[2 models of indomethacin-induced arterial hypertension in rats in chronic experiments].
Chronic administration of small doses of prostaglandin-synthesis inhibitor indometacin against the background of a salt load or unilateral nephrectomy induces the development of arterial hypertension in rats. Arterial pressure increases (two fold on the average) on the 6th week of the experiment in 60-80% of the animals. Arterial hypertension developing against the background of a salt load is marked by retention of sodium in the organism and increase the intravascular volume, while that developing in unilateral nephrectomy--by increased sodium excretion and reduced intravascular volume. Depressed activity of the renin-angiotensin-aldosterone system and conspicious changes in the renal vascular channel are noted in both forms of arterial hypertension. It is assumed that disorders in the metabolism of cyclic nucleotides underlie the changes occurring in the renal vessels due to the effect of indometacin. Similar generalized changes in the peripheral vascular channel on the whole may be the cause of the increased vascular resistance and one of the causative factors of the hypertension development.
D000450:Aldosterone / Q000378:metabolism; D000809:Angiotensins / Q000378:metabolism; D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced*; D007213:Indomethacin; D007668:Kidney / Q000503:physiopathology; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D009392:Nephrectomy; D011453:Prostaglandins / Q000378:metabolism; D051381:Rats; D012083:Renin / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D000809:Angiotensins; D011453:Prostaglandins; D000450:Aldosterone; D012964:Sodium; D000242:Cyclic AMP; D012083:Renin; D007213:Indomethacin
2 modeli arterial'noĭ gipertonii u krys, vyzvannoĭ indometatsinom v khronicheskom opyte.