Characteristics of biphasic slow depolarizing and slow hyperpolarizing potential in frog taste cell induced by parasympathetic efferent stimulation

When the velocity of capillary blood flow in the frog tongue declined to an intermediate range of 0.2-0.7 mm/s, the glossopharyngeal nerve stimulation induced a biphasic slow depolarizing and slow hyperpolarizing potential (HP) in taste cells. The objective of this work was to examine the generative mechanisms of the biphasic slow potentials. The biphasic slow response was always preceded by a slow depolarizing potential (DP) component and followed by a slow HP component. Intravenous injection of tubocurarine completely blocked the biphasic slow responses, suggesting that both components of the biphasic slow potentials are evoked by the parasympathetic nerve (PSN) fibers. Membrane conductance of taste cells increased during slow DPs and decreased during slow HPs. The reversal potential of either component of a biphasic slow response was the almost same value of -12 mV. An antagonist, L-703,606, for neurotransmitter substance P neurokinin(1) receptor completely blocked both components of the biphasic slow responses. An antagonist, flufenamic acid, for nonselective cation channels on the taste cell membrane completely blocked the biphasic slow responses. These results suggest that PSN-induced biphasic slow responses are postsynaptically elicited in taste cells by releasing substance P at the PSN axon terminals. It is concluded that the slow DP component may be generated by opening one type of nonselective cation channel on taste cells and that the slow HP component may be generated by closing the other type of nonselective cation channel. We discussed that a second messenger inositol 1,4,5-trisphosphate might be related to a slow DP component and another second messenger diacylglycerol might be related to a slow HP component.     

Analysis of slow depolarizing potential in frog taste cell induced by parasympathetic efferent stimulation under hypoxia

Strong electrical stimulation (ES) of the frog glossopharyngeal (GP) efferent nerve induced slow depolarizing potentials (DPs) in taste cells under hypoxia. This study aimed to elucidate whether the slow DPs were postsynaptically induced in taste cells. After a block of parasympathetic nerve (PSN) ganglia by tubocurarine, ES of GP nerve never induced slow DPs in the taste cells, so slow DPs were induced by PSN. When Ca(2+) in the blood plasma under hypoxia was decreased to approximately 0.5 mM, the slow DPs reduced in amplitude and lengthened in latency. Increasing the normal Ca(2+) to approximately 20 mM increased the amplitude of slow DPs and shortened the latency. Addition of Cd(2+) to the plasma greatly reduced the amplitude of slow DPs and lengthened the latency. These data suggest that the slow DPs depend on Ca(2+) and Cd(2+) concentration at the presynaptic PSN terminals of taste disk. Antagonists, [D-Arg(1), D-Trp(7,9), Leu(11)]-substance P and L-703 606, of neurotransmitter substance P neurokinin(1) receptor completely blocked the slow DPs. Intravenous application of substance P induced a DP of approximately 7 mV and a reduction of membrane resistance of approximately 48% in taste cells. A nonselective cation channel antagonist, flufenamic acid, completely blocked the slow DPs. These findings suggest that the slow DPs are postsynaptically initiated in frog taste cells under hypoxia by opening nonselective cation channels on the postsynaptic membrane after substance P is probably released from the presynaptic PSN axon terminals.     

Analysis of slow hyperpolarizing potentials in frog taste cells induced by glossopharyngeal nerve stimulation

Electrical stimulation of the frog glossopharyngeal (GP) nerve evoked slow hyperpolarizing potentials (HPs) in taste cells. This study aimed to clarify whether slow HPs were postsynaptically induced in taste cells. The slow HPs were recorded intracellularly with a microelectrode. When Ca2+ concentration in the blood plasma was decreased to approximately 0.5 mM, the amplitude of slow HPs reduced and their latency lengthened. When the Ca2+ concentration was increased to approximately 20 mM, the amplitude of slow HPs increased and their latency shortened. Addition of Cd2+ to the plasma greatly reduced the amplitude of slow HPs and lengthened their latency. These data suggest that the slow HPs are dependent on presynaptic activities in the GP nerve terminals in the taste disk. Of various antagonists injected intravenously for blocking receptors of neurotransmitter biogenic amines and peptides, only antagonists for substance P blocked the slow HPs at 2-4 mg/kg body wt. Application of substance P of 2 mg/kg to the plasma induced hyperpolarizing responses in taste cells, whose amplitude was the same as that of the slow HPs induced by GP nerve stimulation. Application of a nonselective cation channel antagonist, flufenamic acid, to the plasma blocked the slow HPs. These results suggest that the slow HPs are generated by closing the nonselective cation channels in the postsynaptic membrane of taste cells following possible release of substance P from the GP nerve terminals in the taste disk.     

