Effects of histamine on rat isolated atria

1980 ◽  
Vol 58 (9) ◽  
pp. 1114-1116 ◽  
Author(s):  
I. Laher ◽  
J. H. McNeill
Keyword(s):  
Muscarinic Receptors ◽  
Right Atrium ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Adrenoceptor Antagonist ◽  
Endogenous Noradrenaline ◽  
Isolated Atria ◽  
High Doses ◽  
Indirect Stimulation ◽  
Stimulation Of

The effects of histamine were studied in atria obtained from untreated and reserpine-pretreated rats. At high doses, histamine caused a positive chronotropic response that was not antagonized by either promethazine or cimetidine. In the presence of propranolol or in atria from reserpine-pretreated rats histamine caused an atropine-sensitive negative chronotropic response. Large doses of histamine also caused a positive inotropic response in left atria that were antagonized by the β adrenoceptor antagonist propranolol. Reserpine pretreatment abolished the inotropic response of histamine in the rat heart. The results indicate that in large doses histamine causes an indirect stimulation of β adrenoceptors (right and left atrium) by releasing endogenous noradrenaline and of muscarinic receptors (right atrium) by releasing acetylcholine.

Dietary manipulation of cardiac and aortic smooth muscle reactivity to isoproterenol

1984 ◽  
Vol 246 (3) ◽  
pp. H369-H373 ◽  
Author(s):  
J. T. Herlihy
Keyword(s):  
Body Weight ◽  
The Body ◽  
Heart Weight ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Fischer 344 ◽  
Isolated Atria ◽  
Group A ◽  
The Right ◽  
Right Atria

The responsiveness to isoproterenol of isolated atria and aortic strips was examined in two groups of male Fischer 344 rats. Group A (control) was composed of 5-mo-old rats fed ad libitum; group R (experimental) was composed of rats whose food intake had been restricted for 2 mo to 60% of that consumed by group A. Aortic strips obtained from group R and preconstricted with 30 mM K+ relaxed by 18% when challenged by a maximal concentration of isoproterenol (1 microM). This relaxation was significantly less than the 28% relaxation observed with strips from group A. No effect on the inotropic response of the left atria or on the chronotropic response of the right atria to maximal concentrations of isoproterenol was observed. A slight but statistically significant increase in sensitivity to isoproterenol was observed in the inotropic response of the left atria. The 50% effective concentration (EC50) for the isoproterenol-stimulated increase in force development observed with group R was 0.87 +/- 0.16 X 10(-8) M, which was significantly less than the value of 1.56 +/- 0.28 X 10(-8) M obtained with atria from group A. Food restriction exerted no significant effect on the EC50 for the chronotropic response of right atria to isoproterenol. Both the body weight and the heart weight of group A were greater than those of group R. However, the ratio of heart weight to body weight was significantly greater in group R than in group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Unchanged sensitivity to noradrenaline in isolated tissues from cold-acclimated rats

1970 ◽  
Vol 48 (9) ◽  
pp. 657-660 ◽  
Author(s):  
Jean Himms-Hagen ◽  
I. M. Mazurkiewicz-Kwilecki
Keyword(s):  
Left Atrium ◽  
Vas Deferens ◽  
Contractile Response ◽  
Cardiovascular Responses ◽  
Maximum Response ◽  
Inotropic Response ◽  
Chronotropic Response ◽  
Isolated Atria ◽  
Isolated Tissues

Acclimation of rats to cold did not alter either the sensitivity to noradrenaline or the size of the maximum response to noradrenaline of three isolated tissue preparations (chronotropic response of isolated atria; inotropic response of left atrium; contractile response of vas deferens). It is concluded that a change in the response of the heart to exogenous noradrenaline is an unlikely explanation for the modified cardiovascular responses to noradrenaline known to occur in intact cold-acclimated rats.

