Resistance Resting membrane potential

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

Tetrodotoxin is believed to be synthesized by a bacterial or dinoflagellate species. Tetrodotoxin blocks axonal transmission by lowering the conductance of sodium at nodes of Ranvier. It is a selective sodium channel blocker that can block nerve and muscle conduction action potentials are blocked while resting membrane potentials and resting membrane resistance are not affected. Tetrodotoxin does not... 

Fig. 27. Intracellular recordings from a granule cell in the hippocampal slice to show the response to the iontophoretic application of GABA. (A) Voltage record made on moving film to show the way in which an intracellular injection of a depolarizing ramp of current is used to test the cell s excitability. Every alternate second a hyperpolarizing current pulse is used to measure the input resistance. As shown more clearly in the single shots in (B) and (C), the application of GABA inhibited the spike discharge evoked by the ramp, caused a substantial decrease in the input resistance, and produced a small depolarization with respect to resting membrane potential [dotted line in (B)]. (From Assaf et ai, 1981.)...

Fig. 41. Opioid peptide (D.ALA) blocks spontaneous ipsp s in hippocampal pyramidal cell. The responses were recorded on running film with a 3 M KCl-filled microelectrode in the absence of pentobarbital. To block spontaneous action potentials the membrane was hyper-polarized to - 69 mV while the film records were obtained. Switching to a solution containing 5 pM D.ALA for 6 min eliminates the spontaneous depolarizing potentials. Addition of 2 xM naloxone to the D.ALA-containing solution reverses the depressant action of D.ALA. The resting membrane potential was - 53 mV in control, - 56 mV in D.ALA, and - 50 mV in D.ALA + NAL. The faster decay of the potentials in D.ALA + NAL was due to a fall in membrane resistance resulting from imperfect sealing of the electrode when these records were obtained. (From Nicoll et al., 1980.)...

Diazoxide is an effective and relatively long-acting parenterally administered arteriolar dilator that is occasionally used to treat hypertensive emergencies. Injection of diazoxide results in a rapid fall in systemic vascular resistance and mean arterial blood pressure associated with substantial tachycardia and increase in cardiac output. Studies of its mechanism suggest that it prevents vascular smooth muscle contraction by opening potassium channels and stabilizing the membrane potential at the resting level. 

Calcium performs a variety of cellular functions in muscle and nerve that ultimately result in muscular contraction. Excellent descriptions of calcium s function in muscle and nerve are to be found in the reviews by Hoyle (37), Cohen (38), and Robertson (39). At the neuromuscular junction, the excitable cells are very sensitive to changes in extracellular concentrations of calcium. Curtis (40) and Luttgau (41) described a fall in the resting action potential and electrical resistance when the extracellular calcium concentration fell below 10 M. The action potential and electrical resistance returned to normal following addition of calcium to this vitro preparation. The magnitude of the Initial muscle membrane action potential, that which regulates the propagation of further muscle contraction, is also mediated by the extracellular calcium concentration. While the inward flow of sodium ions from the extracellular space remains the dominant factor in the mechanism of muscle membrane depolarization, calcium ion flux appears to mediate the cell s permeability to sodium ions. This effect is particularly true in cardiac tissue (W). 

The nerve cell membrane, which is about 5 nm thick, consists primarily of lipids and proteins. When at rest it is permeable basically to potassium ions (although its resistance in this state is rather high, ca. 10 fl cm ), and therefore the electric potential difference between the inner and outer solutions (this difference is called the membrane potential or simply the potential) is negative at rest and amounts to a few tens of mV (about -60 mV on the giant axon). The membrane capacitance is of the order of 1 /iF/cm. Thus a neuron membrane is already polarized when at rest. If some external action shifts the potential from its value at rest to more negative values (its absolute value increasing), the resultant situation is usually called hyperpolarization. Potential shift in the positive direction is called depolarization. If the potential reverses its sign and becomes positive the term is overshoot. ... 

The standing potential is maintained because, although there are both electrical and concentration gradients (a variation of high to low concentration) that induce the excess sodium cations to enter the cell and potassium cations to migrate out, the channels for such movements are normally closed so that the neural cell membrane remains impermeable or highly resistant to ion passage in the rest state. 

An intrinsic ionic charge gradient across the membrane exists because of semipermeable nature of membrane, which maintains a difference in the concentration of the ions between the cytosol and the extracellular matrix. This difference results in a definite potential across membrane of the normal cells, which is called the resting potential. Normal plant cells, mammalian muscle cells, and neurons have resting potential values of about —120, —90, and —70 mV, respectively. Along with the resistance to the flow of ions, membrane also exhibits a capacitance. Cm, which is given by... 

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