Taste cell responses in the frog are modulated by parasympathetic efferent nerve fibers

We studied the anatomical properties of parasympathetic postganglionic neurons in the frog tongue and their modulatory effects on taste cell responses. Most of the parasympathetic ganglion cell bodies in the tongue were found in extremely small nerve bundles running near the fungiform papillae, which originate from the lingual branches of the glossopharyngeal (GP) nerve. The density of parasympathetic postganglionic neurons in the tongue was 8000-11,000/mm(3) of the extremely small nerve bundle. The mean major axis of parasympathetic ganglion cell bodies was 21 microm, and the mean length of parasympathetic postganglionic neurons was 1.45 mm. Electrical stimulation at 30 Hz of either the GP nerve or the papillary nerve produced slow hyperpolarizing potentials (HPs) in taste cells. After nicotinic acetyl choline receptors on the parasympathetic ganglion cells in the tongue had been blocked by intravenous (i.v.) injection of D-tubocurarine (1 mg/kg), stimulation of the GP nerve did not induce any slow HPs in taste cells but that of the papillary nerve did. A further i.v. injection of a substance P NK-1 antagonist, L-703,606, blocked the slow HPs induced by the papillary nerve stimulation. This suggests that the parasympathetic postganglionic efferent fibers innervate taste cells and are related to a generation of the slow HPs and that substance P is released from the parasympathetic postganglionic axon terminals. When the resting membrane potential of a taste cell was hyperpolarized by a prolonged slow HP, the gustatory receptor potentials for NaCl and sugar stimuli were enhanced in amplitude, but those for quinine-HCl and acetic acid stimuli remained unchanged. It is concluded that frog taste cell responses are modulated by activities of parasympathetic postganglionic efferent fibers innervating these cells.     

Depression of gustatory receptor potential in frog taste cell by parasympathetic nerve-induced slow hyperpolarizing potential

Parasympathetic nerve (PSN) innervates taste cells of the frog taste disk, and electrical stimulation of PSN elicited a slow hyperpolarizing potential (HP) in taste cells. Here we report that gustatory receptor potentials in frog taste cells are depressed by PSN-induced slow HPs. When PSN was stimulated at 30 Hz during generation of taste cell responses, the large amplitude of depolarizing receptor potential for 1 M NaCl and 1 mM acetic acid was depressed by approximately 40% by slow HPs, but the small amplitude of the depolarizing receptor potential for 10 mM quinine-HCl (Q-HCl) and 1 M sucrose was completely depressed by slow HPs and furthermore changed to the hyperpolarizing direction. The duration of the depolarizing receptor potentials depressed by slow HPs prolonged with increasing period of PSN stimulation. As tastant-induced depolarizing receptor potentials were increased, the amplitude of PSN-induced slow HPs inhibiting the receptor potentials gradually decreased. The mean reversal potentials of the slow HPs were approximately -1 mV under NaCl and acetic acid stimulations, but approximately -14 mV under Q-HCl and sucrose stimulations. This implies that when a slow HP was evoked on the same amplitude of depolarizing receptor potentials, the depression of the NaCl and acetic acid responses in taste cells was larger than that of Q-HCl and sucrose responses. It is concluded that slow HP-induced depression of gustatory depolarizing receptor potentials derives from the interaction between gustatory receptor current and slow hyperpolarizing current in frog taste cells and that the interaction is stronger for NaCl and acetic acid stimulations than for Q-HCl and sucrose stimulations.     