Characterization of angiotensin receptors in rabbit isolated atria

1976 ◽  
Vol 54 (3) ◽  
pp. 229-237 ◽  
Author(s):  
F. Rioux ◽  
W. K. Park ◽  
D. Regoli
Keyword(s):  
Smooth Muscles ◽  
Rabbit Aorta ◽  
Angiotensin Receptors ◽  
Response Curves ◽  
Renin Substrate ◽  
Inotropic Effects ◽  
Isolated Atria ◽  
High Doses ◽  
The Right ◽  
Stimulation Of

Rabbit isolated left atria have been used to study the inotropic action of angiotensin II (ATII). The peptide is active at doses ranging from 1.0 × 10−9 to 2.8 × 10−6 M and its inotropic effect is not modified by sotalol, phentolamine, burimamide, and indomethacin. We therefore propose that this effect results from the stimulation of receptors specific for ATIIDose–response curves of ATII obtained in presence of increasing concentrations of 8-Gly-ATII are gradually displaced to the right, but high doses of the antagonist depressed the maximum contractions caused by ATII.pA2 value for 8-Gly-ATII in this preparation is similar to those observed in vascular and intestinal smooth muscles. Order of potency of analogues of ATII (2-, 3- and 5-Ala-ATII), acting as full agonists, but with reduced affinity, is similar to that found in rabbit aorta strips. It is therefore proposed that receptors for ATII in rabbit isolated left atria are pharmacologically similar to those present in vascular smooth muscles.Positive inotropic effects of angiotensin I, undecapeptide (1-11), dodecapeptide (1-12) and tetradecapeptide (1-14) renin substrate are antagonized by 8-Gly-ATII in a similar way as the effect of ATIIThis suggests that the action of these peptides is mainly due to stimulation of receptors for ATII. The contribution of myocardial converting enzyme to the action of these peptides is discussed.

Evidence for the involvement of α1-adrenoceptors in negative feedback regulation of noradrenergic transmitter release in rat atria

1985 ◽  
Vol 68 (s10) ◽  
pp. 111s-115s ◽  
Author(s):  
D. F. Story ◽  
C. A. Standford-Starr ◽  
M. J. Rand
Keyword(s):  
Transmitter Release ◽  
Feedback Regulation ◽  
Sympathetic Nerves ◽  
Field Stimulation ◽  
Negative Feedback Regulation ◽  
Rat Atria ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Isolated Atria ◽  
Stimulation Of

1. Experiments were undertaken to determine if prejunctional α1-adrenoceptors are involved in autoinhibitory regulation of transmitter noradrenaline release in rat atria. 2. The noradrenergic transmitter stores in rat isolated atria were radiolabeled with [3H]noradrenaline and transmitter release was deduced from the efflux of the radiolabel evoked by field stimulation of the atrial intramural sympathetic nerves. 3. Phentolamine (3 μmol/l) and prazosin (0.1 and 3 μmol/l) enhanced the release of radiolabel evoked by stimulation with trains of 4, 8 and 16 pulses, whereas idazoxan (10 μmol/l) enhanced release evoked by stimulation with 8 and 16 pulses. Idazoxan and prazosin were about equieffective in enhancing the evoked release but phentolamine produced much greater enhancement than either idazoxan or prazosin. 4. Combination of idazoxan (10 μmol/l) and prazosin enhanced the stimulation-evoked release with 4, 8 and 16 pulses to the same extent as phentolamine (3 μmol/l). 5. The selective α1-adrenoceptor agonist methoxamine (10 μmol/l) inhibited stimulation-evoked release and this effect was blocked by the α1-adrenoceptor antagonist prazosin (0.1 μmol/l). 6. The findings indicate that α1-adrenoceptors may contribute to autoinhibitory feedback regulation of transmitter release in rat atria.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

Testosterone-augmented contractile responses to α1- and β1-adrenoceptor stimulation are associated with increased activities of RyR, SERCA, and NCX in the heart

2009 ◽  
Vol 296 (4) ◽  
pp. C766-C782 ◽  
Author(s):  
Sharon Tsang ◽  
Stanley S. C. Wong ◽  
Song Wu ◽  
Gennadi M. Kravtsov ◽  
Tak-Ming Wong
Keyword(s):  
Ventricular Myocytes ◽  
Left Ventricular ◽  
Contractile Responses ◽  
Adrenoceptor Antagonist ◽  
Cardiac Contractile ◽  
Plasmic Reticulum ◽  
Adrenoceptor Agonist ◽  
Intracellular Ca ◽  
Developed Pressure ◽  
Stimulation Of

