By Robert G. Carroll
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Extra resources for Elsevier’s Integrated Physiology
4-5). Characterization of a signaling molecule as an endocrine, autocrine, or paracrine agent is difﬁcult, since one molecule can serve each of these purposes in the same system. Norepinephrine released at a sympathetic nerve terminal will bind to an α2-adrenergic receptor on the presynaptic axon CELL MEMBRANE terminal (autocrine), bind to the postsynaptic cell receptor (neurotransmitter), and diffuse away from the synaptic cleft, where it can bind to receptors on adjacent cells (paracrine) or diffuse into the circulation, where it can be carried to distant cells (endocrine) (Fig.
An increase in plasma H+ (acidosis) causes an increase in H+ entry into cells and an increase in K+ movement out of cells. Acidosis is often associated with hyperkalemia. 25 26 BODY FLUID DISTRIBUTION Urinary K+ excretion is determined in the short term by tubular load, by luminal pH, and by aldosterone (see Chapter 11). The long-term control of K+ balance also relies on tubular load and on aldosterone. Hypokalemia can be caused by hyperaldosteronism, and hyperkalemia by impaired aldosterone secretion in Addison’s disease.
Negatively charged compared with the outside. In contrast, positively charged K+ would be attracted toward the inside of a cell whose inside was negatively charged compared with the outside. Two separate gradients affect K+ movement: the chemical driving force from diffusion and an electrostatic driving force from the electrical charge. There can be a balance between these driving forces, so that the outward diffusional tendency TABLE 4-1. 0001 mEq/L +144 mV Cl– 110 mEq/L 20 mEq/L –46 mV for K+ is offset by the inward electrostatic attraction.