Non-synaptic transformation of gustatory receptor potential by stimulation of the parasympathetic fiber of the frog glossopharyngeal nerve

When the glossopharyngeal nerve (GP) in the frog was strongly stimulated electrically, slow potentials were elicited from the tongue surface and taste cells in the fungiform papillae. Injection of atropine completely blocked these slow potentials. The present and previous data indicate that the slow potentials induced in the tongue surface and taste cells are due to a liquid junction potential between saliva secreted from the lingual glands due to parasympathetic fiber activity and an adapting solution on the tongue surface. Intracellularly recorded depolarizing receptor potentials in taste cells induced by 0.5 M NaCl and 3 mM acetic acid were enhanced by depolarizing slow potentials induced by GP nerve stimulation, but were depressed by the hyperpolarizing slow potentials. On average, the receptor potential of taste cells for 0.5 M NaCl was increased by 25% by the GP nerve-induced slow potential, but the receptor potential of taste cells for 3 mM acetic acid was decreased by 1% by the slow potential. These transformations of receptor potentials in frog taste cells were not due to a synaptic event initiated between taste cells and the efferent nerve fiber, but due to a non-synaptic event, a lingual junction potential generated in the dorsal lingual epithelium by GP nerve stimulation.     

The origin of slow potentials on the tongue surface induced by frog glossopharyngeal efferent fiber stimulation

When the glossopharyngeal (GP) nerve of the frog was stimulated electrically, electropositive slow potentials were recorded from the tongue surface and depolarizing slow potentials from taste cells in the fungiform papillae. The amplitude of the slow potentials was stimulus strength- and the frequency-dependent. Generation of the slow potentials was not related to antidromic activity of myelinated afferent fibers in the GP nerve, but to orthodromic activity of autonomic post-ganglionic C fibers in the GP nerve. Intravenous injection of atropine abolished the positive and depolarizing slow potentials evoked by GP nerve stimulation, suggesting that the slow potentials were induced by the activity of parasympathetic post-ganglionic fibers. The amplitude and polarity of the slow potentials depended on the concentration of adapting NaCl solutions applied to the tongue surface. These results suggest that the slow potentials recorded from the tongue surface and taste cells are due to the liquid junction potential generated between saliva secreted from the lingual glands by GP nerve stimulation and the adapting solution on the tongue surface.     

The role of fast and slow potassium currents in electrical activity of amphibian myelinated nerve fibres

The paper reviews the information about the role of fast and slow potassium currents in electrical activity of amphibian myelinated nerve fibres. It demonstrates the importance of discovering of fast and slow potassium currents and their following pharmacological separation (by potassium channels blockers 4-aminopyridine and tetraethylammonium) in investigation of mechanisms of biological potentials generation. The information about the existence of fast and slow potassium channels in the nerve membrane and about the properties of 4-aminopyridine and tetraethylammonium action served as a base for determination the nature of biological potentials and discovering the mechanism of potential-dependent action of 4-aminopyridine that for tens of years suffered from the lack of adequate explanation.     

Tonic activity of parasympathetic efferent nerve fibers hyperpolarizes the resting membrane potential of frog taste cells

We investigated the relationship between the membrane potential of frog taste cells in the fungiform papillae and the tonic discharge of parasympathetic efferent fibers in the glossopharyngeal (GP) nerve. When the parasympathetic preganglionic fibers in the GP nerve were kept intact, the mean membrane potential of Ringer-adapted taste cells was -40 mV but decreased to -31 mV after transecting the preganglionic fibers in the GP nerve and crushing the postganglionic fibers in the papillary nerve. The same result occurred after blocking the nicotinic acetylcholine receptors on parasympathetic ganglion cells in the tongue and blocking the substance P neurokinin-1 (NK-1) receptors in the gustatory efferent synapses. This indicates that the parasympathetic nerve (PSN) hyperpolarizes the membrane potential of frog taste cells by -9 mV. Repetitive stimulation of a transected GP nerve revealed that a -9-mV hyperpolarization of taste cells maintained under the intact GP nerve derives from an approximately 10-Hz discharge of the PSN efferent fibers. The mean frequency of tonic discharges extracellularly recorded from PSN efferent fibers of the taste disks was 9.1 impulses/s. We conclude that the resting membrane potential of frog taste cells is continuously hyperpolarized by on average -9 mV by an approximately 10-Hz tonic discharge from the parasympathetic preganglionic neurons in the medulla oblongata.     