We hypothesized that testosterone at physiological levels enhances cardiac contractile responses to stimulation of both α1- and β1-adrenoceptors by increasing Ca2+ release from the sarcoplasmic reticulum (SR) and speedier removal of Ca2+ from cytosol via Ca2+-regulatory proteins. We first determined the left ventricular developed pressure, velocity of contraction and relaxation, and heart rate in perfused hearts isolated from control rats, orchiectomized rats, and orchiectomized rats without and with testosterone replacement (200 μg/100 g body wt) in the presence of norepinephrine (10−7 M), the α1-adrenoceptor agonist phenylephrine (10−6 M), or the nonselective β-adrenoceptor agonist isoprenaline (10−7 M) in the presence of 5 × 10−7 M ICI-118,551, a β2-adrenoceptor antagonist. Next, we determined the amplitudes of intracellular Ca2+ concentration transients induced by electrical stimulation or caffeine, which represent, respectively, Ca2+ release via the ryanodine receptor (RyR) or releasable Ca2+ in the SR, in ventricular myocytes isolated from the three groups of rats. We also measured 45Ca2+ release via the RyR. We then determined the time to 50% decay of both transients, which represents, respectively, Ca2+ reuptake by sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and removal via the sarcolemmal Na+/Ca2+ exchanger (NCX). We correlated Ca2+ removal from the cytosol with activities of SERCA and its regulator phospholamban as well as NCX. The results showed that testosterone at physiological levels enhanced positive inotropic and lusitropic responses to stimulation of α1- and β1-adrenoceptors via the androgen receptor. The increased contractility and speedier relaxation were associated with increased Ca2+ release via the RyR and faster Ca2+ removal out of the cytosol via SERCA and NCX.

Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Antigen Challenge ◽  
Saline Control ◽  
Control Group ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
Volume Blood ◽  
M2 Muscarinic Receptors ◽  
Stimulation Of

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Electrical Stimulation for Immune Modulation in Cancer Treatments

2022 ◽  
Vol 9 ◽  
Author(s):  
Ritopa Das ◽  
Sofia Langou ◽  
Thinh T. Le ◽  
Pooja Prasad ◽  
Feng Lin ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Immune System ◽  
Immune Modulation ◽  
Cancer Treatments ◽  
Different Types ◽  
Specific Antigens ◽  
High Doses ◽  
T Cell Transfer ◽  
Deficient Mice ◽  
Stimulation Of

Immunotherapy is becoming a very common treatment for cancer, using approaches like checkpoint inhibition, T cell transfer therapy, monoclonal antibodies and cancer vaccination. However, these approaches involve high doses of immune therapeutics with problematic side effects. A promising approach to reducing the dose of immunotherapeutic agents given to a cancer patient is to combine it with electrical stimulation, which can act in two ways; it can either modulate the immune system to produce the immune cytokines and agents in the patient’s body or it can increase the cellular uptake of these immune agents via electroporation. Electrical stimulation in form of direct current has been shown to reduce tumor sizes in immune-competent mice while having no effect on tumor sizes in immune-deficient mice. Several studies have used nano-pulsed electrical stimulations to activate the immune system and drive it against tumor cells. This approach has been utilized for different types of cancers, like fibrosarcoma, hepatocellular carcinoma, human papillomavirus etc. Another common approach is to combine electrochemotherapy with immune modulation, either by inducing immunogenic cell death or injecting immunostimulants that increase the effectiveness of the treatments. Several therapies utilize electroporation to deliver immunostimulants (like genes encoded with cytokine producing sequences, cancer specific antigens or fragments of anti-tumor toxins) more effectively. Lastly, electrical stimulation of the vagus nerve can trigger production and activation of anti-tumor immune cells and immune reactions. Hence, the use of electrical stimulation to modulate the immune system in different ways can be a promising approach to treat cancer.

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