Reactive arthritis (ReA) is typically preceded by sexually transmitted disease or gastrointestinal infection. An association has also been reported with bacterial and viral respiratory infections. Herein, we report the first case of ReA after the he severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This male patient is in his 50s who was admitted with COVID-19 pneumonia. On the second day of admission, SARS-CoV-2 PCR was positive from nasopharyngeal swab specimen. Despite starting standard dose of favipiravir, his respiratory condition deteriorated during hospitalisation. On the fourth hospital day, he developed acute respiratory distress syndrome and was intubated. On day 11, he was successfully extubated, subsequently completing a 14-day course of favipiravir. On day 21, 1 day after starting physical therapy, he developed acute bilateral arthritis in his ankles, with mild enthesitis in his right Achilles tendon, without rash, conjunctivitis, or preceding diarrhoea or urethritis. Arthrocentesis of his left ankle revealed mild inflammatory fluid without monosodium urate or calcium pyrophosphate crystals. Culture of synovial fluid was negative. Plain X-rays of his ankles and feet showed no erosive changes or enthesophytes. Tests for syphilis, HIV, anti-streptolysin O (ASO), Mycoplasma, Chlamydia pneumoniae, antinuclear antibody, rheumatoid factor, anticyclic citrullinated peptide antibody and Human Leukocyte Antigen-B27 (HLA-B27) were negative. Gonococcal and Chlamydia trachomatis urine PCR were also negative. He was diagnosed with ReA. Nonsteroidal Anti-Inflammatory Drug (NSAID)s and intra-articular corticosteroid injection resulted in moderate improvement.

1. After blocking both the hyperpolarization-activated current and the membrane K+ conductance, depolarizations from -80 mV to between -70 and -50 mV induced a sustained current in sino-atrial node cells. We have tentatively designated this current ISt. 2. I't was blocked by both organic and inorganic Ca2+ channel blockers, but was insensitive to tetrodotoxin (30 uM). Isoprenaline increased ISt. 6. The transitional sino-atrial node cell had minimal amplitude of I't.7. These characteristics of ISt are qualitatively comparable to those of the monovalent cation conductance of the L-type Ca2+ channel induced by depleting external divalent cations to the micromolar range. We conclude that ISt is generated by a novel subtype of L-type Ca2+ channel.

Individual types of ion channels play a unique role in generating membrane excitation based on their gating and conductance properties. The contribution of a given ion channel has been extensively discussed in original experimental papers. However, the complicated interactions of more than 10 ionic current systems through a common membrane potential make it difficult to clarify their roles in membrane excitability. ; I ext , current applied through the electrode (pA); I ha , hyperpolarization-activated cation current (pA); I Kl , inward rectifier K ϩ current (pA); I KACh , ACh-activated K ϩ current (pA); I KATP , ATP-sensitive K ϩ current (pA); I Kpl , non-specific, voltage-dependent outward current (plateau current) (pA); I Kr , delayed rectifier K ϩ current, rapid component (pA); I Ks , delayed rectifier K ϩ current, slow component (pA); I l , total of background current (time-independent) components (pA); I l(Ca) , Ca 2ϩ -activated background cation current (pA); I Na , Na ϩ current (pA); I NaCa , Na ϩ /Ca 2ϩ exchange current (pA); I NaK , Na ϩ /K ϩ pump current (pA); I net X, whole cell current carried by ion X (pA); I RyR , Ca 2ϩ release through the RyR channel in SR (pA); I SR L, Ca 2ϩ leak from the SR (pA); I SR U, Ca 2ϩ uptake in the SR (pA); I SR T, Ca 2ϩ transfer from the SR uptake site to the release site (pA); I st , sustained inward current (pA); I to , transient outward current (pA); I tot , total current of ion channels and ion exchangers (pA); K mX , Michaelis constant for ion X binding; N, total number of channels; P x , convert factor (pA mM Ϫ1 ); p(X), probability of state X in a multiple states gate; R, gas constant, 8.3143 C mV K Ϫ1 mmol Ϫ1; SA factor, scaling factor for SA node cell sarcoplasmic reticulum (0.03); T, absolute temperature K; T, T*, TCa, TCa*, the 4 states of NL model (1996) ).

