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| Untersuchte Arbeit: Seite: 25, Zeilen: 1ff (entire page) |
Quelle: Lang et al 2006 Seite(n): 1151, 1152, 1163, Zeilen: 1151: last lines, 1152: 1ff; 1163: figure |
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Figure nr. 3 - Dual role of SGK1 in the maintenance of salt homeostasis and blood pressure. SGK1 plays a dual role in the regulation of salt balance, i.e., in the stimulation of both renal Na+ reabsorption and salt appetite. SGK1 contributes to aldosterone- and insulin-induced stimulation of renal Na+ reabsorption. The increased extracellular fluid volume (ECV) enhances the cardiac output (C.O.), thus increasing mean arterial blood pressure (MAP). The enhanced blood pressure leads to pressure natriuresis and thus secondarily increases renal salt excretion, eventually counteracting renal salt retention. A II, angiotensin II; R, total peripheral vascular resistance. SGK1 participate in the regulation of transport, hormone release, neuroexcitability, cell proliferation, and apoptosis. SGK1 contributes to Na+ retention and K+ elimination of the kidney, mineralocorticoid stimulation of salt appetite, glucocorticoid stimulation of intestinal Na+/H+ exchanger and nutrient transport, insulin-dependent salt sensitivity of blood pressure and salt sensitivity of peripheral glucose uptake, memory consolidation, and cardiac repolarization. |
SGKs participate in the regulation of transport, hormone release, neuroexcitability, cell proliferation, and apoptosis. SGK1 contributes to Na+ retention and K+ elimination of the kidney,
[page 1152] mineralocorticoid stimulation of salt appetite, glucocorticoid stimulation of intestinal Na+/H+ exchanger and nutrient transport, insulin-dependent salt sensitivity of blood pressure and salt sensitivity of peripheral glucose uptake, memory consolidation, and cardiac repolarization. [page 1163]
FIG. 5. Dual role of SGK1 in the maintenance of salt homeostasis and blood pressure. SGK1 plays a dual role in the regulation of salt balance, i.e., in the stimulation of both renal Na+ reabsorption and salt appetite. SGK1 contributes to aldosterone- and insulin-induced stimulation of renal Na+ reabsorption. The increased extracellular fluid volume (ECV) enhances the cardiac output (C.O.), thus increasing mean arterial blood pressure (MAP). The enhanced blood pressure leads to pressure natriuresis and thus secondarily increases renal salt excretion, eventually counteracting renal salt retention. A II, angiotensin II; R, total peripheral vascular resistance. |
The source is not mentioned. |
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