10.1016/s0022-2828(86)80491-6.

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4

Boivin-Jahns, V., A. Schlipp, S. Hartmann, P. Panjwani, K. Klingel, M. J. Lohse, G. Ertl, and R. Jahns. "Antibodies to cardiac receptors." Herz 37, no. 8 (November 28, 2012): 843–48. http://dx.doi.org/10.1007/s00059-012-3699-5.

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5

Woo, Sun-Hee, and Tran Nguyet Trinh. "P2 Receptors in Cardiac Myocyte Pathophysiology and Mechanotransduction." International Journal of Molecular Sciences 22, no. 1 (December 29, 2020): 251. http://dx.doi.org/10.3390/ijms22010251.

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ATP is a major energy source in the mammalian cells, but it is an extracellular chemical messenger acting on P2 purinergic receptors. A line of evidence has shown that ATP is released from many different types of cells including neurons, endothelial cells, and muscle cells. In this review, we described the distribution of P2 receptor subtypes in the cardiac cells and their physiological and pathological roles in the heart. So far, the effects of external application of ATP or its analogues, and those of UTP on cardiac contractility and rhythm have been reported. In addition, specific genetic alterations and pharmacological agonists and antagonists have been adopted to discover specific roles of P2 receptor subtypes including P2X4-, P2X7-, P2Y2- and P2Y6-receptors in cardiac cells under physiological and pathological conditions. Accumulated data suggest that P2X4 receptors may play a beneficial role in cardiac muscle function, and that P2Y2- and P2Y6-receptors can induce cardiac fibrosis. Recent evidence further demonstrates P2Y1 receptor and P2X4 receptor as important mechanical signaling molecules to alter membrane potential and Ca2+ signaling in atrial myocytes and their uneven expression profile between right and left atrium.
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6

Li, De-Pei, David B. Averill, and Hui-Lin Pan. "Differential roles for glutamate receptor subtypes within commissural NTS in cardiac-sympathetic reflex." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 3 (September 1, 2001): R935—R943. http://dx.doi.org/10.1152/ajpregu.2001.281.3.r935.

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Ischemic stimulation of cardiac receptors evokes excitatory sympathetic reflexes. Although the nucleus of the solitary tract (NTS) is an important site for integration of visceral afferents, its involvement in the cardiac-renal sympathetic reflex remains to be fully defined. This study examined the role of glutamate receptor subtypes in the commissural NTS in the sympathetic responses to stimulation of cardiac receptors. Renal sympathetic nerve activity (RSNA) was recorded in anesthetized rats. Cardiac receptors were stimulated by epicardial application of bradykinin (BK; 10 μg/ml). Application of BK significantly increased the mean arterial pressure from 78.2 ± 2.2 to 97.5 ± 2.9 mmHg and augmented RSNA by 38.5 ± 2.5% ( P < 0.05). Bilateral microinjection of 10 pmol of 6-cyano-7-nitroquinoxaline-2,3-dione, a non- N-methyl-d-aspartate (NMDA) antagonist, into the commissural NTS eliminated the pressor and RSNA responses to BK application in 10 rats. However, microinjection of 2-amino-5-phosphonopentanoic acid (0.1 and 1 nmol, n = 8), an NMDA- receptor antagonist, or α-methyl-4-carboxyphenylglycine (0.1 and 1 nmol, n = 5), a glutamate metabotropic receptor antagonist, failed to attenuate significantly the pressor and RSNA responses to stimulation of cardiac receptors with BK. Thus this study suggests that non-NMDA, but not NMDA and glutamate metabotropic, receptors in the commissural NTS play an important role in the sympathoexcitatory reflex response to activation of cardiac receptors during myocardial ischemia.
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7

Smith, William H. T., R. Unnikrishnan Nair, Dawn Adamson, Mark T. Kearney, Stephen G. Ball, and Anthony J. Balmforth. "Somatostatin receptor subtype expression in the human heart: differential expression by myocytes and fibroblasts." Journal of Endocrinology 187, no. 3 (December 2005): 379–86. http://dx.doi.org/10.1677/joe.1.06082.

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In acromegaly, somatostatin receptor ligands (SRLs) can ameliorate left ventricular hypertrophy (LVH) and their use is associated with demonstrable improvements in various parameters of cardiac function. It remains unclear as to whether these beneficial effects are principally attributable to falling GH and IGF-I levels, or whether SRLs exert independent direct effects on the heart via somatostatin receptors. To help address this issue, we have sought to investigate somatostatin receptor expression in human heart. A human heart cDNA library was probed using PCR techniques to determine expression of somatostatin receptor subtypes. Subsequently, human heart biopsies and human cardiac fibroblasts and myocytes were analysed to determine whether expression differed between cardiac chambers or cell types. mRNAs for four of the five somatostatin receptor subtypes (sst1, sst2, sst4 and sst5) were shown to be co-expressed by the human heart. These receptors were present in both atrial and ventricular tissue. Human cardiac myocytes expressed mRNA for only sst1 and sst2, while human cardiac fibroblasts expressed all four subtypes found in whole heart tissue. The expression of functional somatostatin receptors on human cardiac fibroblasts was confirmed by mobilisation of intracellular calcium in response to somatostatin. The presence of cardiac somatostatin receptors raises the possibility of a direct effect of somatostatin analogues on the heart. Furthermore, the differential expression of somatostatin receptor subtypes by human cardiac myocytes and fibroblasts opens up the possibility of differential modulation of the cell types in the heart by subtype-specific somatostatin analogues.
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8

Sagawa, Toshio, Kazuko Sagawa, James E. Kelly, Robert G. Tsushima, and J. Andrew Wasserstrom. "Activation of cardiac ryanodine receptors by cardiac glycosides." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 3 (March 1, 2002): H1118—H1126. http://dx.doi.org/10.1152/ajpheart.00700.2001.

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This study investigated the effects of cardiac glycosides on single-channel activity of the cardiac sarcoplasmic reticulum (SR) Ca2+ release channels or ryanodine receptor (RyR2) channels and how this action might contribute to their inotropic and/or toxic actions. Heavy SR vesicles isolated from canine left ventricle were fused with artificial planar lipid bilayers to measure single RyR2 channel activity. Digoxin and actodigin increased single-channel activity at low concentrations normally associated with therapeutic plasma levels, yielding a 50% of maximal effect of ∼0.2 nM for each agent. Channel activation by glycosides did not require MgATP and occurred only when digoxin was applied to the cytoplasmic side of the channel. Similar results were obtained in human RyR2 channels; however, neither the crude skeletal nor the purified cardiac channel was activated by glycosides. Channel activation was dependent on [Ca2+] on the luminal side of the bilayer with maximal stimulation occurring between 0.3 and 10 mM. Rat RyR2 channels were activated by digoxin only at 1 μM, consistent with the lower sensitivity to glycosides in rat heart. These results suggest a model in which RyR2 channel activation by digoxin occurs only when luminal [Ca2+] was increased above 300 μM (in the physiological range). Consequently, increasing SR load (by Na+ pump inhibition) serves to amplify SR release by promoting direct RyR2 channel activation via a luminal Ca2+-sensitive mechanism. This high-affinity effect of glycosides could contribute to increased SR Ca2+ release and might play a role in the inotropic and/or toxic actions of glycosides in vivo.
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9

Thompson, G. W., D. B. Hoover, J. L. Ardell, and J. A. Armour. "Canine intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (November 1, 1998): R1683—R1689. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1683.

