OBJECTIVETo explore the impact of niflumic acid (NFA) on connexin 43 (Cx43) expression in smooth muscle cells of mesenteric small artery from spontaneously hypertensive rats (SHR).

METHODSBlood pressure of Wistar rats and spontaneously hypertensive rats (SHR) was measured by the tail cuff method. Relaxation and contraction of mesenteric small artery from Wistar rat and SHR were evaluated by pressure myograph system under various concentrations of NFA. Protein Cx43 expression on primary cultured mesenteric smooth muscle cells from Wistar rats and SHR was detected in the absence and presence of various NFA concentrations by Western blot.

RESULTSPhenylephrine resulted in mesenteric small arteries contraction [(193 ± 13.5) µm], while NFA (3×10(-4) mol/L) could relax the artery [(275 ± 17.1) µm]. The relaxation response in Wistar rats was significantly stronger than that in SHR (P < 0.05). Cx43 expression of the first level branch and the third branch mesenteric artery of SHR were higher than the corresponding branch vessels of Wistar rats, and the Cx43 expression of the third branches of mesenteric artery was higher than that of the first branch (F = 1 014.43, P < 0.01). Cx43 expression in primary cultured mesenteric smooth muscle cells was significantly downregulated post NFA treatment in a concentration dependent manner.

CONCLUSIONIn the SHR mesenteric small arteries, Cx43 may be involved in smooth muscle cells communication, thereby affecting vascular contraction and relaxation responses.NFA could downregulate the expression of Cx43 in SHR mesenteric artery vascular smooth muscle cells and induce vasodilation.

Animals ; Connexin 43 ; metabolism ; Male ; Mesenteric Arteries ; drug effects ; metabolism ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; drug effects ; metabolism ; Niflumic Acid ; pharmacology ; Rats ; Rats, Inbred SHR ; Rats, Wistar ; Vasodilator Agents ; pharmacology

OBJECTIVEThe present study was to investigate the effects of acute hypoxia on the electrophysiological properties and outward current of spiral ganglion cell (SGC).

METHODSSGC of newborn's Sprague Dawley (SD) rats were isolated and digested, primary cultured neurons for 8 h. By perfusion with physical saline solution containing no glucose and low oxygen, SGNs model of acute hypoxia was established. The whole-cell patch clamp recording was used to clarify the effect of hypoxia on the outward currents of SGC.

RESULTSThe outward current of SGC showed characteristics of outward rectification, which contained two major components, one sensitive to the big conductance Ca²⁺-activated K⁺ channels (BKCa) which blocked by TEA, and the other could be suppressed by the KV channel blocker 4-AP. When holding at -60 mV, acute hypoxia increased the outward current of SGC in a voltage-dependent manner, which mainly increased the amplitude of the current activated by the votage ranged from 0 mV to +60 mV, and increased the amplitude of outward current from (1 160.0 ± 129.1) pA to (2 428 ± 239.3) pA (n = 9, P < 0.01) at holding potential of -60mV. By perfusion with the Potassium channel blocker TEA or 4-AP, the former could significantly reduced the increasing of outward currents induced by hypoxia on the SGC, the latter had no significant effect on the outward current increased by the hypoxia.

CONCLUSIONSThese results suggest that acute hypoxia causes neuron hyperpolarization possibly by activating big conductance BKCa of the SGC. When the BKca channels are activated, K⁺ effluxes increase, which induces cell membrane hyperpolarization, and decreases cell excitability, which may affect the conducting function of SGC.

Animals ; Hypoxia ; physiopathology ; Neurons ; cytology ; metabolism ; Patch-Clamp Techniques ; Potassium Channels ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spiral Ganglion ; cytology ; physiopathology