1. Circular muscle strips of the guinea-pig gastric muscle produced spontaneous electrical activity in the form of slow waves. The slow wave amplitude, maximum rate of rise, duration, and frequency were 31 mV, 60 mV sec^-1, 4.3 sec, and 4.3 min^-1 on average, respectively. These parameters were not appreciably affected by 3μM nifedipine or nicardipine, even following membrane depolarization with 60mM K⁺.
2. Ni²⁺ (1-100μM) increased slow wave amplitude and frequency, but reduced the rate of rise, accompanied by membrane depolarization. The rate of rise and depolarization slowly recovered to the control values in the continuous presence of Ni²⁺, but slow wave frequency remained high. The recovery after wash-out was very poor particularly when a high concentration of Ni²⁺ was applied.
3. The effects of Co²⁺ were fundamentally the same as those of Ni²⁺.
4. Removal of external Ca²⁺ slowly reduced the rate of rise and amplitude of the slow waves in the absence and the presence of Ni²⁺ and Co²⁺, although the effects were reduced in the presence of these metal ions.
5. Concentrations of Ni²⁺ and Co²⁺ greater than 1mM suppressed the slow waves. However, when the external Na⁺ was replaced with N-methyl-D-glucamine during the suppression, nearly normal electrical activity was resumed.
6. Since slow waves were not significantly affected by nifedipine (3μM) and Ni²⁺ (100 μM), the inward currents generating slow waves do not seem to flow through L-type Ca²⁺ channels or typical T-type Ca²⁺ channels. Slow waves are probably potentiated by Ni²⁺ and Co²⁺ acting intracellularly. These ions at higher concentrations seem to inhibit the pacemaker activity more powerfully than they do the inward currents responsible for slow wave generation.

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The facial vein in several species has been shown to have unusual properties, including exhibition of spontaneous myogenic tone and relaxation to norepinephrine (NE). The present study was undertaken to characterize the relaxant effect of 5-hydroxytryptamine (5-HT) on the rabbit facial vein. An isolated ring preparation of the rabbit facial vein exhibited intrinsic tone when it was stretched and the spontaneous contraction continued for hours. 5-HT concentration-dependently relaxed facial veins exhibiting spontaneous contraction. The relaxation was not inhibited by rubbing the endothelium or by N^G-nitro-L-arginine (10^-4 M), a nitric oxide (NO) synthase inhibitor. The 5-HT-induced relaxation was also unaffected by pretreatment with indomethacin (10^-5 M), a cyclooxygenase inhibitor, and propranolol (10^-6 M), a both β-adrenoceptor and 5-HT_1B-receptor antagonist. In contrast, 5-HT-induced relaxation of the facial vein was concentration-dependently antagonized by methysergide (10^-7 M and 10^-6 M), a non-selective 5-HT₁- and 5-HT₂- receptor antagonist, but not by NAN-190 (10^-6M) and SDZ-205, 557 (10^-6M), antagonists for 5-HT_1A and 5-HT₄-receptors, respectively. A higher (10^-6M), but not lower (3×10^-7M) concentration of ketanserin, a 5-HT₂-receptor antagonist, slightly inhibited the 5-HT-induced relaxation. These results indicate that 5-HT-induced relaxation is not due to indirect mechanisms mediated by NE released from the sympathetic nerve terminals, or by endogenous prostanoid and endothelium-derived relaxing factor (EDRF=NO) released from the vascular tissues, but due to a direct effect on the 5-HT receptors located on vascular smooth muscle cells. However, the subtype of 5-HT receptor that produces relaxation of the rabbit facial vein remains to be clarified.

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Muscarinic receptor subtypes that involved in cholinergic responses in rat iris were identified by reverse transcription-polymerase chain reaction (RT-PCR) analysis. mRNAs encoding m2, m3, and m4 subtypes were abundantly expressed in iris, whereas ml and m5 subtypes were not detected. Selective amplification of the coding regions of m2, m3, and m4 subtypes in iris was carried out using specific primers based on the sequence of each subtype previously cloned from rat brain and heart by RT-PCR. The amino acid sequence for iris m2 was different from published heart and genomic m2 by nine and one residue (s), respectively. It was also found that the sequence for m2 that in brain, heart, and several smooth muscles determined in the present study is completely identical to that in iris but not to that reported previously in heart. The sequence for iris m4 was completely identical to that for m4 in brain. The sequence identity between m3 subtype in iris and that in brain is 99.3%, with four amino acid substitutions at the sites of the position 165 and 184 in the edge of second intracellular loop and the sites of the position 337 and 406 in the central of i3 loop.It was found that iris m3 is slightly but substantially different in amino acid sequence from that in brain of the rat.

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Eugenol (≤0.1 mM) inhibited the contractions induced by various stimulants, such as 90 mM extracellular K⁺ solution ([K⁺] ₀), histamine and noradrenaline in the rabbit ear artery. Inhibitory actions of eugenol occurred in a concentration-dependent manner, however, eugenol more dominantly inhibited the histamine-induced contraction than those induced by either 90 mM [K⁺] ₀ solution or noradrenaline. Removal of both endothelium and adventitia did not change the inhibitory actions of eugenol on the 90 mM [K⁺] ₀- and noradrenaline-induced contractions, however, attenuated those on the histamine-induced contraction. Chlorphenylamine abolished the histamine-induced contraction, but neither cimetidine, ranitidine nor thioperamide modified the eugenol actions on the contractions induced by histamine. Pretreatment with nitric oxide syntheses inhibitor N^G-nitro-L-arginine (LNNA;100μM), but not soluble guanylate cyclase inhibitor methylene blue (MB;10μM), prevented endothelium/adventitia-dependent augmentation of the eugenol-induced relaxation on the histamine-induced contraction. When an intact tissue, but not an endothelium/ adventitia-denuded tissue, was placed at the up-stream close to the other denuded preparation (test preparation), histamine-induced contraction observed in the test preparation tended to be augmented. Similarly, eugenol-induced relaxation was also augmented by the same treatment.
Eugenol (0.3 mM) inhibited the excitatory junction potentials (EJPs) without hyperpolarization of the membrane. However, a high concentration of eugenol (1 mM) slightly hyperpolarized the membrane (ca. 5 mV). No transient enhancement of amplitude of EJP was recorded.
These results suggest that eugenol may inhibit the histamine-induced muscle contraction directly, and the inhibition is augemented by the adventitia and endothelium partly by vasoactive substances, which were released from the adventitia/endothelium-derived substances in rabbit ear artery.

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