Ca2+dependence of positive inotropic responses of guinea pig isolated cardiac preparations to cAMP-generating and cAMP-independent agonists

1984 ◽  
Vol 62 (1) ◽  
pp. 105-108 ◽  
Author(s):  
L. F. Yao ◽  
K. M. MacLeod ◽  
J. H. McNeill
Keyword(s):  
Guinea Pig ◽  
Papillary Muscles ◽  
Similar Magnitude ◽  
Myocardial Cells ◽  
Receptor Stimulation ◽  
Histamine Response ◽  
Β Receptor ◽  
Inotropic Responses ◽  
Stimulation Of

The effects of procedures which diminish Ca2+ influx into myocardial cells on responses of isolated cardiac preparations to cAMP-independent histamine H1 receptor stimulation and cAMP-generating β-receptor stimulation were measured. The histamine response of guinea pig left atria, which appears to be primarily mediated by H1 receptors, was depressed to a greater extent than was the response of this preparation to isoproterenol by decreasing the extracellular Ca2+ concentration, and by the Ca2+ influx blocker D-600. Similarly, while the H1 agonist 2-pyridylethylamine dihydrochloride (PEA) produced increases in tension of a similar magnitude as the partial β-agonist salbutamol in both left atria and in papillary muscles, responses of both preparations to PEA were depressed to a significantly greater extent by decreasing the extracellular Ca2+ concentration than were responses to salbutamol. Overall, both the basal developed force of papillary muscles and the responses of these preparations to H1 and β-receptor stimulation appeared to be less depressed by decreasing the extracellular Ca2+ concentration than were those of left atria. These results indicate that responses mediated via cAMP-independent H1 receptors, like those arising from α-receptor stimulation, are more sensitive to procedures which diminish Ca2+ influx than are responses arising from stimulation of cAMP-generating β-receptors. This may reflect differences in the mechanisms by which stimulation of H1, α-, and β-receptors give rise to positive inotropic responses. In addition, left atria may be more dependent than papillary muscles on extracellular Ca2+ for the support of contraction.

Takotsubo Cardiomyopathy: Its Possible Impact during Adult Donor Care

2011 ◽  
Vol 21 (4) ◽  
pp. 344-349
Author(s):  
David J. Powner ◽  
Hanh Truong
Keyword(s):  
Calcium Channels ◽  
Brain Death ◽  
Takotsubo Cardiomyopathy ◽  
Cardiac Contractility ◽  
Circulatory Support ◽  
Receptor Stimulation ◽  
Treatment Methods ◽  
Biochemical Processes ◽  
Β Receptor ◽  
Stimulation Of

Takotsubo cardiomyopathy, the syndrome caused by an extreme release and circulation of catecholamines, shares several histopathological and clinical similarities with cardiac changes after brain death noted in animal investigations and human observation. Overwhelming stimulation of myocardial inotropic β receptors may alter their responsiveness and induce other biochemical processes, producing reduced cardiac contractility. Treatment methods in Takotsubo cardiomyopathy that use extracorporeal circulatory support and medications that do not rely on β-receptor stimulation and preemptive blockade of β receptors or calcium channels before brain death may be relevant to donor care.

β-Receptor-mediated increase in venous return in humans

1987 ◽  
Vol 65 (8) ◽  
pp. 1658-1665 ◽  
Author(s):  
Frans H. H. Leenen ◽  
Richard A. Reeves
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Positive Inotropic Effect ◽  
Venous Return ◽  
Left Ventricular ◽  
Receptor Stimulation ◽  
Selective Blockade ◽  
Healthy Humans ◽  
Β Receptor ◽  
Stimulation Of