Interaction Between Gustatory Depolarizing Receptor Potential and Efferent-Induced Slow Depolarizing Synaptic Potential in Frog Taste Cell

Electrical stimulation of parasympathetic nerve (PSN) efferent fibers in the glossopharyngeal nerve induced a slow depolarizing synaptic potential (DSP) in frog taste cells under hypoxia. The objective of this study is to examine the interaction between a gustatory depolarizing receptor potential (GDRP) and a slow DSP. The amplitude of slow DSP added to a tastant-induced GDRP of 10 mV was suppressed to 60% of control slow DSPs for NaCl and acetic acid stimulations, but to 20–30% for quinine–HCl (Q-HCl) and sucrose stimulations. On the other hand, when a GDRP was induced during a prolonged slow DSP, the amplitude of GDRPs induced by 1 M NaCl and 1 M sucrose was suppressed to 50% of controls, but that by 1 mM acetic acid and 10 mM Q-HCl unchanged. It is concluded that the interaction between GDRPs and efferent-induced slow DSPs in frog taste cells under hypoxia derives from the crosstalk between a gustatory receptor current across the receptive membrane and a slow depolarizing synaptic current across the proximal subsynaptic membrane of taste cells.     

Local development of action potentials in slow muscle fibres after complete or partial denervation.

Pyriformis muscles of Rana temporaria were completely or partially denervated by cutting the sciatic nerve or some of the small nerve branches entering the muscle. One stimulating and one to three recording microelectrodes were inserted along the fibres in order to compare the electrical activity at these points. In an early period following denervation action potentials of variable size and shape could be observed; these action potentials were often composed of two, sometimes of three or four, components. The size of individual components depended on the position of the recording microelectrode. Individual components could occasionally be triggered separately by adjusting the strength of the stimulating current pulse; propagation of these "all or none" responses was absent. In other fibres one component of the action potential could trigger another one several millimetres apart, thus indicating propagation. Conduction velocities were approximately 0.4 m/s. In partially denervated slow fibres, endplate potentials were confined to one lateral segment of the fibres, while the action potential occupied the denervated part of the membrane. The amplitudes of endplate and action potentials varied inversely with distance. Rough estimates of the length constant of the slow fibre membrane were calculated from the spatial decay of action potentials, endplate potentials and hyperpolarizing electrotonic potentials; mean values obtained were 2.5, 4.8 and 7.7 mm respectively. The results suggest that following denervation Na channels are built into discrete areas of the slow fibre membrane and that this process depends on the amount of denervation in individual fibres.     

Spontaneous and repetitive driver potentials in crab cardiac ganglion neurons

Summary Driver potentials (DP), TTX-resistant voltage-activated slow depolarizations probably involving Ca⁺⁺-influx, have previously been shown to play an essential role in the organization of spike bursts in crustacean cardiac ganglia. The work reported here suggests that the DP system may also constitute an important component of the ganglionic oscillator.DPs were recorded intracellularly from neurons in ganglia isolated from two brachyurans,Portunus sanguinolentus and Podophthalmus vigil. InPortunus, full-sized DPs can be evoked in TTX by brief stimulus pulses only at invervals of several seconds; a single DP is triggered during a long (3-s) current pulse, and spontaneous DPs never occur. In contrast, nearly one half ofPodophthalmus preparations show spontaneous high-frequency trains of DPs lasting up to 5 min and recurring at irregular intervals. In allPodophthalmus preparations repetitive DPs are evoked during a 3-s pulse, and increase in frequency as current strength is increased. Portunus ganglia can be made to exhibit repetitive DPs in response to current if perfused with TEA (which suppresses a rectifying K⁺-current) in a medium with reduced Na⁺ (which is likely to enhance the inward Ca⁺⁺-current); neither TEA alone nor low-Na⁺ alone permits repetitive DPs. IfPortunus large cells are first conditioned at more negative voltages than normal, subsequent depolarizing current tends to induce large oscillations, and a second full DP may result in normal medium containing TTX.InPodophthalmus ganglia, single evoked DPs rise more rapidly and are shorter in duration than inPortunus; they are less effectively suppressed by Mn⁺⁺, but show similar Ca⁺⁺-dependency at lowered Ca⁺⁺ levels. Conditioning hyperpolarization slows the rate of rise of single evoked DPs and delays the onset of repetitive DPs during a 3-s pulse. A fast-K⁺ current appears to be more strongly activated inPodophthalmus.The results suggest (1) that oscillatory capability of the DP system may itself play an important role in the generation of rhythmic output by cardiac ganglia; and (2) differences in the V-dependence of Ca^{+ +}, delayed rectifying K⁺ and fast K⁺ currents may be responsible in diverse species for different tendency of the DP system to oscillate in TTX.Abbreviations DP driver potential - Rm membrane resistance - TEA tetraethylammonium - TTX tetrodotoxin - Vm membrane potential     

