The pacemaker activity generating the intrinsic myogenic contraction of the dorsal vessel of Tenebrio molitor (Coleoptera)

Combined intracellular and extracellular recordings from various parts of the isolated dorsal vessel of Tenebrio molitor revealed some of the following electrophysiological properties of the heart and the aorta. (i) The wave of depolarization causing forward pulsation of the dorsal vessel was always transmitted from posterior to anterior, with a conduction velocity of 0.014 m s(−1) in the heart and 0.001 m s(−1) in the aorta when the heart rate was 60 beats min(−1). (ii) There was no pacemaker activity in the aorta. (iii) The duration of the compound action potential in the aortic muscle depended on the duration of the pacemaker action potential generated in the heart. (iv) Isolated parts of the heart continued to contract rhythmically for hours, indicating powerful pacemaker activity in individual cardiac segments. (v) There was a direct relationship between action potential duration and the length of the preceding diastolic interval. (vi) The rhythmic wave of depolarization was dependent on the influx of Ca(2+). (vii) The recovery of the electrical properties of myocardial cells that had been disrupted by sectioning was rapid. (viii) In hearts sectioned into two halves, the rhythmic pacemaker action potentials recorded simultaneously from the two isolated halves eventually drifted out of phase, but they had the same intrinsic frequency. In the light of these data, we discuss two alternative models for the generation of spontaneous rhythmic pumping movements of the heart and aorta.

Analysis of the effects of vagal stimulation on the sinus venosus of the toad

In amphibians and mammals, vagal stimulation leads to the release of acetylcholine, ACh, which causes bradycardia. However, the responses to nerve stimulation are not well mimicked by exogenously applied ACh. These observations have led to the suggestion that there are subpopulations of muscarinic receptors on pacemaker cells and that during vagal stimulation neuronally released ACh caused slowing by suppressing inward current flow during diastole. After the generation of action potentials has been prevented by applying an organic calcium antagonist, vagal stimulation causes a hyperpolarization and an increase in membrane resistance: this observation suggests that the hyperpolarization results from a supression of inward, presumably Na + , current flow. In this study we describe the effects of vagal stimulation on membrane potentials recorded from arrested and beating hearts by using a computer model. The model of Noble & Noble ( Proc. R. Soc. Lond. B 222, 295 (1984)) was modified to describe the shape of amphibian pacemaker action potentials. A voltage-dependent Na conductance was included as well as two voltage-independent conductances, a background Na conductance and a background K conductance. Subsequently the hypothesis that the changes in membrane potential recorded during vagal stimulation from arrested preparations resulted from a reduction in Na conductance and this represented the sole action of vagally released ACh, was tested. If this were so, the changes in membrane conductance that occur during vagal inhibitory junction potentials recorded from arrested preparations should produce changes in pacemaker action potentials similar to those recorded experimentally from beating preparations. This was found to be the case. Thus the analyses are consistent with the idea that vagal inhibition of pacemaker cells results solely from a suppression of the two pacemaker sodium currents.

Effects of extracellular Mg2+ on T- and L-type Ca2+ currents in single atrial myocytes

Whole cell voltage-clamp techniques were used to study the effects of extracellular Mg2+ on T- and L-type Ca2+ currents recorded from single atrial myocytes from cat heart. T and L currents were distinguished primarily by their voltage dependence. With 5.4 mM Ca2+ as charge carrier, maximal T- and L-current densities were 1.0 +/- 0.06 and 9.7 +/- 0.4 pA/pF, respectively. Nickel (Ni2+, 50 microM) inhibited maximal T current (-65.6 +/- 5.9%) more than L current (-15.7 +/- 2.4%), and 10 microM cadmium (Cd2+) inhibited L current (-65.5 +/- 5.9%) without significant effect on T current (-8.7 +/- 8.1%). Mg2+ elicited a dose-dependent inhibition of both T and L currents. Mg2+ less than 8.4 mM inhibited T current more than L current. At Mg2+ greater than or equal to 8.4 mM, T-current inhibition reach a plateau at approximately 52%, whereas L current was further inhibited (-65%) at 16.8 mM Mg2+. Mg2+ elicited a dose-dependent positive shift in half-maximal voltages of activation and inactivation for both T and L currents. Mg2(+)-induced inhibition of both T and L currents was greater in lower (2.7 mM) external Ca2+. Finally, 4.2 mM Mg2+ and 50 microM Ni2+ elicited a similar decrease in the late diastolic slope of subsidiary pacemaker action potentials, whereas 10 microM Cd2+ markedly inhibited action potential amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

The pacemaker cell of the sinoatrial node of the rabbit

Rabbit sinoatrial nodes were isolated and studied in an attempt to determine the cell of origin of the true pacemaker potential. Cells of the sinoatrial node of the rabbit giving rise to the characteristic true pacemaker potential were iontophoretically tagged with lanthanum. The lanthanum appeared within the cytoplasm of cells, which morpholigically are (P) cells. The lanthanum appeared as small, amorphous, electron-dense globules. It is concluded from this study that the P or pale cell is the source of the true pacemaker action potential of the sinoatrial node.