The results suggest that non-fatal, whole-body gamma-irradiation suppresses large conductance, calcium-activated potassium channels, which control the driving force for Ca2+ entry and therefore Ca2+ dependent nitric oxide (NO) synthesis in endothelial cells. This may contribute, in part, to radiation-induced endothelium dysfunction and an increase in arterial blood pressure.

The effects of hypoxia on whole‐cell current in single smooth muscle cells and on a high K+‐induced contraction of strips of the guinea‐pig taenia caeci were studied. In physiological salt solution (PSS) and K+‐based pipette solution, hypoxia (PO2= 20 mmHg) reversibly inhibited both the inward Ca2+ current (ICa) and outward Ca2+‐activated K+ current (IK(Ca)) components of the whole‐cell current. In PSS and Cs+‐based pipette solution, hypoxia reversibly suppressed ICa by 30 ± 5% at 0mV. When Ba2+ was used as a charge carrier, the IBa was suppressed by hypoxia in a potential‐dependent manner, with the maximum of 40 ± 7% at +10mV. Alterations of concentrations of egta, GDBβS or ATP in the pipette solution did not change the inhibitory effects of hypoxia on ICa and IBa. In PSS with 2 mm CaCl2 replaced by CoCl2, hypoxia did not affect the Ca2+ influx‐independent potassium current. In cells voltage clamped at ‐20 mV hypoxia reversibly inhibited the spontaneous transient outward currents. The response of high K+‐contracted taenia caeci to hypoxia was composed of an initial rapid relaxation followed by a small transient contraction and slow relaxation. The transient contraction was blocked by atropine (1–10 μm), while relaxations were unaffected by atropine and guanethidine (10 μm). The results show that hypoxia reversibly inhibits ICa and secondarily suppresses IK(Ca) due to decreased Ca2+ influx through Ca2+ channels. It is suggested that inhibition of ICa was responsible for the rapid relaxation, whereas transient contraction may have been due to release of acetylcholine from nerve terminals upon hypoxia.

1 The effects of nifedipine (Nif) and its illuminated nitroso product nitrosopine (NTP) were investigated on lipid peroxidation, KCl elevated smooth muscle tension, and ionic currents of single smooth muscle cells. 2 Illumination of Nif at 400-700 nm within 24-48 h changed it completely to a potent antioxidant, NTP. 3 Nif relaxed the KCl-induced contractions of guinea-pig taenia caeci and rat aorta and reduced the amplitude of the evoked inward Ca2" current of taenia caeci cells in a concentration-dependent manner.NTP (up to 100 pM) was ineffective in this respect. Pretreatment by NTP (10 pM) did not affect the actions of Nif. 4 The evidence suggests that NTP, generated by day-light illumination from Nif, exerts antioxidant activity but is devoid of voltage-dependent Ca2" channel (VDC) blocking property and does not interfere with the action of Nif on the smooth muscle cell membrane VDC.

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