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To determine whether intrinsic cardiac neurons involved in cardiac regulation possess neurokinin (NK) receptor subtypes, we administered selective NK receptor agonists individually (100 μM; 0.1 ml) into the coronary arterial blood supply of right atrial intrinsic cardiac neurons of 18 anesthetized dogs. The selective NK1 receptor agonist [Sar9,Met(O2)11]-substance P depressed the spontaneous activity of right atrial neurons (26.7 ± 6.7 to 13.0 ± 4.0 impulses/min; P < 0.05) in 11 dogs and augmented such activity in the other 5 dogs (8.0 ± 3.1 to 27.8 ± 8.7 impulses/min; P < 0.05). Local administration of the selective NK2 receptor agonist [β-Ala8]-NKA-(4—10) depressed right atrial neuronal activity (27.3 ± 6.4 to 14.7 ± 3.8 impulses/min; P < 0.05), whereas the selective NK3 receptor agonist senktide augmented such activity (18.9 ± 6.4 to 53.1 ± 12.0 impulses/min; P < 0.05). Left ventricular chamber pressure fell when selective NK1 and NK2 receptor agonists were administered. Increases in heart rate and right ventricular intramyocardial systolic pressure occurred when the selective NK3 receptor agonist was studied. Administration of a selective NK1or NK2 receptor antagonist altered neuronal activity, with no subsequent change in activity occurring after administration of its respective receptor agonist. Receptor autoradiography demonstrated tachykinin receptors associated with ventral right atrial intrinsic cardiac neurons. It is concluded that intrinsic cardiac neurons involved in cardiac regulation possess NK1, NK2, and NK3 receptors and that some intrinsic cardiac neurons receive tonic input via endogenously released NKs.
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10

Garcia, M. Iveth, and Darren Boehning. "Cardiac inositol 1,4,5-trisphosphate receptors." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1864, no. 6 (June 2017): 907–14. http://dx.doi.org/10.1016/j.bbamcr.2016.11.017.

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11

DRESEL, PETER E. "Cardiac Alpha Receptors and Arrhythmias." Anesthesiology 63, no. 6 (December 1, 1985): 582–83. http://dx.doi.org/10.1097/00000542-198512000-00005.

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12

Smith, F. M., A. S. McGuirt, D. B. Hoover, J. A. Armour, and J. L. Ardell. "Chronic decentralization of the heart differentially remodels canine intrinsic cardiac neuron muscarinic receptors." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 5 (November 1, 2001): H1919—H1930. http://dx.doi.org/10.1152/ajpheart.2001.281.5.h1919.

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The objective of the study was to determine if chronic interruption of all extrinsic nerve inputs to the heart alters cholinergic-mediated responses within the intrinsic cardiac nervous system (ICN). Extracardiac nerve inputs to the ICN were surgically interrupted (ICN decentralized). Three weeks later, the intrinsic cardiac right atrial ganglionated plexus (RAGP) was removed and intrinsic cardiac neuronal responses were evaluated electrophysiologically. Cholinergic receptor abundance was evaluated using autoradiography. In sham controls and chronic decentralized ICN ganglia, neuronal postsynaptic responses were mediated by acetylcholine, acting at nicotinic and muscarinic receptors. Muscarine- but not nicotine-mediated synaptic responses that were enhanced after chronic ICN decentralization. After chronic decentralization, muscarine facilitation of orthodromic neuronal activation increased. Receptor autoradiography demonstrated that nicotinic and muscarinic receptor density associated with the RAGP was unaffected by decentralization and that muscarinic receptors were tenfold more abundant than nicotinic receptors in the right atrial ganglia in each group. After chronic decentralization of the ICN, intrinsic cardiac neurons remain viable and responsive to cholinergic synaptic inputs. Enhanced muscarinic responsiveness of intrinsic cardiac neurons occurs without changes in receptor abundance.
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13

Enders, Julio E., Patricia Paglini, Alicia R. Fernandez, Fernanda Marco, and José A. Palma. "Cardiac beta-receptors in experimental Chagas' disease." Revista do Instituto de Medicina Tropical de São Paulo 37, no. 1 (February 1995): 59–63. http://dx.doi.org/10.1590/s0036-46651995000100009.

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Experimental Chagas' disease (45 to 90 days post-infection) showed serious cardiac alterations in the contractility and in the pharmacological response to beta adrenergic receptors in normal and T. cruzi infected mice (post-acute phase). Chagasic infection did not change the beta receptors density (78.591 ± 3.125 fmol/mg protein and 73.647 ± 2.194 fmol/mg protein for controls) but their affinity was significantly diminished (Kd = 7.299 ± 0.426 nM and Kd = 3.759 ± 0.212 nM for the control) p < 0.001. This results demonstrate that the alterations in pharmacological response previously reported in chagasic myocardium are related to a significantly less beta cardiac receptor affinity. During this experimental period serious cardiac cell alterations take place and functional consequences will be detected in the chronic phase.
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14

Lee, H. T., C. I. Thompson, A. Hernandez, J. L. Lewy, and F. L. Belloni. "Cardiac desensitization to adenosine analogues after prolonged R-PIA infusion in vivo." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (December 1, 1993): H1916—H1927. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h1916.

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To determine the effects of chronic in vivo stimulation of adenosine receptors, R-(-)-N6-(2-phenylisopropyl)adenosine (R-PIA), a selective A1 receptor agonist, was administered to rats as a continuous 7-day infusion (200 nmol/h). Inotropic and chronotropic responses of isolated atria to adenosine receptor agonists were markedly desensitized compared with the responses of atria from age-matched control animals. Carbachol's negative chronotropic effect was also attenuated, indicating a heterologous mode of desensitization. Antagonist radioligand binding assays indicated a 52% reduction in A1 adenosine receptor maximum binding, and competition binding assays revealed a significant loss of G protein-coupled high-affinity A1 receptors in atria from R-PIA-treated rats. Inhibitory G proteins (Gi) were significantly reduced, as quantified by immunoblot analysis, with no change in the amount of stimulatory G proteins. Ventricular membranes from R-PIA rats showed loss of Gi and uncoupling of A1 receptors, without a significant change in A1 receptor density. Thus chronic R-PIA infusion desensitized rat atrial muscle to the effects of adenosine receptor agonists via several regulatory adaptations, including downregulation of A1 adenosine receptors, uncoupling of A1 receptors from their associated G proteins, and loss of Gi proteins.
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15

Gallagher, Ann Marie, Tristram D. Bahnson, Hisahiro Yu, Noel N. Kim, and Morton P. Printz. "Species variability in angiotensin receptor expression by cultured cardiac fibroblasts and the infarcted heart." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 3 (March 1, 1998): H801—H809. http://dx.doi.org/10.1152/ajpheart.1998.274.3.h801.

