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K-mediated aldosterone secretion

An increase in the extracellular K+ concentration from 2 to 8 mM (the limits of the physiological range) leads to a 4-5-fold increase in the rate of aldosterone secretion by the adrenal glomerulosa cell [24,25]. This increase in [K+] leads to a depolarization of the plasma membrane of the cell. This depolarization causes the opening of two types of voltage-dependent Ca2+ channel in this membrane, and thus to a 4-fold increase in the rate of Ca2+ influx. The total cell calcium and the [Ca2+]j both [Pg.103]

Glucagon has a number of effects on various aspects of hepatocyte metabolism. Many of these are covered in other parts of this treatise. The focus of our present attention is the identity of the intracellular messengers which mediate the effects of glucagon. In considering this question, it is first necessary to recognize that different mechanisms operate when cells are exposed to low or high concentrations of glucagon. [Pg.105]

When hepatocytes are exposed to a low concentration of glucagon (1012 M), the hormone interacts with one class of receptors linked to phospholipase C and the hydrolysis of PIP2 [26]. These events lead to an increase in Insl,4,5P3, and presumably to both a mobilization of intracellular Ca2+ and an increase in Ca2+ influx rate. Hence, low concentrations of glucagon act exclusively via the PI system. [Pg.105]


See other pages where K-mediated aldosterone secretion is mentioned: [Pg.103]    [Pg.106]   


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