To assess the involvement of β1 and β2-receptors in the regulation of venous return in humans, changes in left ventricular end-diastolic (LVED) dimension were determined during β-receptor stimulation either by exogenous catecholamines or by increased endogenous sympathetic activity after hydralazine, after placebo and during nonselective versus β1 -selective blockade. Taking changes in heart rate and LV emptying into account, the three β-agonists (isoproterenol, terbutaline, and epinephrine) as well as hydralazine increased venous return as inferred from LVED dimension. After hydralazine, nonselective and β1-selective blockade were equally effective in blunting the increases in venous return, in heart rate, and in positive inotropic response. β1-Selective blockade did not affect the increase in heart rate caused by epinephrine and partially inhibited the positive inotropic effect and the increase in venous return. Nonselective blockade not only blocked the increase in venous return owing to epinephrine but actually led to a decrease, as evidenced by a decrease in LVED dimension despite the marked bradycardia and high afterload with this combination. The present findings in healthy humans indicate that stimulation of both β1- and β2-receptors increases venous return, heart rate, and myocardial contractility. β1-Receptors appeal to predominate in the response to neuronal sympathetic activity.

scholarly journals Muscarinic-receptor stimulation enhances polyphosphoinositide breakdown in guinea-pig ileum smooth muscle

1984 ◽  
Vol 223 (2) ◽  
pp. 527-531 ◽  
Author(s):  
M C Sekar ◽  
B D Roufogalis
Keyword(s):  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Longitudinal Muscle ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Exchange Chromatography ◽  
Guinea Pig Ileum ◽  
Receptor Stimulation ◽  
Inositol 1 ◽  
Stimulation Of

Muscarinic-receptor stimulation by 0.1 mM-carbachol in longitudinal muscle of the guinea-pig ileum increases the incorporation of [3H]inositol into inositol-containing phospholipid. This effect was blocked by 16 microM-atropine. After 60 min incubation, carbachol increased the accumulation of total inositol phosphates 20-fold in the presence of 10 mM-Li+. Less than 20% of the total inositol phosphate corresponded to inositol 1-phosphate by ion-exchange chromatography, whereas of the remainder about two-thirds corresponded to inositol bisphosphate and one third to inositol trisphosphate. It is concluded that stimulation of muscarinic receptors in guinea-pig ileum enhances breakdown of polyphosphoinositides, suggesting that this may be a primary event associated with Ca2+ mobilization in the guinea-pig ileum.

scholarly journals Vasopressin V1-Receptor Stimulation Produces a Positive Inotropic Response without Affecting pHi in Guinea Pig Papillary Muscles

1995 ◽  
Vol 68 (2) ◽  
pp. 217-221 ◽  
Author(s):  
Hiroshi Yamaguchi ◽  
Hiroko Uemura ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
Haruaki Nakaya
Keyword(s):  
Guinea Pig ◽  
Papillary Muscles ◽  
Inotropic Response ◽  
Receptor Stimulation

scholarly journals Role of β1- and β2-adrenergic receptors in regulation of Cl− and Ca2+ channels in guinea pig ventricular myocytes

1997 ◽  
Vol 273 (4) ◽  
pp. H1669-H1676 ◽  
Author(s):  
Livia C. Hool ◽  
Robert D. Harvey
Keyword(s):  
Guinea Pig ◽  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Ventricular Myocytes ◽  
Receptor Stimulation ◽  
Receptor Agonists ◽  
High Concentrations ◽  
Β Receptor ◽  
Ca2 Channels