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Cardiac fibroblasts, an abundant cell of the left ventricle (LV), proliferate and synthesize collagen in the heart after acute injury and during pressure overload hypertrophy. From many studies, angiotensin II (ANG II) receptors have been implicated in promoting collagen formation by the rat cardiac fibroblast. The present study examined species variability in ANG II receptor expression. Cultured rat fibroblasts expressed 43,000 ± 15,000 ANG II (AT1-specific) receptors per cell (dissociation constant = 0.92 ± 0.34 nM), whereas rabbit and neonate human cardiac fibroblast cultures expressed few receptors. Angiotensin increased intracellular Ca2+ concentration in rats but not in rabbit or human cardiac fibroblasts and stimulated arachidonic acid release in rat but not rabbit fibroblasts. In situ, 6 days after coronary artery ligation, angiotensin receptor expression was increased 34.8 ± 13.4-fold in the infarcted area relative to the noninfarcted tissue in the rat LV, whereas rabbit hearts demonstrated only a 3.2 ± 1.6-fold increase in ANG II binding within the infarcted tissue. These species differences in receptor expression raise questions as to the role of angiotensin as a mediator of collagen formation across species and as a direct target of angiotensin-converting enzyme inhibitors to regulate cardiac fibroblast function.
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16

Dubey, Raghvendra K., Delbert G. Gillespie, and Edwin K. Jackson. "A2B Adenosine Receptors Mediate the Anti-Mitogenic Effects of Adenosine in Cardiac Fibroblasts." Hypertension 36, suppl_1 (October 2000): 708. http://dx.doi.org/10.1161/hyp.36.suppl_1.708-b.

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P85 Adenosine inhibits growth of CFs; however, the adenosine receptor subtype that mediates this anti-mitogenic effect remains undefined. Using specific ADE receptor antagonists and agonists and antisense oligonucleotides (OLIGO) against A2B receptors, we investigated the role of A2B receptors in inhibiting cardiac fibroblast growth. PDGF (25ng/ml)-induced DNA synthesis, cell number and collagen synthesis in CFs were inhibited by A2 (chloroadenosine [Cl-Ad]and MECA), but not by A1 (CPA), A2a ( CGS21680 ) or A3 (AB-MECA),receptor agonists.The inhibitory effects of 1μM MECA and Cl-Ad were reversed by A1/A2 (DPSPX; 10nM), but not by A1 (DPCPX; 10nM), receptor antagonists. In CFs treated with antisense, but not sense or scrambled, OLIGOs to the A2B receptor, both basal and PDGF-induced DNA synthesis was enhanced by 70±4% and 64±5% respectively. Moreover, the inhibitory effects of Cl-Ad and MECA were completely abolished in CFs treated with antisense, but not sense and scrambled, OLIGOs. In conclusion, A2B receptors mediate the anti-mitogenic effects of adenosine suggesting that A2B receptors are importantly involved in the regulation of CF biology. Thus, A2B receptors may play a critical role in regulating cardiac remodeling associated with CF proliferation.
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17

Li, X., G. Eschun, D. Bose, H. Jacobs, J. J. Yang, R. B. Light, and S. N. Mink. "Histamine H3 activation depresses cardiac function in experimental sepsis." Journal of Applied Physiology 85, no. 5 (November 1, 1998): 1693–701. http://dx.doi.org/10.1152/jappl.1998.85.5.1693.

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In the heart, histamine (H3) receptors may function as inhibitory presynaptic receptors that decrease adrenergic norepinephrine release in conditions of enhanced sympathetic neural activity. We hypothesized that H3-receptor blockade might improve cardiovascular function in sepsis. In a canine model of Escherichia coli sepsis, we found that H3-receptor blockade increased cardiac output (3.6 to 5.3 l/min, P< 0.05), systemic blood pressure (mean 76 to 96 mmHg, P < 0.05), and left ventricular contractility compared with pretreatment values. Plasma histamine concentrations increased modestly in the H3-blocker–sepsis group compared with values obtained in a nonsepsis–time-control group. In an in vitro preparation, histamine H3 activation could be identified under conditions of septic plasma. We conclude that activation of H3 receptors may contribute to cardiovascular collapse in sepsis.
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18

KOOSHKABADI, MOHAMMAD, PATRICK WHALEN, DALE YOO, and JONATHAN LANGBERG. "Stretch-Activated Receptors Mediate Cardiac Memory." Pacing and Clinical Electrophysiology 32, no. 3 (March 2009): 330–35. http://dx.doi.org/10.1111/j.1540-8159.2008.02240.x.

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19

Ludbrook, J. "Cardiovascular reflexes from cardiac sensory receptors." Australian and New Zealand Journal of Medicine 20, no. 4 (August 1990): 597–606. http://dx.doi.org/10.1111/j.1445-5994.1990.tb01325.x.

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20

Vincent, Anne, Catherine Sportouch, Aurélie Covinhes, Christian Barrère, Laura Gallot, Viviana Delgado-Betancourt, Benoît Lattuca, et al. "Cardiac mGluR1 metabotropic receptors in cardioprotection." Cardiovascular Research 113, no. 6 (February 27, 2017): 644–55. http://dx.doi.org/10.1093/cvr/cvx024.

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21

Christiansen, James L., Wesley Covitz, Holland V. Moore, and Robert S. Aronstam. "CARDIAC MUSCARINIC RECEPTORS IN CONOTRUNCAL ABNORMALITIES." Pediatric Research 21, no. 4 (April 1987): 187A. http://dx.doi.org/10.1203/00006450-198704010-00128.

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22

Lasley, R. "Cardiac Myocyte Adenosine Receptors and Caveolae." Trends in Cardiovascular Medicine 11, no. 7 (October 2001): 259–63. http://dx.doi.org/10.1016/s1050-1738(01)00120-7.

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23

Nishio, Hiroaki. "5-HT4 receptors and cardiac functions." Japanese Journal of Pharmacology 82 (2000): 37. http://dx.doi.org/10.1016/s0021-5198(19)47626-9.

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24

Selyanko, A. A., and V. I. Skok. "Acetylcholine receptors in rat cardiac neurones." Journal of the Autonomic Nervous System 40, no. 1 (August 1992): 33–47. http://dx.doi.org/10.1016/0165-1838(92)90223-4.

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25

Guerra, L., E. Cerbai, M. Barbieri, K. Varani, P. A. Borea, and A. Mugelli. "Cardiac beta-adrenergic receptors during ageing." Pharmacological Research 31 (January 1995): 202. http://dx.doi.org/10.1016/1043-6618(95)87068-7.

