Cytosolic Ca2+, Na+/H+ antiport, protein kinase C trio in essential hypertension.
In: American journal of hypertension, Jg. 7 (1994-02-01), Heft 2, S. 205-12
academicJournal
Zugriff:
The relationships among the cytosolic free Ca2+ (Cai), protein kinase C (PKC), and the Na+/H+ antiport may hold the key to unraveling the causes and origin of essential hypertension. Increased cellular Ca2+, accelerated Cai turnover rate, or both occur in concert with activation of PKC and the Na+/H+ antiport in a variety of cells. In the vascular smooth muscle cell a rise in Cai produces increased tone and in the kidney it enhances sodium retention through stimulation of the Na+/H+ antiport in the renal tubules. In skeletal muscle increased Cai and augmented PKC activity produces insulin resistance, which is a major characteristic of essential hypertension. Moreover, elevation of Cai, in conjunction with increased activities of PKC and the Na+/H+ antiport, may exert trophic effects on the vasculature and the heart, thereby explaining the narrowing of the vascular lumen in peripheral arteries and the cardiac hypertrophy of long-standing hypertension. Because essential hypertension is a common disorder, its evolutionary advantage in primeval times could rest in skeletal muscle, where higher Ca2+ stores and increased Na+/H+ antiport activity enhanced muscular performance and provided a crucial survival element.
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Cytosolic Ca2+, Na+/H+ antiport, protein kinase C trio in essential hypertension.
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Autor/in / Beteiligte Person: | Aviv, A |
Zeitschrift: | American journal of hypertension, Jg. 7 (1994-02-01), Heft 2, S. 205-12 |
Veröffentlichung: | 2013- : Oxford : Oxford University Press ; <i>Original Publication</i>: [New York, NY] : Elsevier, [c1988-, 1994 |
Medientyp: | academicJournal |
ISSN: | 0895-7061 (print) |
DOI: | 10.1093/ajh/7.2.205 |
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