Beta Adrenergic Control of Extrarenal Potassium Disposal

Nephron ◽  
1986 ◽  
Vol 43 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Margaret Johnson Bia ◽  
David Lu ◽  
Karen Tyler ◽  
Ralph A. De Fronzo
Keyword(s):  
Beta Adrenergic ◽  
Adrenergic Control

IL-1 inhibits beta-adrenergic control of cardiac calcium current: role of L-arginine/nitric oxide pathway

1994 ◽  
Vol 267 (5) ◽  
pp. H1753-H1758 ◽  
Author(s):  
G. J. Rozanski ◽  
R. C. Witt
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventricular Myocytes ◽  
Interleukin 1 ◽  
Cell Voltage ◽  
Cellular Mechanisms ◽  
Beta Adrenergic ◽  
Nitric Oxide Synthase Inhibitor ◽  
Adrenergic Control ◽  
Oxide Synthase

Modulation of the beta-adrenergic control of cardiac L-type Ca2+ current (Ica) by human recombinant interleukin-1 beta (IL-1) was examined in adult guinea pig ventricular myocytes using the whole cell voltage-clamp technique. ICa was elicited in Cs(+)-loaded myocytes by depolarizing pulses from a holding potential of -40 mV. Isoproterenol (0.01 and 1 microM) exposed to myocytes pretreated with 1 ng/ml IL-1 evoked a significantly smaller increase in ICa density compared with control cells. This IL-1-mediated decrease in beta-responsiveness was usually observed with pretreatment periods of > 1 h and varied as a function of the L-arginine concentration of the pretreatment medium. In addition, it was prevented by 1) IL-1 receptor antagonist, 2) substituting D-arginine for L-arginine, or 3) incubating cells with the nitric oxide synthase inhibitor NG-monomethyl-L-arginine. Thus the present data illustrate that IL-1 significantly alters the beta-adrenergic control of cardiac Ca2+ channels by cellular mechanisms that involve the activation of nitric oxide synthase. These mechanisms may play a role in altering ventricular function during cytokine-mediated inflammatory processes affecting the heart.

beta-Adrenergic control of lipolysis in primate white fat cells: a comparative study with nonprimate mammals

1994 ◽  
Vol 267 (1) ◽  
pp. R115-R123 ◽  
Author(s):  
A. Bousquet-Melou ◽  
J. Galitzky ◽  
C. Carpene ◽  
M. Lafontan ◽  
M. Berlan
Keyword(s):  
Fat Cells ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Homogeneous Population ◽  
Beta Adrenoceptor ◽  
Adrenergic Control ◽  
Cgp 12177 ◽  
Adrenoceptor Agonists ◽  
Beta 2 ◽  
White Fat

The beta-adrenoceptor subtypes involved in the control of lipolysis in white fat cells of rat, dog, marmoset (Callithrix jacchus), baboon (Papio papio), macaque (Macaca fascicularis), and human were compared. In all species [3H]CGP-12177 binding (up to 3 nM) indicated the existence of a homogeneous population of binding sites in fat cell membranes, and competition studies showed that beta 1- and beta 2-adrenoceptors were present. Selective beta 1 or beta 2-adrenoceptor agonists induced lipolysis. The efficiencies of isoproterenol and norepinephrine were similar. The use of selective beta 3-adrenoceptor agonists revealed that BRL-37344 and CL-316243 were full agonists, whereas CGP-12177 and SR-58611A were partial agonists in rat and dog white fat cells. beta 3-Agonists partially stimulated lipolysis in the marmoset, while CGP-12177 was weakly active in the baboon. In macaque and human fat cells, beta 3-agonists were ineffective. The lipolytic effect of norepinephrine involves beta 1-and/or beta 2-adrenoceptors in baboon, macaque, and human. The baboon and macaque constitute valuable models for studying the beta-adrenergic control of lipolysis.

scholarly journals A kinetic model of beta-adrenergic control in cardiac myocytes

Physiome ◽  
2021 ◽  
Author(s):  
Shelley Fong ◽  
Jeffrey J. Saucerman
Keyword(s):  
Kinetic Model ◽  
Cardiac Myocytes ◽  
System Of Equations ◽  
Beta Adrenergic ◽  
Adrenergic Control

The system of equations and figures presented in Saucerman et al. (2003) are verified and reproduced in this paper's curation effort. These checks are performed in MATLAB. With some parameter additions and modifications, we can reproduce all figures with small mismatches.