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SUMMARY1. A class of Ca2+-activated non-selective cation channel was identified in ventricular cells, which were dissociated from adult guinea-pig hearts using collagenase.2. Under cell-attached conditions the patch electrode filled with a Na+-rich solution recorded no obvious single-channel current at the resting membrane potential. Subsequent superfusion of the ventricular cell with a Na+-free Tyrode solution induced an inward-going single-channel current as well as contracture of the cell. Kinetics of this channel were not affected by varying the membrane potential.3. Single-channel currents showing a conductance similar to those observed in the cell-attached patches were recorded in isolated inside-out membrane patches when the inner side of the membrane was exposed to a free Ca2+ concentration ([Ca2+]i) higher than 0 3 /LM. The slope conductance of the channel was 14-8 + 2-9 pS (mean+s.D., n = 17) at 20-25 'C.4. The reversal potential examined in the inside-out patch was about 0 mV irrespective of the Na+-rich, K+-rich, Li+-rich or Cs+-rich solutions on either side of the membrane, thereby indicating that the channel was almost equally permeable to these cations. 7. Contribution of the channel to the whole-cell current was discussed based on an estimation of the channel density, presumably about 0-04 -04//sm2. Maximum activation of the channel would produce 7-2 72 nS of membrane conductance, which would explain the reported magnitude of the Ca2+-mediated background

A rapidly activating component of delayed rectifier K+ current (IK,r) was dissected using a selective blocker, E-4031, during the action potential clamp (AP clamp) in rabbit sinoatrial node cells. Application of E-4031 induced a large compensation current, of which amplitude was similar to or larger than the net current during repolarization and was maximum (2.2 +/- 0.2 pA/pF) at -46.0 +/- 1.8 mV (n = 13). During the slow diastolic depolarization, the compensation current gradually decayed and then abruptly decreased at the peak of action potential. The time-dependent change of IK,r was calculated using a mathematical model, in which independent gates of activation and inactivation were assumed based on the whole cell voltage-clamp experiments. The reconstructed IK,r corresponded well with the E-4031-sensitive current measured by the AP clamp method. Partial block of IK,r by E-4031 in spontaneously beating cells decreased the action potential amplitude, maximum rate of rise, and maximum rate of repolarization and induced a positive shift of the maximum diastolic potential. Complete block of IK,r terminated the spontaneous action potential at -37.4 +/- 2.9 mV (n = 3). It is concluded that IK,r plays an essential role in determining the maximum diastolic potential and ensures the firing of the following action potential in sinoatrial node cells.

Systemic inflammation induces various adaptive responses including tachycardia. Although inflammation-associated tachycardia has been thought to result from increased sympathetic discharge caused by inflammatory signals of the immune system, definitive proof has been lacking. Prostanoids, including prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2) and thromboxane (TX) A(2), exert their actions through specific receptors: DP, EP (EP(1), EP(2), EP(3), EP(4)), FP, IP and TP, respectively. Here we have examined the roles of prostanoids in inflammatory tachycardia using mice that lack each of these receptors individually. The TXA(2) analog I-BOP and PGF(2alpha) each increased the beating rate of the isolated atrium of wild-type mice in vitro through interaction with TP and FP receptors, respectively. The cytokine-induced increase in beating rate was markedly inhibited in atria from mice lacking either TP or FP receptors. The tachycardia induced in wild-type mice by injection of lipopolysaccharide (LPS) was greatly attenuated in TP-deficient or FP-deficient mice and was completely absent in mice lacking both TP and FP. The beta-blocker propranolol did not block the LPS-induced increase in heart rate in wild-type animals. Our results show that inflammatory tachycardia is caused by a direct action on the heart of TXA(2) and PGF(2alpha) formed under systemic inflammatory conditions.