| Literature DB >> 4039776 |
Abstract
The hypothesis outlined below shows how an underlying functional (genetic or acquired) defect in renal excretion (undetectable by standard renal function tests) can, in the presence of an excessive salt load, lead to the development of hypertension. The initial tendency toward salt and water retention and extracellular fluid volume expansion is compensated by the secretion of a natriuretic hormone that promotes Na excretion by inhibiting Na pumps in renal tubule cells. The hormone also inhibits Na pumps in other types of cells, however, including vascular smooth muscle cells, so that the intracellular Na concentration rises in these cells. Then, because the vascular smooth muscle cells contain a Na/Ca exchange transport system in their plasma membranes, more Ca than normal will be delivered to these cells. This will cause the increased contractility and reactivity that underlies increased vascular tone and peripheral vascular resistance which is the direct cause of the elevated blood pressure.Entities:
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Year: 1985 PMID: 4039776
Source DB: PubMed Journal: Klin Wochenschr ISSN: 0023-2173