Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
2142790
Knihovny.cz E-resources
- MeSH
- Aldosterone blood MeSH
- Biological Transport MeSH
- Dinoprost urine MeSH
- Adult MeSH
- Potassium urine MeSH
- Erythrocytes metabolism MeSH
- Furosemide pharmacology MeSH
- Hypertension metabolism MeSH
- Kallikreins urine MeSH
- Humans MeSH
- Natriuresis MeSH
- Renin blood MeSH
- Sodium blood metabolism MeSH
- Thromboxanes urine MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Aldosterone MeSH
- Dinoprost MeSH
- Potassium MeSH
- Furosemide MeSH
- Kallikreins MeSH
- Renin MeSH
- Sodium MeSH
- Thromboxanes MeSH
Urinary excretion of sodium, potassium and some hormones influencing their transport was investigated before and after i.v. furosemide administration in 10 offsprings of normotensive subjects who had a normal Na(+)-K+ cotransport activity and in 26 normotensive men with a positive family history of essential hypertension. The latter group was divided into two subgroups with regard to the activity of red cell Na(+)-K+ cotransport. The Co[-] subjects with a decreased Na(+)-K+ cotransport activity had lower urinary excretion of sodium and vasodilators (kallikrein, dopamine, PGE2 and prostacyclin) after furosemide administration. The urinary excretion of vasopressor factors (PGF2 alpha, thromboxane) was unchanged as compared with that in the control group. There was a significant correlation between Na(+)-K+ cotransport activity and kallikrein excretion. These results suggest a deficit in the secretion of renal substances with vasodilating or natriuretic effects in Co[-] subjects. This could negatively affect their sodium excretion.