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26

Gavi, Shai, Dezhong Yin, Elena Shumay, Hsien-yu Wang, and Craig C. Malbon. "Insulin-Like Growth Factor-I Provokes Functional Antagonism and Internalization of β1-Adrenergic Receptors." Endocrinology 148, no. 6 (June 1, 2007): 2653–62. http://dx.doi.org/10.1210/en.2006-1569.

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Hormones that activate receptor tyrosine kinases have been shown to regulate G protein-coupled receptors, and herein we investigate the ability of IGF-I to regulate the β1-adrenergic receptor. Treating Chinese hamster ovary cells in culture with IGF-I is shown to functionally antagonize the ability of expressed β1-adrenergic receptors to accumulate intracellular cAMP in response to stimulation by the β-adrenergic agonist Iso. The attenuation of β1-adrenergic action was accompanied by internalization of β1-adrenergic receptors in response to IGF-I. Inhibiting either phosphatidylinositol 3-kinase or the serine/threonine protein kinase Akt blocks the ability of IGF-I to antagonize and to internalize β1-adrenergic receptors. Mutation of one potential Akt substrate site Ser412Ala, but not another Ser312Ala, of the β1-adrenergic receptor abolishes the ability of IGF-I to functionally antagonize and to sequester the β1-adrenergic receptor. We also tested the ability of IGF-I to regulate β1-adrenergic receptors and their signaling in adult canine cardiac myocytes. IGF-I attenuates the ability of β1-adrenergic receptors to accumulate intracellular cAMP in response to Iso and promotes internalization of β1-adrenergic receptors in these cardiac myocytes.
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Jesmin, Subrina, Sohel Zaedi, Nobutake Shimojo, Motoyuki Iemitsu, Koichi Masuzawa, Naoto Yamaguchi, Chishimba N. Mowa, Seiji Maeda, Yuichi Hattori, and Takashi Miyauchi. "Endothelin antagonism normalizes VEGF signaling and cardiac function in STZ-induced diabetic rat hearts." American Journal of Physiology-Endocrinology and Metabolism 292, no. 4 (April 2007): E1030—E1040. http://dx.doi.org/10.1152/ajpendo.00517.2006.

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Abnormal alterations in cardiac expression of vascular endothelial growth factor (VEGF) as well as its receptors and impairment in the development of coronary collaterals have recently been reported in diabetic subjects. However, the presence of pharmacological intervention on these defects in diabetes remains unsettled. Here, we studied the effect of endothelin (ET) receptor blockade on cardiac VEGF signaling pathways and cardiac function in Sprague-Dawley rats 5 wk after induction of type I diabetes with streptozotocin (65 mg/kg ip) in comparison with age-matched control rats. After streptozotocin (1 wk), some diabetic rats were treated with the ET receptor antagonist SB-209670 (1 mg/day) for 4 wk. VEGF, its receptors, and its angiogenic signaling molecules [phosphorylated Akt and endothelial nitric-oxide synthase (eNOS)] were analyzed by Western blot, ELISA, real-time PCR, and immunohistochemistry, and cardiac function was evaluated by echocardiography. Coronary capillary morphology was assessed by lectin and enzymatic double staining. We found significant decreases in cardiac expression of VEGF, its receptors, phosphorylation of Akt and eNOS, and coronary capillary density in diabetic rats compared with controls. Treatment of diabetic rats with SB-209670 reversed these alterations to the control levels and ameliorated impairment of cardiac function. From a molecular point of view, the present study is the first to indicate the potential usefulness of an ET receptor antagonist in the treatment of cardiac dysfunction in type I diabetes.
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28

Foster, Simon R., Eugeni Roura, Peter Molenaar, and Walter G. Thomas. "G protein-coupled receptors in cardiac biology: old and new receptors." Biophysical Reviews 7, no. 1 (January 13, 2015): 77–89. http://dx.doi.org/10.1007/s12551-014-0154-2.

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29

Gøtzsche, Liv Bjørn-Hansen. "β-Adrenergic receptors, voltage-operated Ca 2+-channels, nuclear triiodothyronine receptors and triiodothyronine concentration in pig myocardium after long-term low-dose amiodarone treatment." Acta Endocrinologica 129, no. 4 (October 1993): 337–47. http://dx.doi.org/10.1530/acta.0.1290337.

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Similar features during chronic amiodarone treatment and hypothyroidism suggest that amiodarone induces a state of "triiodothyronine (T3)-resistance" or "cardiac hypothyroidism", which may predispose the heart to pump failure under conditions with severe strain, such as recovery after cardiac surgery. Disagreements exist as to how amiodarone, and possibly its main metabolite desethylamiodarone, act upon the various receptor systems in the heart. The aim of the present study was to elucidate whether chronic amiodarone treatment leads to a functional reduction in the number of myocardial nuclear T3 receptors, the myocardial tissue T3 concentration and the number of β-receptors and voltage-operated Ca2+-channels. Finally, special attention was drawn to any changes that could contribute to explain previous reports on reduced haemodynamic reserve in animals exposed to severe cardiac strain, such as cardiac surgery. Pigs (72±2 kg) were assigned randomly to amiodarone treatment (20 mg·kg−1·day−1 for 30±1 days, N = 8); controls received no medical treatment (N = 6). The left ventricle was evaluated for β-adrenergic receptors, voltage-operated Ca2+-channels, T3 nuclear receptors and tissue T3 concentration. Maximum binding capacity for β-receptors and Ca2+-channels was reduced in amiodarone-treated pigs (by 38%, p<0.05, and by 52%, p<0.01) and correlated with tissue drug concentrations for both receptor types (p<0.05). No changes were observed concerning nuclear T3 receptors. In vitro competition studies revealed that amiodarone, but not desethylamiodarone, possessed binding properties to Ca2+-channels, whereas neither of the compounds bound to β-receptors. Desethylamiodarone, but not amiodarone, competitively inhibited T3 binding to its nuclear receptors. Myocardial T3 was undetectable (<0.05 nmol/kg wet wt) in amiodarone-treated pigs. From our observations we suggest that the active metabolite desethylamiodarone, rather than the parent drug, is mainly responsible for the observed local hypothyroid-like effects during amiodarone treatment. The observed changes after treatment with low-dose amiodarone in pigs are likely to have biological implications. Functionally, the changes may imply reduced cardiac reserve during conditions of extraordinary strain.
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30

Middlekauff, Holly R., Scott A. Rivkees, Helen E. Raybould, Melo Bitticaca, Joshua I. Goldhaber, and James N. Weiss. "Localization and functional effects of adenosine A1 receptors on cardiac vagal afferents in adult rats." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 2 (February 1, 1998): H441—H447. http://dx.doi.org/10.1152/ajpheart.1998.274.2.h441.