Interleukin-1 enhances beta-responsiveness of cardiac L-type calcium current suppressed by acidosis

1994 ◽  
Vol 267 (4) ◽  
pp. H1361-H1367 ◽  
Author(s):  
G. J. Rozanski ◽  
R. C. Witt
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Interleukin 1 ◽  
External Solution ◽  
Cellular Mechanisms ◽  
Solution Ph ◽  
Acid Media ◽  
Beta Adrenergic ◽  
Kinase C ◽  
Adrenergic Control

Modulation of the beta-adrenergic control of the cardiac L-type Ca2+ current (ICa) by human recombinant interleukin-1 beta (IL-1) was examined in guinea pig ventricular myocytes using the whole cell voltage-clamp technique. ICa was evoked in Cs(+)-loaded myocytes by depolarizing pulses from a holding potential of -40 mV. In the presence of an acidic external solution (pH 5.8), the response of ICa to isoproterenol (Iso; 0.01 and 1 microM) was markedly decreased compared with control myocytes studied at pH 7.4. However, when cells were pretreated with 1 ng/ml IL-1 and then exposed to acid media, beta-responsiveness was significantly increased compared with untreated cells. Despite this effect of IL-1, maximum ICa density with 0.01 and 1 microM Iso was still 51 and 58%, respectively, less than that measured at pH 7.4. The enhanced beta-responsiveness produced by IL-1 was eliminated by adding amiloride to block Na+/H+ exchange or protein kinase C inhibitors staurosporine (10 nM) and calphostin C (50 nM). However, a direct activator of protein kinase C, phorbol 12-myristate 13-acetate, did not mimic the effects of the cytokine. These data demonstrate that IL-1 partially restores the beta-adrenergic control of cardiac Ca2+ channels suppressed under acidic conditions. Moreover, they suggest that IL-1 acts by enhancing Na+/H+ exchange through a second messenger pathway that may involve protein kinase C. These cellular mechanisms may play a role in altering ventricular function during cytokine-mediated inflammatory processes that are initiated by myocardial ischemia.

Role of adrenergic-dependent H+ release from red cells in acidosis induced by hypoxia in trout

1987 ◽  
Vol 252 (2) ◽  
pp. R269-R275 ◽  
Author(s):  
B. Fievet ◽  
R. Motais ◽  
S. Thomas
Keyword(s):  
Blood Lactate ◽  
Beta Blocker ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Second Phase ◽  
Beta Adrenergic ◽  
Blood Ph ◽  
Adrenergic Control ◽  
Net Uptake

The response to severe hypoxia is characterized in trout by a sudden drop in blood pH, which is of metabolic origin, and by an increase in the blood concentration of adrenaline. This acidification is biphasic in nature. The first phase of acidification is not associated with a rise in the blood lactate concentration and no longer occurs after pretreatment of the fish with a beta-blocker agent, propranolol. Thus an acid other than lactic acid is released into the blood at the onset of hypoxia and this release, which is under beta-adrenergic control, is responsible for the first phase of acidification. On the other hand the second phase of acidification is related to an increase in blood lactate and is not modified by a beta-blocker agent. We have also demonstrated that deep hypoxia promotes a rapid increase in red blood cell volume and that this cell enlargement is coincident with a large net uptake of Na+ and Cl-. In the presence of beta-blocking agents the Na+ uptake is blocked and the swelling of the cells is considerably inhibited. The residual swelling is clearly due to the chloride shift induced by both deoxygenation of hemoglobin and change in blood pH. In the light of data obtained in vitro on the effect of catecholamines on trout erythrocytes, it can be considered that the first phase of acidification occurring at the onset of hypoxia, and that is under beta-adrenergic control, is due essentially to the release of H+ by red blood cells in exchange with external sodium mediated by a beta-adrenergic-stimulated Na+-H+ exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)

Sign in / Sign up

Export Citation Format

Share Document