The characterization of cardiac histaminergic chronotropic receptors in the rabbit

1981 ◽  
Vol 59 (1) ◽  
pp. 14-18 ◽  
Author(s):  
Alicia Polanin ◽  
Thomas E. Tenner Jr. ◽  
John H. McNeill
Keyword(s):  
Histamine Receptor ◽  
Receptor Blockade ◽  
Chronotropic Response ◽  
Atrial Rate ◽  
Chronotropic Effects ◽  
Rabbit Atria ◽  
Stimulation Of

The effects of selective histamine receptor analogs were studied in spontaneously beating rabbit atria. Atrial rate was increased by histamine (an H1 and H2 agonist), 4-methylhistamine and impromidine (H2 agonists), and 2-pyridylethylamine (PEA, an H1 agonist). The responses to histamine, 4-methylhistamine, and impromidine were not affected by propranolol (1 × 10−7 M) or reserpine pretreatment. However, the response to PEA was nearly abolished upon pretreatment with propranolol or reserpine.Cimetidine pretreatment (H2 receptor blockade) competitively antagonised the positive chronotropic effects of histamine, 4-methylhistamine, and impromidine. Promethazine pretreatment (H1 receptor blockade) competitively blocked the chronotropic effects of histamine but had no effect on the responses to 4-methylhistamine or impromidine. These results suggest that stimulation of H1 and H2 receptors will cause a positive chronotropic response.

The effect of pH on rabbit atrial response to histamine

1976 ◽  
Vol 54 (2) ◽  
pp. 118-127 ◽  
Author(s):  
M. J. Hughes ◽  
I. A. Coret
Keyword(s):  
Histamine Receptor ◽  
Maximum Response ◽  
Force Of Contraction ◽  
Histamine Concentration ◽  
Adenyl Cyclase Activity ◽  
Chronotropic Response ◽  
Spontaneous Rate ◽  
Histamine Response ◽  
Ph Range ◽  
Rabbit Atria

The chronotropic response of isolated rabbit atria in normal Tyrode's medium increases monotonically with increasing doses of histamine (9 × 10−7–9 × 10−4 M). Plots of the inverse of response against the inverse of concentration were linear; and from these plots were derived values for the theoretical maximum response at 'infinite' dose and for the histamine concentration required to evoke a half maximum response. Alteration of pH by changing [HCO3−] at constant pCO2, [Na+] and osmolality did not appreciably affect the response to histamine in the range pH 7.0–7.6. However, at pH below 7.0 the magnitude of histamine response was reduced at all concentrations of histamine tested. In the pH range 7.0–7.6, additions of NaHCO3 at constant pCO2 increased the spontaneous rate of rabbit atria (in the absence of histamine); however, there was little effect of changing pH (in this range) by altering [HCO3−] at constant pCO2 when [Na+] and osmolality were kept constant. Immersion in solutions at pH's less than 7.0 led to decline in spontaneous rate and force of contraction. It is probable that depression of adenyl cyclase activity rather than a specific change in ionization of histamine receptor is responsible for a decreased response to histamine at pH 6.9.

Characterization of the histamine receptors in rabbit left atria

1981 ◽  
Vol 59 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Alicia Polanin ◽  
John H. McNeill
Keyword(s):  
Left Atrial ◽  
Histamine Receptor ◽  
Histamine Receptors ◽  
Receptor Blockade ◽  
Inotropic Response ◽  
Receptor Stimulation ◽  
Inotropic Effects ◽  
Receptor Antagonism ◽  
Positive Inotropic Effects

The effects of selective histamine receptor analogs were studied in electrically paced rabbit left atria. Atrial tension was increased by histamine (an H1 and H2 agonist), 4-methylhistamine and impromidine (H2 agonists), and 2-pyridylethylamine (PEA) (an H1 agonist). The responses to histamine and impromidine were not altered by propranolol (1 × 10−7 M) or reserpine pretreatment. However, the responses to 4-methylhistamine and PEA were significantly decreased upon pretreatment with propranolol or reserpine. Promethazine pretreatment (H1 receptor blockade) antagonized the inotropic effects of histamine and PEA but had no effect on the responses to 4-methylhistamine or impromidine. Cimetidine pretreatment (H2 receptor antagonism) competitively blocked the positive inotropic effects of histamine, 4-methylhistamine, and impromidine. These results suggest that the left atrial inotropic response is mediated through H1 and H2 receptor stimulation.

Histamine and the heart

1984 ◽  
Vol 62 (6) ◽  
pp. 720-726 ◽  
Author(s):  
John H. McNeill
Keyword(s):  
Histamine Receptor ◽  
Histamine Receptors ◽  
Ion Concentration ◽  
Free Calcium ◽  
Guinea Pig Heart ◽  
Release Of Noradrenaline ◽  
Chronotropic Effects ◽  
Calcium Ion Concentration ◽  
Right Atria ◽  
Stimulation Of

Histamine has been known as a cardiac stimulant for over 70 years. Work in our laboratory over the past decade has established that histamine receptors exist in the hearts of various species. The type of histamine receptor varies not only between species but also in the various regions of the heart. In the guinea pig heart H1 receptors are found in left atria and ventricles while H2 receptors are found in right atria and are the predominant histamine receptor in the ventricles. Rabbit atria contain both H1 and H2 receptors while the ventricles appear to possess only H1. Rat and cat heart do not seem to have histamine receptors and the positive inotropic and chronotropic effects elicited by histamine in cardiac preparations of these species are due to the release of noradrenaline. Dog heart contains H1 receptors while human heart has H2 receptors. In all cases H2 receptors are associated with adenylate cyclase and stimulation of such receptors results in an increase in cyclic AMP levels. H1 receptors are not associated with cyclic nucleotides in the heart. There are certain similarities between β-adrenergic and H2-histaminergic receptors as well as between α-adrenergic and H1-histaminergic receptors. Stimulation of either histamine receptor must result in an increase in the free calcium ion concentration in the cardiac cell but the mechanisms involved are obviously different.

Characterization of early and late cerebral evoke responses (CEP) to stimulation of afferent esophageal pathways in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A630-A630
Author(s):  
C DIENEFELD ◽  
R BECKER ◽  
M KAMATH ◽  
G TOUGAS ◽  
M HAUPTS ◽  
...  
Keyword(s):  
Stimulation Of

CATECHOLAMINE ANTAGONISM TO OXYTOCIN-INDUCED MILK-EJECTION

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr
Keyword(s):  
Receptor Blockade ◽  
Milk Ejection ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Beta Receptors ◽  
Alpha Receptors ◽  
Adrenergic Blockers ◽  
Beta Receptor Blockade ◽  
Second Pain ◽  
Stimulation Of

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.

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