The role of β1- and β2-adrenergic receptor stimulation in modulating adenosine 3′,5′-cyclic monophosphate (cAMP)-regulated Cl− and Ca2+ currents was investigated with use of guinea pig ventricular myocytes. Activation of the Cl− current by the nonselective β-receptor agonist isoproterenol (Iso) was not affected by the β2-receptor antagonist ICI-118,551 (ICI), but it was blocked by the β1-receptor antagonist atenolol. The inability of β2-receptor stimulation to activate the Cl− current was confirmed by the lack of response to the selective β2-receptor agonists salbutamol and zinterol. Responses to β2-adrenergic receptor stimulation were also looked for in pertussis toxin (PTX)-treated myocytes because PTX increases the sensitivity of responses to Iso, and PTX has been reported to increase the responsiveness to β2- but not β1-receptor stimulation. PTX treatment increased the sensitivity of the Cl− current to activation by Iso in the presence of ICI, indicating that PTX increases β1-receptor responsiveness. PTX treatment also resulted in the ability of salbutamol to activate the Cl− current. However, the response to salbutamol was blocked by atenolol but not by appropriate concentrations of ICI, suggesting that salbutamol was activating β1-receptors. These results indicate that PTX treatment increases the sensitivity to β1-receptor stimulation, without affecting β2-responsiveness. To verify that the lack of response to β2-receptor stimulation was not unique to the Cl− current, the effects of β2-receptor agonists on the L-type Ca2+current were also examined. The Ca2+ current was only affected by high concentrations of zinterol or salbutamol, and such responses were blocked by atenolol, but not by ICI, suggesting that activation of β1-receptors was involved. These results indicate that β1- but not β2-adrenergic receptor stimulation plays an important role in modulating the cAMP-regulated Cl− and Ca2+ currents in guinea pig ventricular myocytes.

Effect of a-Receptor Stimulation on Cl Transport by Rat Submandibular Acini

1988 ◽  
Vol 67 (3) ◽  
pp. 561-564 ◽  
Author(s):  
J.R. Martinez ◽  
P. Reed
Keyword(s):  
Steady State ◽  
Enzymatic Digestion ◽  
Receptor Blocker ◽  
K Channel ◽  
Dependent Manner ◽  
Receptor Stimulation ◽  
Contrast Exposure ◽  
Β Receptor ◽  
Isotope Content ◽  
Stimulation Of

Dispersed salivary acini isolated from the rat submandibular gland by enzymatic digestion were used to study the effects of a-receptor stimulation on transmembrane transport of 36Cl. In the absence of secretagogue, the tracer accumulated in the cells in a time-dependent manner until a steady-state content of 6.8 ± 0.1 nmol/mg protein was attained after 3-5 min of incubation. Epinephrine (1 μmol/L) alone did not modify 36Cl accumulation but in the presence of the β-receptor blocker propranolol (1 μmol/L) caused a significant (21%) reduction in the isotope content of the cells to 5.2 ± 0.1 nmol/mg protein. In acini pre-loaded with 36Cl for 12 min, 1 μmol/L epinephrine caused a rapid but transient net efflux of tracer, but the isotope content subsequently increased to pre-stimulation levels. In the presence of propranolol, however, the efflux of 36Cl induced by epinephrine was larger and more sustained and was partially inhibited by the K-channel blocker quinidine (1 mmol/L) and significantly by the absence of Ca2+ in the incubation medium. The a-agonist phenylephrine (10 μmol/L) also significantly reduced the steady-state 36Cl content of tracer-pre-loaded cells. By contrast, exposure of the acini to epinephrine in the presence of the a-receptor blocker phentolamine, or the β-agonist isoproterenol, increased the tracer content of the cells, whether the drugs were added at time zero or to tracer-pre-loaded cells. The results indicate that stimulation of a-receptors in salivary acinar cells causes a Ca2+-dependent efflux of Cl which seems to be functionally linked to K release. These effects are similar to those observed following stimulation of cholinergic receptors. The lack of effect of β-receptor stimulation on Cl efflux suggests that this response is not regulated by a cAMP-mediated pathway in salivary cells. The extent of stimulation-induced Cl efflux is likely to be relevant in terms of the amount of saliva secreted upon stimulation.

κ Opioid Receptor Stimulation of [35S] GTPγS Binding in Guinea Pig Brain

1998 ◽  
Vol 56 (1) ◽  
pp. 113-120 ◽  
Author(s):  
Steven R Childers ◽  
Ruoyu Xiao ◽  
Leslie Vogt ◽  
Laura J Sim
Keyword(s):  
Guinea Pig ◽  
Opioid Receptor ◽  
Receptor Stimulation ◽  
Pig Brain ◽  
Gtpγs Binding ◽  
Guinea Pig Brain ◽  
Stimulation Of
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