The calcium channel agonist, Bay K-8644, antagonizes effects of diacetyl monoxime on cardiac tissues

1985 ◽  
Vol 63 (10) ◽  
pp. 1267-1270 ◽  
Author(s):  
Hideaki Sada ◽  
Shigiko Sada ◽  
Nicholas Sperelakis
Keyword(s):  
Maximum Rate ◽  
Bay K 8644 ◽  
Embryonic Chick ◽  
Cardiac Tissues ◽  
Amplitude Maximum ◽  
Slow Channel ◽  
Long Time ◽  
Diacetyl Monoxime ◽  
Maximum Rate Of Rise ◽  
Slow Action Potential

Effects of a novel slow channel activator, Bay K-8644 (Bay K), were studied on slow action potential (APs) in young and old embryonic chick hearts, and on its antagonism of the effects of diacetyl monoxime (DAM). The slow APs of young hearts are mediated by slow Na+ channels, whereas those of old hearts are mediated by slow Ca2+ channels. In slow APs of old (13–18 days old) embryonic chick hearts superfused with a high (22 mM) K+ solution, Bay K (10−6 M) gradually increased the amplitude, maximum rate of rise [Formula: see text], and duration of the slow APs. The actions of Bay K persisted for a long time (>30 min) after washout of the drug. DAM (10 mM) depressed the [Formula: see text], duration and amplitude of the slow APs. Some of the changes in slow AP parameters produced by DAM, e.g., [Formula: see text] decrease, were antagonized by the addition of Bay K (10−6 M). In 3-day-old embryonic chick hearts, Bay K potentiated the slow APs and DAM depressed them; Bay K antagonized these effects of DAM. Thus, the actions of Bay K and DAM are likely to be produced, respectively, via the activation and depression of slow Ca2+ channels in old embryonic chick hearts. In addition, the drugs seem to influence slow Na+ channels found in young embyronic chick hearts.

An opiate receptor on frog sciatic nerve axons

1979 ◽  
Vol 57 (10) ◽  
pp. 1171-1174 ◽  
Author(s):  
E. G. Hunter ◽  
G. B. Frank
Keyword(s):  
Sciatic Nerve ◽  
Action Potential ◽  
Maximum Rate ◽  
Opiate Receptor ◽  
Resting Potential ◽  
Amplitude Maximum ◽  
Gap Technique ◽  
Sucrose Gap ◽  
Frog Sciatic Nerve ◽  
Maximum Rate Of Rise

The effect of meperidine (3 × 10−4 M) on the action potential of frog sciatic nerve was examined by means of the double sucrose gap technique. Meperidine decreased the amplitude, maximum rate of depolarization, and maximum rate of repolarization of the action potential but had no effect on the resting potential. This depression in amplitude and maximum rate of rise was partially blocked by naloxone (1 × 10−8 M) while the maximum rate of depolarization was further depressed. The data suggest that the effect of meperidine is due to two mechanisms, a nonspecific local anaesthetic like effect and an opiate receptor mediated effect.

Neuronal and Extraneuronal Uptake of 3H-Norepinephrine in the Heart of the Active Bat: An Electron Microscopic Radioautographic Study

1973 ◽  
Vol 31 ◽  
pp. 522-523
Author(s):  
Martin Hagopian ◽  
Michael D. Gershon ◽  
Eladio A. Nunez
Keyword(s):  
Smooth Muscle ◽  
Monoamine Oxidase ◽  
Vascular Smooth Muscle ◽  
Cardiac Muscle ◽  
Maximum Rate ◽  
External Medium ◽  
Extraneuronal Uptake ◽  
Electron Microscopic ◽  
Cardiac Tissues ◽  
High Affinity

The ability of cardiac tissues to take up norepinephrine from an external medium is well known. Two mechanisms, called Uptake and Uptake respectively by Iversen have been differentiated. Uptake is a high affinity system associated with adrenergic neuronal elements. Uptake is a low affinity system, with a higher maximum rate than that of Uptake. Uptake has been associated with extraneuronal tissues such as cardiac muscle, fibroblasts or vascular smooth muscle. At low perfusion concentrations of norepinephrine most of the amine taken up by Uptake is metabolized. In order to study the localization of sites of norepinephrine storage following its uptake in the active bat heart, tritiated norepinephrine (2.5 mCi; 0.064 mg) was given intravenously to 2 bats. Monoamine oxidase had been inhibited with pheniprazine (10 mg/kg) one hour previously to decrease metabolism of norepinephrine.