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There is evidence to suggest that during ischemia adenosine acts on cardiac vagal afferent neurons to activate systemic reflexes and to modulate cardiac nociception. The purpose of this study was to determine whether adenosine receptors are present and have direct cellular electrophysiological actions on cardiac vagal afferent neurons. In radioreceptor assays of nodose ganglion tissue from rats, binding was detectable for A1 (39.6 ± 1.2 fmol/mg protein) but not A2aadenosine receptors. These findings were confirmed using the complementary approach of receptor-labeling autoradiography. Using in situ hybridization, we saw specific labeling over ∼50% of neurons in the nodose ganglia, but not over nonneuronal cells. In colabeling studies, cardiac vagal afferent neurons were identified by retroneuronal labeling with fluororuby. Of cardiac vagal afferents approximately one-half were strongly positive for A1 adenosine receptors (immunocytochemistry). In patch-clamping experiments, adenosine inhibited peak inward calcium current in 7 of 11 cells by 48 ± 13%. In conclusion, adenosine A1receptors reside on a subset of vagal afferent neurons, including cardiac vagal afferents, and have electrophysiological effects that modulate neuroexcitability in cultured nodose ganglion neurons.
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31

O'Hagan, K. P., L. B. Bell, S. W. Mittelstadt, and P. S. Clifford. "Cardiac receptors modulate the renal sympathetic response to dynamic exercise in rabbits." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 507–15. http://dx.doi.org/10.1152/jappl.1994.76.2.507.

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Activation of cardiac sensory receptors with vagal afferents can result in inhibition of sympathetic outflow to the peripheral circulation. This study investigated whether the regulation of renal sympathetic nerve activity (RSNA) during dynamic exercise was modulated by cardiac sensory receptors. RSNA, blood pressure, and heart rate were measured in seven New Zealand White rabbits during treadmill exercise while cardiac receptors were intact (saline), during cardiac neural block with 2% procaine (2% PCN), and during cardiac efferent receptor block with methscopolamine and atenolol (M + A). Drugs were infused into the pericardial space via a chronic catheter. Two exercise protocols were used: 7 m/min (5 min) and 12 m/min (2 min) at 0% grade. The increases in HR during exercise at 7 and 12 m/min were attenuated with 2% PCN or M + A. At 12 m/min, blood pressure was significantly lower with 2% PCN (76 +/- 4 mmHg) or M + A (76 +/- 3 mmHg) than with saline (86 +/- 2 mmHg). Abolition of cardiac afferent input with 2% PCN resulted in a potentiated RSNA response to exercise at 7 m/min (+134 +/- 37%) and 12 m/min (+234 +/- 45%) relative to saline (+62 +/- 24 and +101 +/- 28%) or M + A (+19 +/- 9 and +52 +/- 19%, P < 0.05). These results suggest that cardiac sensory receptors attenuate sympathetic drive to the kidney during dynamic exercise in conscious rabbits.
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32

Zakharov, S. I., J. L. Overholt, R. A. Wagner, and R. D. Harvey. "Tetramethylammonium activation of muscarinic receptors in cardiac ventricular myocytes." American Journal of Physiology-Cell Physiology 264, no. 6 (June 1, 1993): C1625—C1630. http://dx.doi.org/10.1152/ajpcell.1993.264.6.c1625.

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Replacement of extracellular Na+ with tetramethylammonium (TMA) reduces the magnitude of the Cl- current activated by beta-adrenergic receptor stimulation in guinea pig ventricular myocytes. However, the effects of replacing Na+ appear to be associated with the presence of TMA, rather than the absence of Na+. Direct addition of TMA to extracellular solutions, without changing the Na+ concentration, was able to inhibit the Cl- current activated by isoproterenol (Iso) in a concentration-dependent manner. The concentration of TMA that caused half-maximal inhibition was 327 microM when the Cl- current was activated by 1 microM Iso and 29 microM when the Cl- current was activated by 0.03 microM Iso. The effect of TMA was also blocked by atropine, suggesting that TMA exerts its effect through stimulation of the muscarinic receptors. Furthermore, TMA inhibited the Iso-activated Ca2+ current, as would be expected for an effect involving muscarinic receptor stimulation. The response to complete Na+ replacement with TMA could not be overcome by increasing the concentration of Iso 1,000-fold, and direct addition of TMA was able to antagonize the Cl- current activated independently of the beta-adrenergic receptor, using forskolin and histamine. These results are consistent with the hypothesis that TMA does not exert its effects through a competitive mechanism at the beta-adrenergic receptor. It is concluded that TMA is able to antagonize adenosine 3',5'-cyclic monophosphate-dependent activation of ion channels in the heart through activation of muscarinic receptors.
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Ganguly, P. K., K. Mukherjee, and Y. Chen. "Altered renal dopamine receptors during development of cardiac hypertrophy." American Journal of Physiology-Endocrinology and Metabolism 262, no. 5 (May 1, 1992): E569—E573. http://dx.doi.org/10.1152/ajpendo.1992.262.5.e569.

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The characteristics of dopamine receptors were studied in heart and kidney using the radiolabeled receptor assay of [3H]spiperone during the development of cardiac hypertrophy. Male Sprague-Dawley rats (175-200 g) underwent abdominal aortic constriction above the renal arteries and were studied 3, 14, and 28 days thereafter. Sham-operated animals without aortic constriction were used as control. Although the ratio of left ventricular weight to total body weight was significantly increased 14 and 28 days after aortic constriction in animals, [3H]spiperone binding in left ventricular membrane was increased as early as 3 days after aortic constriction. At 14 days, the binding was still elevated and, by 28 days, it returned to control values. In contrast, membranes obtained from kidney cortex showed an elevation of [3H]spiperone binding only at 28 days after aortic constriction; at 3 days the binding values were decreased. A reciprocal correlation was found between the number of dopamine receptors and the activity of Na(+)-K(+)-ATPase at 28 days of aortic constriction; the enzyme activity, as measured by the release of 32Pi from [gamma-32P]ATP, was decreased in kidney cortex. Autoradiographic data also showed an increased number of dopamine receptors in kidney at 28 days after abdominal aortic constriction. These results suggest that the dopamine receptor is increased very early in heart in response to pressure overload as a result of a compensatory response to maintain an optimal left ventricular output. Kidney dopamine receptors are triggered at a later stage possibly to maintain fluid homeostasis secondary to the cardiac hypertrophic process.
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34

Sonin, Dmitry, Si-Yuan Zhou, Chunxia Cronin, Tatiana Sonina, Jeffrey Wu, Kenneth A. Jacobson, Achilles Pappano, and Bruce T. Liang. "Role of P2X purinergic receptors in the rescue of ischemic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (September 2008): H1191—H1197. http://dx.doi.org/10.1152/ajpheart.00577.2008.