The role of slow potassium current in phenomena of voltage-dependent action of 4-aminopyridine in amphibian myelinated nerve fibres

The mechanism underlying the voltage-dependent action of 4-aminopyridine (4-AP) is investigated in experiments on amphibian myelinated nerve fibres (Rana ridibunda Pallas) by way of extracellular recording of electrical activity and using activators of potassium current (potassium-free solution and nitric oxide NO) and inhibitors of sodium current (tetrodotoxin). Measurement of action potential (AP) areas was used to evaluate the extent of general membrane depolarization during the activity of nerve fibres. Tetrodotoxin-induced decrease in general membrane depolarization (when the action potential amplitude was reduced by less than 20%) leads to an increase in the duration of depolarizing after-potential (DAP). This supports the dependence of time course of DAP in the presence of 4-AP on ratio of fast and slow potassium channels. In the absence of 4-AP, potassium-free solution and NO increase the potassium current through fast potassium channels (decreasing AP duration, reducing DAP and sometimes producing fast hyperpolarizing after-potential (HAP) after shortened AP), and in the presence of 4-AP these activators increase potassium current through unblocked slow potassium channels (making the development of slow HAP induced by 4-AP more rapid). The increase of slow HAP induced by 4-AP under the influence of potassium-free solution with NO supports the idea that slow HAP is due to activation of slow potassium channels and argues against the notion of removal of block of fast potassium channels. All analyzed phenomena of voltage-dependent action of 4-AP in amphibian myelinated nerve fibers can be accounted for by the activation of slow potassium current produced by membrane depolarization and a decrease of the amount of fast potassium channels involved in the membrane repolarization.     

The positive inotropic action of transmural electrical stimulation of the heart ventricles in the ontogeny of the frog Rana temporaria

Studies have been made of the effect of transmural electrical stimulation on twitch tension produced by atropinized ventricular preparations from tadpoles and adult frogs. In preparations from tadpoles at stage 42 and all the following stages, as well as in adult frogs, transmural electrical stimulation evoked positive inotropic responses which consisted of a slow propranolol-sensitive component or of a slow and fast components. It is highly probable that the slow component is induced by adrenergic transmitter. The fast propranolol-resistant component appears at stage 43. It may be prevented by bretilium being probably induced by a comediator which is released together with the adrenergic transmitter from the sympathetic nerve endings.     

The electrical and mechanical properties of the proleg retractor muscle of the Chinese oak silkmoth larva

ABSTRACT. The main proleg retractor muscle (y) of Antheraea pernyi Guer. (Lepidoptera, Saturniidae) larvae consists of three layers of fibres. The innermost layer of fibres is dually innervated. Cobalt backfills of the two motor neurones, in nerve 2d, showed the somata to be situated ventrally and anteriorly in the same segmental ganglion, ipsilateral to the filled nerve. Intramuscular microelectrode recordings showed excitatory junction potentials (EJPs) of two distinct amplitudes, both of which were relatively slow. However, 26% of the larger amplitude EJPs had an active membrane response. The EJPs and mechanical responses both summated at low stimulation frequencies. Large EJPs resulted in a much greater development of tension than small ones. Extracellular stimulation of nerve lbiii modulated peak tension and peak rate of relaxation.     

Characterization of the neurotoxic constituents of Conus geographus (L) venom

The crude venom of the marine gastropod Conus geographus (L) has been separated into three lethal constituents and their actions at the mammalian neuromuscular junction examined.Chromatography of the venom of Sephadex G-50 gave one toxic fraction, which was resolved by ion exchange chromatography on SP-Sephadex into three toxic components. These components were individually purified by diafiltration and Sephadex G-15 chromatography to give Toxins I,II and III. Toxins I and II in concentrations greater than 5 ug/ml reduced the amplitude of end-plate potentials and miniature end-plate potentials; Toxin I also blocked the depolarization of muscle fibres produced by carbachol; neither toxin affected the generation of action potentials in muscle fibres. Toxin III in concentrations greater than 5 ug/ml rapidly and reversibly blocked the generation of action potentials in muscle fibres; it had no effect on resting membrane potential nor on the amplitude of epps or mepps. It also slowly blocked the compound action potential recorded from isolated sciatic nerves but this was not reversible in the experiments. The rate at which this toxin blocked action potentials was increased by stimulation of the preparation. It is suggested that Toxin III acts by blocking the inward movement of sodium during activity. Toxin III appeared to be a nonadeca or eicosa peptide possibly having a cystine residue in the N-terminal position.     

