Recent aspects in the genetic renal mechanisms involved in hypertension
The kidney plays an important role in the blood pressure regulation primarily by modulating tubular sodium reabsorption. Various hormones, vasoactive peptides, autacoids and transporters or channels in renal tubules are involved in this process. Genes associated with renal tubular sodium handling are possibly related to the development of hypertension. Genes of the renin-angiotensin-aldosterone system are thought to be especially important as causal genes of hypertension. Na-K-ATPase, biochemically equal to Na pump, exists on the basolateral membrane of renal epithelial cells. It plays a central role in Na reabsorption and creates a driving force for transepithelial transport. Na-K-ATPase activity is regulated by adducin, a membrane-bound skeletal protein, as well as by several hormones such as dopamine, endogenous ouabain-like factor or cytochrome P450 metabolites. Genes of these factors involved in Na-K-ATPase regulation should be related to the development of hypertension. The endothelin system, atrial natriuretic peptide and nitric oxide regulate the tonus of blood vessels as well as renal sodium excretion. Several reports have indicated that genes of these substances are crucial in the pathogenesis of hypertension.
Medienart: |
Artikel |
---|
Erscheinungsjahr: |
1999 |
---|---|
Erschienen: |
1999 |
Enthalten in: |
Zur Gesamtaufnahme - volume:38 |
---|---|
Enthalten in: |
Internal medicine (Tokyo, Japan) - 38(1999), 12 vom: 01. Dez., Seite 919-26 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Satoh, T [VerfasserIn] |
---|
Anmerkungen: |
Date Completed 27.01.2000 Date Revised 16.05.2019 published: Print Citation Status MEDLINE |
---|
Förderinstitution / Projekttitel: |
|
---|
PPN (Katalog-ID): |
NLM105581097 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM105581097 | ||
003 | DE-627 | ||
005 | 20231222134952.0 | ||
007 | tu | ||
008 | 231222s1999 xx ||||| 00| ||eng c | ||
028 | 5 | 2 | |a pubmed24n0352.xml |
035 | |a (DE-627)NLM105581097 | ||
035 | |a (NLM)10628927 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Satoh, T |e verfasserin |4 aut | |
245 | 1 | 0 | |a Recent aspects in the genetic renal mechanisms involved in hypertension |
264 | 1 | |c 1999 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
338 | |a Band |b nc |2 rdacarrier | ||
500 | |a Date Completed 27.01.2000 | ||
500 | |a Date Revised 16.05.2019 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a The kidney plays an important role in the blood pressure regulation primarily by modulating tubular sodium reabsorption. Various hormones, vasoactive peptides, autacoids and transporters or channels in renal tubules are involved in this process. Genes associated with renal tubular sodium handling are possibly related to the development of hypertension. Genes of the renin-angiotensin-aldosterone system are thought to be especially important as causal genes of hypertension. Na-K-ATPase, biochemically equal to Na pump, exists on the basolateral membrane of renal epithelial cells. It plays a central role in Na reabsorption and creates a driving force for transepithelial transport. Na-K-ATPase activity is regulated by adducin, a membrane-bound skeletal protein, as well as by several hormones such as dopamine, endogenous ouabain-like factor or cytochrome P450 metabolites. Genes of these factors involved in Na-K-ATPase regulation should be related to the development of hypertension. The endothelin system, atrial natriuretic peptide and nitric oxide regulate the tonus of blood vessels as well as renal sodium excretion. Several reports have indicated that genes of these substances are crucial in the pathogenesis of hypertension | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Review | |
650 | 7 | |a Biological Factors |2 NLM | |
650 | 7 | |a Calmodulin-Binding Proteins |2 NLM | |
650 | 7 | |a Cardenolides |2 NLM | |
650 | 7 | |a Endothelins |2 NLM | |
650 | 7 | |a Receptors, Angiotensin |2 NLM | |
650 | 7 | |a Saponins |2 NLM | |
650 | 7 | |a Sodium Channels |2 NLM | |
650 | 7 | |a adducin |2 NLM | |
650 | 7 | |a digoxin-like factors |2 NLM | |
650 | 7 | |a Nitric Oxide |2 NLM | |
650 | 7 | |a 31C4KY9ESH |2 NLM | |
650 | 7 | |a Digoxin |2 NLM | |
650 | 7 | |a 73K4184T59 |2 NLM | |
650 | 7 | |a Nitric Oxide Synthase |2 NLM | |
650 | 7 | |a EC 1.14.13.39 |2 NLM | |
650 | 7 | |a Peptidyl-Dipeptidase A |2 NLM | |
650 | 7 | |a EC 3.4.15.1 |2 NLM | |
650 | 7 | |a Dopamine |2 NLM | |
650 | 7 | |a VTD58H1Z2X |2 NLM | |
700 | 1 | |a Owada, S |e verfasserin |4 aut | |
700 | 1 | |a Ishida, M |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Internal medicine (Tokyo, Japan) |d 1996 |g 38(1999), 12 vom: 01. Dez., Seite 919-26 |w (DE-627)NLM012606731 |x 1349-7235 |7 nnns |
773 | 1 | 8 | |g volume:38 |g year:1999 |g number:12 |g day:01 |g month:12 |g pages:919-26 |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 38 |j 1999 |e 12 |b 01 |c 12 |h 919-26 |