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Evidence is accumulating to support the presence of P2X purinergic receptors in the heart. However, the biological role of this receptor remains to be defined. The objectives here were to determine the role of cardiac P2X receptors in modulating the progression of post-myocardial infarction ischemic heart failure and to investigate the underlying mechanism. The P2X4 receptor (P2X4R) is an important subunit of native cardiac P2X receptors, and the cardiac-specific transgenic overexpression of P2X4R (Tg) was developed as a model. Left anterior descending artery ligation resulted in similar infarct size between Tg and wild-type (WT) mice ( P > 0.1). However, Tg mice showed an enhanced cardiac contractile performance at 7 days, 1 mo, and 2 mo after infarction and an increased survival at 1 and 2 mo after infarction ( P < 0.01). The enhanced intact heart function was manifested by a greater global left ventricular developed pressure and rate of contraction of left ventricular pressure in vitro and by a significantly increased fractional shortening and systolic thickening in the noninfarcted region in vivo ( P < 0.05). The salutary effects on the ischemic heart failure phenotype were seen in both sexes and were not the result of any difference in infarct size in Tg versus WT hearts. An enhanced contractile function of the noninfarcted area in the Tg heart was likely an important rescuing mechanism. The cardiac P2X receptor is a novel target to treat post-myocardial infarction ischemic heart failure.
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35

Gergs, Ulrich, Timo Gerigk, Jonas Wittschier, Constanze T. Schmidbaur, Clara Röttger, Mareen Mahnkopf, Hanna Edler, Hartmut Wache, and Joachim Neumann. "Influence of Serotonin 5-HT4 Receptors on Responses to Cardiac Stressors in Transgenic Mouse Models." Biomedicines 9, no. 5 (May 18, 2021): 569. http://dx.doi.org/10.3390/biomedicines9050569.

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The current study aimed to deepen our knowledge on the role of cardiac 5-HT4 receptors under pathophysiological conditions. To this end, we used transgenic (TG) mice that overexpressed human 5-HT4a receptors solely in cardiac myocytes (5-HT4-TG mice) and their wild-type (WT) littermates that do not have functional cardiac 5-HT4 receptors as controls. We found that an inflammation induced by lipopolysaccharide (LPS) was detrimental to cardiac function in both 5-HT4-TG and WT mice. In a hypoxia model, isolated left atrial preparations from the 5-HT4-TG mice went into contracture faster during hypoxia and recovered slower following hypoxia than the WT mice. Similarly, using isolated perfused hearts, 5-HT4-TG mice hearts were more susceptible to ischemia compared to WT hearts. To study the influence of 5-HT4 receptors on cardiac hypertrophy, 5-HT4-TG mice were crossbred with TG mice overexpressing the catalytic subunit of PP2A in cardiac myocytes (PP2A-TG mice, a model for genetically induced hypertrophy). The cardiac contractility, determined by echocardiography, of the resulting double transgenic mice was attenuated like in the mono-transgenic PP2A-TG and, therefore, largely determined by the overexpression of PP2A. In summary, depending on the kind of stress put upon the animal or isolated tissue, 5-HT4 receptor overexpression could be either neutral (genetically induced hypertrophy, sepsis) or possibly detrimental (hypoxia, ischemia) for mechanical function. We suggest that depending on the underlying pathology, the activation or blockade of 5-HT4 receptors might offer novel drug therapy options in patients.
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Heger, Jacqueline, and Klaus-Dieter Schlüter. "Renin and the IGFII/M6P Receptor System in Cardiac Biology." Scientific World Journal 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/260298.

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Nonenzymatic cardiac activities of renin are well described during the last years and contribute either to cardiac-specific effects of the renin-angiotensin-aldosterone-system (RAAS) or to the pharmacological effects of RAAS inhibition. The interaction of renin with insulin-like growth factor II/mannose-6-phosphate (IGFII/M6P) receptors participates in nonclassical renin effects and contributes to cardiac remodelling caused by RAAS activation. The current findings suggest an important role for renin IGFII/M6P receptor interaction in cardiac adaptation to stress and support the idea that excessive accumulation of renin during inhibition of RAAS directly contributes to blood pressure-independent effects of these pharmacological interventions. It becomes a challenge for future studies focussing on chronic hypertension or myocardial infarction to comprise regulatory adaptations of the kidney, the main source of plasma renin and prorenin, because they directly contribute to key steps in regulation of cardiac (mal)adaptation via IGFII/M6P receptors. This receptor system is part of peptide/receptor interactions that modifies and possibly limits adverse remodelling effects caused by angiotensin II. Evaluation of interactions of renin with other pro-hypertrophic agonists is required to decide whether this receptor may become a target of pharmacological intervention.
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37

Johannessen, Molly, Subramaniam Ramachandran, Logan Riemer, Andrea Ramos-Serrano, Arnold E. Ruoho, and Meyer B. Jackson. "Voltage-gated sodium channel modulation by σ-receptors in cardiac myocytes and heterologous systems." American Journal of Physiology-Cell Physiology 296, no. 5 (May 2009): C1049—C1057. http://dx.doi.org/10.1152/ajpcell.00431.2008.

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The σ-receptor, a broadly distributed integral membrane protein with a novel structure, is known to modulate various voltage-gated K+ and Ca2+ channels through a mechanism that involves neither G proteins nor phosphorylation. The present study investigated the modulation of the heart voltage-gated Na+ channel (Nav1.5) by σ-receptors. The σ1-receptor ligands [SKF-10047 and (+)-pentazocine] and σ1/σ2-receptor ligands (haloperidol and ditolylguanidine) all reversibly inhibited Nav1.5 channels to varying degrees in human embryonic kidney 293 (HEK-293) cells and COS-7 cells, but the σ1-receptor ligands were less effective in COS-7 cells. The same four ligands also inhibited Na+ current in neonatal mouse cardiac myocytes. In σ1-receptor knockout myocytes, the σ1-receptor-specific ligands were far less effective in modulating Na+ current, but the σ1/σ2-receptor ligands modulated Na+ channels as well as in wild type. Photolabeling with the σ1-receptor photoprobe [125I]-iodoazidococaine demonstrated that σ1-receptors were abundant in heart and HEK-293 cells, but scarce in COS-7 cells. This difference was consistent with the greater efficacy of σ1-receptor-specific ligands in HEK-293 cells than in COS-7 cells. σ-Receptors modulated Na+ channels despite the omission of GTP and ATP from the patch pipette solution. σ-Receptor-mediated inhibition of Na+ current had little if any voltage dependence and produced no change in channel kinetics. Na+ channels represent a new addition to the large number of voltage-gated ion channels modulated by σ-receptors. The modulation of Nav1.5 channels by σ-receptors in the heart suggests an important pathway by which drugs can alter cardiac excitability and rhythmicity.
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38

Kaneko, M., D. C. Chapman, P. K. Ganguly, R. E. Beamish, and N. S. Dhalla. "Modification of cardiac adrenergic receptors by oxygen free radicals." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 3 (March 1, 1991): H821—H826. http://dx.doi.org/10.1152/ajpheart.1991.260.3.h821.

