Hormonal regulation of peptide receptors and target cell responses.

Regulation of plasma membrane receptors for peptide hormones by the prevailing ligand concentration often causes altered target cell function. Receptor number is determined by hormone-induced changes in membrane conformation, irreversible ligand binding, and processing of ligand-receptor complexes during hormone action.     

Calcium transients in aequorin-injected frog cardiac muscle.

The Ca2+ -sensitive bioluminescent protein aequorin was microinjected into cells of frog atrial trabeculae to study intracellular calcium transients associated with excitation-contraction coupling. The amplitude of the aequorin signal increased with extracellular Ca2+ concentration and stimulus frequency, but decreased with stretch. Isoprenaline and acetylstrophanthidin both increased the amplitude, but had strikingly different effects on the time course of the signal.     

Hormonal regulation of K+-channel messenger RNA in rat myometrium during oestrus cycle and in pregnancy

The dramatic enhancement of smooth-muscle excitability in the uterus which occurs at oestrus and at term in pregnant rats is closely related to increased blood oestrogen concentrations. How oestrogen alters the electrical properties of myometrial cells is unclear, although electrical coupling between cells has been shown to increase. Many examples are known of changes in cellular excitability involving modification of existing ion channels by second-messenger pathways. Steroid hormones, in contrast, are generally thought to influence cellular processes mainly through effects on gene expression, inducing the synthesis of new proteins. Previous work, using an oocyte translation system, has shown that a very slowly activating, voltage-dependent K+ current can be expressed from the poly(A)+ RNA of oestrogen-treated rat uteri. We report here that the messenger RNA species producing this channel is rapidly and reversibly induced in the presence of oestrogen, as shown by the appearance and disappearance of this mRNA during the oestrous cycle, its emergence at the end of pregnancy, and its presence or absence following hormonal treatments. These results suggest that oestrogen controls the expression of a voltage-dependent ion channel in uterine smooth muscle cells.     

Oscillations of intracellular Ca2+ in mammalian cardiac muscle

Contraction of cardiac muscle depends on a transient rise of intracellular calcium concentration ([Ca2+]i) which is initiated by the action potential. It has, however, also been suggested that [Ca2+]i can fluctuate in the absence of changes in membrane potential. The evidence for this is indirect and comes from observations of (1) fluctuations of contractile force in intact cells, (2) spontaneous cellular movements, and (3) spontaneous contractions in cells which have been skinned to remove the surface membrane. The fluctuations in force are particularly prominent when the cell is Ca2+-loaded, and have been attributed to a Ca2+-induced Ca2+ release from the sarcoplasmic reticulum. In these conditions of Ca2+-loading the normal cardiac contraction is followed by an aftercontraction which has been attributed to the synchronization of the fluctuations. The rise of [Ca2+]i which is thought to underlie the aftercontraction also produces a transient inward current. This current, which probably results from a Ca2+-activated nonspecific cation conductance, has been implicated in the genesis of various cardiac arrhythmias. However, despite the potential importance of such fluctuations of [Ca2+]i their existence has, so far, only been inferred from tension measurements. Here we present direct measurements of such oscillations of [Ca2+]i.     

心肌3种应力的并联桥本构模型

为了深入研究心肌的力学性质,通过理论推导,提出了心肌的并联桥本构模型。该模型包含心肌的被动力、主动力和生长应力三种模型。被动力模型是一个各向异性的非线性弹性模型,其力学性质主要决定于心肌的纤维方向的力学性质;结合自由钙离子浓度演化方程和横桥动力学模型,发展了心肌的主动力模型,在周期化钙离子浓度场的基础上,得到随时间周期变化的主动应力;提出了生长应力的概念,建立基于生长因子表达变化的生长应力模型。研究结果表明,并联桥本构模型完备地反映了心肌的被动力、主动力和生长应力3种应力状态模型。