[Role of prostagladin synthesis inhibitors in the development of arterial hypertension. II].
Arterial hypertension was induced in experiments on rats by chronic injection of indometacin, an inhibitor of prostaglandin synthesis, combined with a salt load or unilateral nephrectomy. A twofold rise in arterial pressure, on average, was noted at the end of the 6th week of the inhibitor injection. The development of arterial hypertension following indometacin injection and a salt load led to reduced excretion of sodium and water, increased intravascular volume, and increased sodium content in the aortic wall. In the group of nephrectomized and indometacin treated animals, on the contrary, sodium and water excretion increased, intravascular volume diminished, and the content of sodium in the aortic wall decreased. Chronic injection of indometacin alone into intact animals did not lead to a rise of arterial pressure within the same periods of time and did not induce changes in the renal excretory function. It is presumed that disorder of water-salt homeostasis is one of the mechanisms of the increase in arterial pressure.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004231:Diuresis / Q000187:drug effects; D006321:Heart / Q000187:drug effects; D006400:Hematocrit; D006973:Hypertension / Q000139:chemically induced* / Q000209:etiology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D010953:Plasma Volume / Q000187:drug effects; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D051381:Rats; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors
D011448:Prostaglandin Antagonists; D012965:Sodium Chloride; D007213:Indomethacin
Rol' ingibitorov sinteza prostaglandinov v razvitii arterial'noĭ gipertonii. Soobshchenie II.