Effects of antidromic activity in gustatory nerve fibers on taste disc cells of the frog tongue

Summary Antidromic electrical stimulation of the lingual branch of the glossopharyngeal (IX) nerve of the frog was carried out while recording intracellular potentials of taste disc cells.Antidromic activation of sensory fibers resulted in depolarization of cells of the upper layer of the disc and most commonly in hyperpolarization of the cells in the lower layer. These changes in potential exhibited latencies greater than 1 s (Fig. 3), and thus cannot be due to electrotonic effects of action potentials in terminals of IX nerve fibers, which have much shorter conduction times. These cell potentials also showed summation, adaptation and post-stimulus rebound (Figs. 3, 4).Depending upon the chemical stimulus used, antidromic activity produced either depression or enhancement of gustatory fiber discharge in response to taste stimuli (Fig. 5).Alteration of the resting membrane potential by current injection did not significantly modify the antidromically evoked potentials (Fig. 8), whereas chemical stimulation of the tongue did (Fig. 7), indicating that these potential changes are not the result of passive electrical processes.These experimental results indicate that the membrane potential of taste disc cells can be modified by antidromic activity in their afferent nerves. This mechanism may be responsible for peripheral interactions among gustatory units of the frog tongue.The research was supported in part by NIH grant NS-09168.     

Hyperpolarizing potentials induced by Ca-mediated K-conductance increase in hamster submandibular ganglion cells.

The mechanisms of three types of hyperpolarizing electrogenesis in hamster submandibular ganglion cells were analyzed with intracellular microelectrodes. These included (1) spike-induced hyperpolarizing afterpotential (S-HAP), (2) spontaneous transient hyperpolarizing potential (HP), and (3) the hyperpolarizing (H) phase of postsynaptic potential (PSP). Most of these hyperpolarizing potentials were due to conductance increases and reversed polarity at membrane potential (Em) between -70 and -85 mV, which was close to the K-equilibrium potential. The average resting potential of ganglion cells was -53 mV. Action potential overshoot increased slightly in high [Ca2+]0 and decreased in low [Ca2+]0. In most neurons action potentials were completely suppressed by 10(-7)-M tetrodotoxin (TTX). The S-HAP has an initial component due to delayed rectification and a late component. The late component is enhanced by increasing [Ca2+]0, or by applying Ca-ionophore (A23187), TEA, caffeine, or dibutyryl cyclic (DBc-) AMP; it is suppressed by decreasing [Ca2+]0, or by applying Mn2+. Perfusion with Cl--free saline reduced membrane potential slightly but did not modify the S-HAP. Depolarizing pulses also induced hyperpolarizing afterpotential (D-HAP), similar to the S-HAP. Spontaneous transient HPs occurred in some neurons at irregular intervals. HPs were insensitive to TTX but were suppressed by Mn2+. Caffeine induced low frequency rhythmic HPs in many neurons, often alternating with periods of repetitive spiking. The PSP was a monophasic depolarizing (D-) potential in some neurons, but in others the D-phase was followed by a small H-phase. Perfusion with A23187, caffeine or DBc-AMP increased the H-phase of the PSP. Perfusion with K+-free saline or treatment with 10(-5)M ouabain did not abolish the H-phase of PSPs. These membrane potential-dependent phenomena appear to be induced mainly by Ca-mediated K-conductance increases. This mechanism contributes to the regulation of low-frequency repetitive firing in submandibular ganglion cells.     

Inhibition of neuromuscular transmission in the guinea-pig saphenous artery by atriopeptin II

In the guinea-pig saphenous artery, stimulation of perivascular nerves elicited contraction and two types of synaptic potentials: the excitatory junction potential and the slow depolarization. The synaptic potentials were inhibited by atriopeptin II but not by sodium nitroprusside. Exogenous noradrenaline induced membrane depolarization and contraction, and both sodium nitroprusside and atriopeptin II inhibited the contraction but not the depolarization. These results suggest that atriopeptin II has an inhibitory effect both presynaptically at the nerve terminals and postsynaptically on the vascular smooth muscle cells.