|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0006675,
umls-concept:C0007634,
umls-concept:C0020538,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0027479,
umls-concept:C0596235,
umls-concept:C0597484,
umls-concept:C0678640,
umls-concept:C1159690,
umls-concept:C1512571
|
|
pubmed:issue |
4A
|
|
pubmed:dateCreated |
1984-11-14
|
|
pubmed:abstractText |
Sodium plays a critical role in the etiology of essential hypertension, but the mechanism by which excess dietary sodium actually leads to the elevation of blood pressure is not understood. The hypothesis described shows how an excessive sodium load can lead to the development of hypertension. The underlying factor must be a genetic or acquired deficiency or limitation in renal sodium excretion that may be undetectable by standard renal function tests. The resultant tendency towards sodium, water, and extracellular fluid volume expansion is compensated by the secretion of a natriuretic hormone that promotes sodium excretion by inhibiting sodium pumps in the kidney tubule cells. The hormone also inhibits sodium pumps in other cells, including vascular smooth muscle cells, causing intracellular sodium to increase. Then, because the vascular smooth muscle cells contain a Na+-Ca2+ exchange transport system in their plasma membranes, more calcium than normal is delivered to these cells. This causes the increased contractility and reactivity that underlies the increased vascular tone and peripheral vascular resistance that elevates the blood pressure.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Oct
|
|
pubmed:issn |
0002-9343
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
5
|
|
pubmed:volume |
77
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
45-59
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:6091450-Biological Transport, Active,
pubmed-meshheading:6091450-Calcium,
pubmed-meshheading:6091450-Cell Membrane,
pubmed-meshheading:6091450-Cell Membrane Permeability,
pubmed-meshheading:6091450-Diet,
pubmed-meshheading:6091450-Humans,
pubmed-meshheading:6091450-Hypertension,
pubmed-meshheading:6091450-Ion Channels,
pubmed-meshheading:6091450-Kidney Tubules,
pubmed-meshheading:6091450-Muscle, Smooth, Vascular,
pubmed-meshheading:6091450-Natriuresis,
pubmed-meshheading:6091450-Natriuretic Agents,
pubmed-meshheading:6091450-Neurons,
pubmed-meshheading:6091450-Proteins,
pubmed-meshheading:6091450-Sodium,
pubmed-meshheading:6091450-Sodium Chloride,
pubmed-meshheading:6091450-Sodium-Potassium-Exchanging ATPase,
pubmed-meshheading:6091450-Vascular Resistance,
pubmed-meshheading:6091450-Water-Electrolyte Balance
|
|
pubmed:year |
1984
|
|
pubmed:articleTitle |
Sodium transport inhibition, cell calcium, and hypertension. The natriuretic hormone/Na+-Ca2+ exchange/hypertension hypothesis.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
|