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To examine the effects of oxygen free radicals on alpha- and beta-adrenergic receptors, rat heart crude membranes were incubated with xanthine plus xanthine oxidase, H2O2, or H2O2 plus Fe2+. The assay of beta-adrenergic receptors involving [3H]dihydroalprenolol (DHA) binding revealed that the maximal number of binding sites (Bmax) and dissociation constant (Kd) were increased by xanthine plus xanthine oxidase. H2O2 increased the Kd value for [3H]DHA binding. When a hydrophilic ligand, [3H]CGP-12177, was used for the beta-adrenergic receptor assay, an increase in Kd value without any changes in Bmax value was evident on treating the membranes with xanthine plus xanthine oxidase. The assay of alpha-adrenergic receptors involving [3H]prazosin binding showed a decrease in the number of binding sites and an increase in Kd value only after a prolonged period of incubation. Both H2O2 and H2O2 plus Fe2+ increased the Kd value for [3H]prazosin without changes in Bmax. Changes in both alpha- and beta-adrenergic receptors similar to those with crude membranes were also seen by employing the purified heart sarcolemmal membranes. These data indicate that adrenergic receptors in the sarcolemmal membranes are modified by oxygen free radicals.
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39

Bacman, Sandra, Leonor Sterin-Borda, Livia Lustig, Berta Denduchis, and Enri Borda. "Antilaminin IgG binds and interacts with cardiac cholinergic receptors." Canadian Journal of Physiology and Pharmacology 68, no. 4 (April 1, 1990): 539–44. http://dx.doi.org/10.1139/y90-078.

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Antilaminin IgG bound to cholinergic muscarinic receptors of normal mice heart and simulated the biological effect of a cholinergic agonist. Antilaminin IgG interfered with the binding of the radiolabelled muscarinic antagonist, (−)-[3H]quinuclidinyl benzilate, in a noncompetitive fashion. The interaction of antilaminin IgG with the muscarinic cholinergic receptor increased production of cGMP and decreased production of cAMP. Antilaminin IgG also decreased the contractile tension of mouse atria. Both the mechanical and enzymatic effect of antilaminin IgG required the activation of the muscarinic cholinergic system because they were blunted by atropine and mimicked by acetylcholine.Key words: antilaminin IgG, cholinergic muscarinic receptors, cGMP, cholinergic binding assay, cAMP, heart contractility.
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40

Maltsev, A. V., and Y. M. Kokoz. "Non-Central Influences of α2-Adrenergic and Imidazoline Agonist Interactions in Isolated ardiomyocytes Cardiac Cells." Kardiologiia 59, no. 4 (April 18, 2019): 52–63. http://dx.doi.org/10.18087/cardio.2019.4.10241.

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Aim: to investigate the functional interaction of α2-adrenergic and imidazoline receptors recently identified on the sarcolemma of isolated cardiomyocytes for regulation of the intracellular calcium and the production of the signal molecule of nitric oxide (NO).Materials and methods:experiments were performed on isolated left ventricular cardiomyocytes of Wistar rats. Potential-dependent Ca2+-currents were measured from the whole-cell by the patch-clamp method in “perforated-patch” configuration. The intracellular calcium and the production of nitric oxide were estimated from the changes in fluorescence intensity of the Ca2+-specific and NO-sensitive dyes at fluorescent or confocal microscope.Results:It has been shown that α2‑adrenergic and imidazoline receptor agonists inhibit L-type Ca2+-currents by themselves, but their effects do not develop against each other’s background. The blockade of key effector molecules: protein kinase B (Akt kinase) for α2‑adrenergic receptors, and protein kinase C for imidazoline receptors causes the action of agonists to become additive. Both the selective α2‑agonist, guanabenz, and the specific agonist of the first type imidazoline receptors, rilmenidine, show an additional inhibition of Ca2+-currents against the basal background already reduced by the activation of one of the two receptor systems. Wherein rilmenidine increases the level of free Ca2+in the cytosol, and guanabenz, on the contrary, decreases it. The action of guanabenz does not develop against the background of rilmenidine, although it, in turn, effectively increases the intracellular level of calcium in guanabenz-pretreated cardiac cells. Activation of α2‑adrenergic receptors leads to significant stimulation of the endothelial isoform of NO-synthase, and as a result to an increase in the NO level. Activation of imidazoline receptors itself does not affect NO synthesis but it prevents the production of NO induced by α2‑agonists.Conclusion:obtained data make it possible to formulate a number of useful recommendations for clinical practice, and also to clarify the non-central peripheral effects arising from the activation of α2‑adrenergic or imidazoline systems under conditions of endogenous hyperactivation on of the two systems.
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41

Nakaya, Michio, Satsuki Chikura, Kenji Watari, Natsumi Mizuno, Koji Mochinaga, Supachoke Mangmool, Satoru Koyanagi, et al. "Induction of Cardiac Fibrosis by β-Blocker in G Protein-independent and G Protein-coupled Receptor Kinase 5/β-Arrestin2-dependent Signaling Pathways." Journal of Biological Chemistry 287, no. 42 (August 10, 2012): 35669–77. http://dx.doi.org/10.1074/jbc.m112.357871.

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G-protein coupled receptors (GPCRs) have long been known as receptors that activate G protein-dependent cellular signaling pathways. In addition to the G protein-dependent pathways, recent reports have revealed that several ligands called “biased ligands” elicit G protein-independent and β-arrestin-dependent signaling through GPCRs (biased agonism). Several β-blockers are known as biased ligands. All β-blockers inhibit the binding of agonists to the β-adrenergic receptors. In addition to β-blocking action, some β-blockers are reported to induce cellular responses through G protein-independent and β-arrestin-dependent signaling pathways. However, the physiological significance induced by the β-arrestin-dependent pathway remains much to be clarified in vivo. Here, we demonstrate that metoprolol, a β1-adrenergic receptor-selective blocker, could induce cardiac fibrosis through a G protein-independent and β-arrestin2-dependent pathway. Metoprolol, a β-blocker, increased the expression of fibrotic genes responsible for cardiac fibrosis in cardiomyocytes. Furthermore, metoprolol induced the interaction between β1-adrenergic receptor and β-arrestin2, but not β-arrestin1. The interaction between β1-adrenergic receptor and β-arrestin2 by metoprolol was impaired in the G protein-coupled receptor kinase 5 (GRK5)-knockdown cells. Metoprolol-induced cardiac fibrosis led to cardiac dysfunction. However, the metoprolol-induced fibrosis and cardiac dysfunction were not evoked in β-arrestin2- or GRK5-knock-out mice. Thus, metoprolol is a biased ligand that selectively activates a G protein-independent and GRK5/β-arrestin2-dependent pathway, and induces cardiac fibrosis. This study demonstrates the physiological importance of biased agonism, and suggests that G protein-independent and β-arrestin-dependent signaling is a reason for the diversity of the effectiveness of β-blockers.
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42

Lau, P. Y., M. G. Cardarelli, and C. Wei. "Expression of Angiotensin II Type 1 and Type 2 Receptor in Human Myocardium with Congestive Heart Failure." Microscopy and Microanalysis 6, S2 (August 2000): 618–19. http://dx.doi.org/10.1017/s1431927600035583.

