[1] We digitized teleseismic and regional records of the 1944 Tonankai earthquake. We used the multiple time window method to invert these records for the spatial and temporal distribution of slip and rake. We assume a 220 Â 140 km fault with a spacing of 20 Â 20 km and a maximum rupture velocity of 2.5 km/s. The inversion resolved an asperity along the accretionary wedge and under the Shima and Atsumi Peninsulas. The rupture propagated from southwest to northeast, and there was little slip near the hypocenter, consistent with the absence of uplift in the overlying submarine forearc basin. The peak slip is 2.3 m, and the total seismic moment is 2.4 Â 10 28 dyn cm (M w 8.2). We compared the predicted and observed vertical geodetic displacements and inferred that the limit of rupture is consistent with the change from subsidence to uplift west of the Atsumi Peninsula. This suggested that the earthquake did not rupture the plate interface in the Tokai gap. We modeled the tsunami using sea-bottom displacements generated from this slip model. The tide gauge amplitudes and frequency content are consistent with those predicted. Resolution tests from inverting synthetic seismograms computed using a simplified slip model indicated that the combination of teleseismic and regional data sets best recovers the asperity locations and peak slips given similar station geometry and degrees of freedom. An inversion of the synthetic regional data set indicates that slip artifacts can occur early in the rupture process due to many clipped records while the inversion of synthetic teleseismic data set had less resolution and recovered only 50% of the peak slip.

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1. Exogenously administered endothelin (ET) modulates the activity of cardiovascular and respiratory neurons in the central nervous system (CNS) and, thus, affects arterial blood pressure (ABP) and ventilation. However, a physiological role(s) for endogenous ET in the CNS has not been elucidated. To address this question, we examined ABP and ventilation in mutant mice deficient in ET-1, ETA and ETB receptors and endothelin-converting enzyme-1, which were made by gene targeting. 2. Respiratory frequency and volume was measured in mice by whole body plethysmography when animals breathed normal room air and hypoxic and hypercapnic gas mixtures. A few days after respiratory measurements, a catheter was implanted into the femoral artery under halothane anaesthesia. On the following day, the ABP of awake mice was measured through the indwelling catheter and heart rate was calculated from the ABP signal. After 2 h ABP measurement, arterial blood was collected through the catheter and pH and the partial pressures of O2 and CO2 were measured by a blood gas analyser. 3. Compared with corresponding controls, the mean (+/- SEM) ABP in ET-1+/- and ETB-deficient mice was significantly higher (118 +/- 2 vs 106 +/- 3 mmHg for ET-1+/- (n = 22) and ET-1+/+ (n = 17) mice, respectively; 127 +/- 3 vs 109 +/- 4 mmHg for ETB-/s (n = 9) and ETB+/s (n = 9) mice, respectively; P < 0.05 for both). In ET-1+/- mice, PCO2 tended to be higher and PO2 was significantly lower than corresponding values in ET-1+/+ mice. Under resting conditions, there was no significant difference in respiratory parameters between mutants and their corresponding controls. However, reflex increases of ventilation to hypoxia and hypercapnia were significantly attenuated in ET-1+/-, ET-1-/- and ETA-/- mice. 4. In another series of experiments in ET-1+/- mice, we found that sympathetic nerve activity (SNA) was augmented and reflex excitation of phrenic nerve activity (PNA) in response to hypoxia and hypercapnia was blunted. Attenuation of the reflex PNA response to hypercapnia was also observed in the medulla-spinal cord preparation from ET-1-/- mice. 5. Elevation of ABP in ETB-deficient mice was most likely due to a peripheral mechanism, because SNA and respiratory reflexes were not different from those in control animals. 6. We conclude that endogenous ET-1 plays an important role in the central neural control of circulation and respiration and that ETA receptors mediate this mechanism.

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