Latch phenomenon

On the basis of the effects of ADP on cross-bridge kinetics, the tight ADP binding in smooth muscles was proposed to explain the latch phenomenon, as metabolic alterations during contraction might involve an increase in MgADP concentration (Nishiye et al.,... 

Constraints imposed by caldesmon that disrupt potentiation may not block myosin docking on actin. This process of modulating ATPase could in turn lead to or permit the development of the latch-state of tension maintenance displayed by tonic smooth muscles and observed at low Ca + concentration. This phenomenon probably involves stable actin-myosin binding and is associated with low actomyosin ATPase activity (Hai and Murphy, 1988 McDaniel et al, 1990). As envisioned, such tension maintenance would be incompatible with a troponin-tropomyosin form of regulation since tropomyosin would in that case block myosin docking at low Ca + concentrations. Hence, the caldesmon-tropomyosin system may be adapted for muscles that enter a latch-state. 

The recruitment of blood-borne cells to evolving atherosclerotic lesions appears to be specific for monocytes and requires the inducement of specific adhesion molecules on both the endothelial cell surface and the recruited monocytes. The adhesion process appears to be a multistep phenomenon. In the initial stages E- or P-selectin expressed by stimulated endothelial cells binds to carbohydrates borne by surface molecules on monocytes. Expression of P-selectin on vascular endothelial cells slows white blood cells and causes them to roll along the endothelial surface. Other cell adhesion molecules, including ICAM-1 and vascular cell adhesion molecule 1, then latch onto and stop the white blood cells completely, prior to their migration out of the blood vessel and into the target tissue. 

Figure 6.12 Figures (a) and (b) demonstrate currents that cause the bistable latch to flip before it is clocked. Current must stay within an acceptable range Umj. - Imji) to prevent this phenomenon.

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