Developmental changes in cardiac contractility in fetal and postnatal sheep: in vitro and in vivo

1984 ◽  
Vol 247 (3) ◽  
pp. H371-H379 ◽  
Author(s):  
P. A. Anderson ◽  
K. L. Glick ◽  
A. Manring ◽  
C. Crenshaw
Keyword(s):  
Maximum Rate ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Developmental Changes ◽  
Common Mechanism ◽  
Postextrasystolic Potentiation ◽  
Maximum Rate Of Rise

Developmental changes in contractility were sought in the fetal and postnatal sheep heart by using postextrasystolic potentiation and force, pressure, and wall-motion measures. Two different preparations were used, isolated myocardium and the chronically instrumented lamb. In the isolated muscle, the following increased significantly with age: force of contraction, the maximum rate of rise of force, and postextrasystolic potentiation. In the intact heart prior to birth [period of study, 20 +/- 4 (SD) days] heart rate (HR) fell significantly, and the following increased significantly: postextrasystolic potentiation [measured with the maximum rate of rise of left ventricular (LV) pressure (Pmax)], LV peak systolic pressure (LVP), end-diastolic dimension (EDD), end-systolic dimension (ESD), and aortic diastolic pressure. After birth, LVP, Pmax, HR, LVEDP, EDD, and ESD increased and postextrasystolic potentiation fell. The latter fall was not found in vitro and probably demonstrates a transient change in contractility, related to hormonal or neural stimulation. Over the subsequent postnatal days (6-122 days), HR fell while potentiation, EDD, and ESD increased significantly. Both in vitro and in vivo, the overall increase in postextrasystolic potentiation demonstrates a similar long-term change in contractility. The similarity of this change to that induced by mild hypertrophy suggests that development and mild hypertrophy alter myocardial contractility through a common mechanism.

Postprandial changes in intestinal slow-wave propagation reflect a decrease in cell coupling

1989 ◽  
Vol 257 (3) ◽  
pp. G463-G469
Author(s):  
D. Terasaka ◽  
A. Bortoff ◽  
L. F. Sillin
Keyword(s):  
Wave Propagation ◽  
Electrical Activity ◽  
Slow Wave ◽  
Propagation Velocity ◽  
Maximum Rate ◽  
Internal Resistance ◽  
Cell Coupling ◽  
Wave Propagation Velocity ◽  
Fasting Level ◽  
Amplitude Maximum

The purpose of these studies was to determine the effects of feeding on jejunal slow-wave propagation velocity (SWPV). Nine cats were instrumented with six pairs of electrodes implanted 4 cm apart on the jejunum. Electrical activity was recorded at the end of an 18-h fast after which each animal was fed 60 g of canned cat food. Recordings were continued during feeding and for several hours thereafter. This procedure was repeated at least twice for each cat. Average SWPV (cm/s) decreased from a fasting level of 2.28 +/- 0.20 (mean of means +/- SE) to 1.93 +/- 0.16 at 10-20 min, 1.51 +/- 0.11 at 1 h, and 1.37 +/- 0.10 at 3 h postprandially. Corresponding SW frequencies (SWFs) were 19.6 +/- 0.3, 18.7 +/- 0.2, 19.2 +/- 0.2, and 19.0 +/- 0.2 cycles/min, respectively. The differences between the fasting SWPV and that at 1 and 3 h were significant (P less than 0.05). When SWPV was plotted as a function of SWF, the slopes of the corresponding curves were also found to decrease postprandially (P less than 0.05, fasting vs. 1 and 3 h). There was no apparent change in SW amplitude, maximum rate of SW depolarization, or threshold. In the absence of changes in these parameters, the divergence of the slopes at lower SWFs indicates that the decrease in SWPV is because of increased internal resistance, probably the result of uncoupling of intestinal muscle cells. The change is rapid in onset and long in duration, suggesting that an uncoupling factor is released during ingestion of a meal, and that its effect persists for several hours.

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