In rat lactotrophs from primary culture an inward-rectifying K¤ current is present which is characterized by sustained inward currents at membrane potentials more positive than −50 mV and by transient K¤ currents at more negative membrane potentials, when measured in high KCl external solution (Corrette et al. 1996). This current is similar to the inward-rectifying K¤ current (IK,IR) in clonal rat pituitary cells (GH×ÏBÜ cells;Bauer et al. 1990). However, in contrast to GH×ÏBÜ cells, the time course of current decay of the inwardrectifying K¤ current in most native lactotrophs exhibited a considerable slowly deactivating current component at negative membrane potentials. Characteristically, the contribution of this slow inward current component varied from cell to cell. A quantitative analysis of this new property of the inward-rectifying K¤ current was not possible because it could not be isolated from the other K¤ currents present in these cells (Corrette et al. 1996).The characteristic gating properties of IK,IR in GH×ÏB6 cells and its selective block by E_4031 and other class III antiarrhythmics (Weinsberg et al. 1997) indicated that it is mediated by K¤ channels expressed by the rat homologue of the human ether-à-go-go-related gene (erg; Sanguinetti et al. 1995;Trudeau et al. 1995). Further experiments provided evidence that the erg-mediated current is indeed a direct correlate of IK,IR in GH×ÏBÜ cells . The pharmacological isolation of the inward-rectifying K¤ current as the E_4031-sensitive current allowed measurement of this current in 5 mÒ external K¤ and demonstrated that in GH×ÏBÜ cells it provides an outward current with a maximum amplitude near −40 mV. This outward current was inhibited by thyrotrophin-releasing hormone (TRH) and this effect is involved in the TRH-induced depolarization characterizing the second phase of the TRH response in GH×ÏBÜ cells (Bauer, 1998 1. The ether-à-go-go-related gene (erg)-like K¤ current in rat lactotrophs from primary culture was characterized and compared with that in clonal rat pituitary cells (GH×ÏBÜ). The class III antiarrhythmic E_4031 known to block specifically erg K¤ channels was used to isolate the erg-like current as the E_4031-sensitive current. The experiments were performed in 150 mÒ K¤ external solution using the patch-clamp technique. 2. The erg-like K¤ current elicited with hyperpolarizing pulses negative to −100 mV consisted of a fast and a pronounced slowly deactivating current component. The contribution of the slow component to the total current amplitude was potential dependent and varied from cell to cell. At −100 mV it ranged from 50 to 85 % and at −140 mV from 21 to 45%. 3. The potential-dependent channel availability curves determined with 2 s prepulses were fitted with the sum of two Boltzmann functions. The function related to the slowly deactivating component of the erg-like current was shifted by more than 40 mV to more negative membrane potentials compared with that of the fast component. 4. In contrast to that of native lactotrophs st...

Besides the known cardiovascular effects of hemorrhagic shock, regular metabolic consequences can be demonstrated in the rabbit: 1. The rise in blood sugar in hemorrhagic shock increases with the amount of blood withdrawn per unit of time. 2. The characteristic rise in blood sugar lasts longer than the phase of the partial exsanguination. 3. In traumatic shock, the rise in blood sugar indicates the degree of severity of the injury earlier than the fall in blood pressure does. The rise in blood sugar is attributable to a reflex increase in glycogenolysis due to catecholamine secretion elicited via baroreceptors in hemorrhagic shock. For the pronounced rise in blood sugar in traumatic shock, an additional receptor is postulated. Supplementary investigation of the blood sugar may possibly enable the extent of the injury to be diagnosed earlier in traumatic shock, and the negative sequelae may be reduced by timely, adequate therapy.