Vasoactive humoral systems and sodium transport in erythrocytes of normotensive offsprings of essential hypertensive subjects.
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.
Janata
V
V
Institute for Clinical and Experimental Medicine, Prague.
Bultasová
H
H
Pinsker
P
P
D000328:Adult; D000450:Aldosterone / Q000097:blood; D001692:Biological Transport; D015237:Dinoprost / Q000652:urine; D004912:Erythrocytes / Q000378:metabolism*; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D007610:Kallikreins / Q000652:urine; D008297:Male; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000097:blood / Q000378:metabolism*; D013931:Thromboxanes / Q000652:urine
D013931:Thromboxanes; D000450:Aldosterone; D005665:Furosemide; D012964:Sodium; D015237:Dinoprost; D007610:Kallikreins; D012083:Renin; D011188:Potassium