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Angiotensin II (AH) is a potent vasoconstrictor and mitogenic factor. AH receptors include type 1 (ATI) and type 2 (AT2) receptors. Recent studies demonstrated that both ATI and AT2 receptors expressed in human myocardium. Circulating and local tissue level of AH was increased in severe congestive heart failure (CHF). However, the expression of ATI and AT2 in cardiac tissue with CHF remains controversial. Therefore, the present study was designed to investigate the protein expression of ATI and AT2 receptors in normal human myocardium and in human cardiac tissue with mild and severe CHF.Human atrial tissues from normal subjects and CHF patients with ischemic cardiomyopathy and dilated cardiomyopathy were obtained from open-heart surgery and cardiac transplantation. ATI and AT2 receptor expression was investigated by immunohistochemical staining (IHCS). The results of IHCS was evaluated by IHCS staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining).
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43

Valentine, Cathleen D., and Peter M. Haggie. "Confinement of β1- and β2-adrenergic receptors in the plasma membrane of cardiomyocyte-like H9c2 cells is mediated by selective interactions with PDZ domain and A-kinase anchoring proteins but not caveolae." Molecular Biology of the Cell 22, no. 16 (August 15, 2011): 2970–82. http://dx.doi.org/10.1091/mbc.e11-01-0034.

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The sympathetic nervous system regulates cardiac output by activating adrenergic receptors (ARs) in cardiac myocytes. The predominant cardiac ARs, β1- and β2AR, are structurally similar but mediate distinct signaling responses. Scaffold protein–mediated compartmentalization of ARs into discrete, multiprotein complexes has been proposed to dictate differential signaling responses. To test the hypothesis that βARs integrate into complexes in live cells, we measured receptor diffusion and interactions by single-particle tracking. Unstimulated β1- and β2AR were highly confined in the membrane of H9c2 cardiomyocyte-like cells, indicating that receptors are tethered and presumably integrated into protein complexes. Selective disruption of interactions with postsynaptic density protein 95/disks large/zonula occludens-1 (PDZ)–domain proteins and A-kinase anchoring proteins (AKAPs) increased receptor diffusion, indicating that these scaffold proteins participate in receptor confinement. In contrast, modulation of interactions between the putative scaffold caveolae and β2AR did not alter receptor dynamics, suggesting that these membrane domains are not involved in β2AR confinement. For both β1- and β2AR, the receptor carboxy-terminus was uniquely responsible for scaffold interactions. Our data formally demonstrate that distinct and stable protein complexes containing β1- or β2AR are formed in the plasma membrane of cardiomyocyte-like cells and that selective PDZ and AKAP interactions are responsible for the integration of receptors into complexes.
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44

Wehrens, X. "Altered function and regulation of cardiac ryanodine receptors in cardiac disease." Trends in Biochemical Sciences 28, no. 12 (December 2003): 671–78. http://dx.doi.org/10.1016/j.tibs.2003.10.003.

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45

Böhm, Michael, Ulrike Mende, Wilhelm Schmitz, and Hasso Scholz. "Cardiac alpha-receptors and cardiac hypertrophy in genetic predisposition to hypertension." American Heart Journal 112, no. 6 (December 1986): 1347–49. http://dx.doi.org/10.1016/0002-8703(86)90392-3.

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46

Huang, Zheng-Gui, Xin Wang, Cory Evans, Allison Gold, Evguenia Bouairi, and David Mendelowitz. "Prenatal Nicotine Exposure Alters the Types of Nicotinic Receptors That Facilitate Excitatory Inputs to Cardiac Vagal Neurons." Journal of Neurophysiology 92, no. 4 (October 2004): 2548–54. http://dx.doi.org/10.1152/jn.00500.2004.

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Nicotinic receptors play an important role in modulating the activity of parasympathetic cardiac vagal neurons in the medulla. Previous work has shown nicotine acts via at least three mechanisms to excite brain stem premotor cardiac vagal neurons. Nicotine evokes a direct increase in holding current and facilitates both the frequency and amplitude of glutamatergic neurotransmission to cardiac vagal neurons. This study tests whether these nicotinic receptor–mediated responses are endogenously active, whether α4β2 and α7 nicotinic receptors are involved, and whether prenatal exposure to nicotine alters the magnitude of these responses and the types of nicotinic receptors involved. Application of neostigmine (10 μM) significantly increased the holding current, amplitude, and frequency of miniature excitatory postsynaptic current (mEPSC) glutamatergic events in cardiac vagal neurons. In unexposed animals, the nicotine-evoked facilitation of mEPSC frequency, but not mEPSC amplitude or holding current, was blocked by α-bungarotoxin (100 nM). Prenatal nicotine exposure significantly exaggerated and altered the types of nicotinic receptors involved in these responses. In prenatal nicotine-exposed animals, α-bungarotoxin only partially reduced the increase in mEPSC frequency. In addition, in prenatal nicotine-exposed animals, the increase in holding current was partially dependent on α-7 subunit–containing nicotinic receptors, in contrast to unexposed animals in which α-bungarotoxin had no effect. These results indicate prenatal nicotine exposure, one of the highest risk factors for sudden infant death syndrome (SIDS), exaggerates the responses and changes the types of nicotinic receptors involved in exciting premotor cardiac vagal neurons. These alterations could be responsible for the pronounced bradycardia that occurs during apnea in SIDS victims.
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Zucchi, Riccardo, Simonetta Ronca-Testoni, Gongyuan Yu, Paola Galbani, Giovanni Ronca, and Mario Mariani. "Interaction between gallopamil and cardiac ryanodine receptors." British Journal of Pharmacology 114, no. 1 (January 1995): 85–92. http://dx.doi.org/10.1111/j.1476-5381.1995.tb14909.x.

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48

Pearce, Paul T., and John W. Funder. "Steroid binding to cardiac Type I receptors." Journal of Hypertension 6, no. 4 (December 1988): S131–133. http://dx.doi.org/10.1097/00004872-198812040-00038.

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49

Marsh, James D., Michael H. Lehmann, Rebecca H. Ritchie, Judith K. Gwathmey, Glenn E. Green, and Rick J. Schiebinger. "Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes." Circulation 98, no. 3 (July 21, 1998): 256–61. http://dx.doi.org/10.1161/01.cir.98.3.256.

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50

Brown, D. A., and W. E. Cascio. "'Leaky' ryanodine receptors and sudden cardiac death." Cardiovascular Research 84, no. 3 (October 8, 2009): 343–44. http://dx.doi.org/10.1093/cvr/cvp330.

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