Effect of captopril on blood pressure, total body sodium and fluid consumption of genetically hypertensive (GH) and normotensive (N) rats.
Captopril was administered in the drinking fluid to normotensive rats and rats of the New Zealand genetically hypertensive (GH) strain. It lowered BP in both strains of rat, particularly in rats deprived of sodium; in these rats BP rose again when the drug was stopped even though there was no access to sodium. Thus captopril appeared to lower blood pressure not by reduction in total exchangeable sodium but by some other mechanism, presumably inhibition of vasoconstriction. Total exchangeable sodium did not change significantly in rats treated with captopril and having access to salt in the drinking fluid, though it fell in rats deprived of sodium. Captopril caused an increase in fluid intake, particularly intake of 0.5% NaCl solution and this may have compensated for any loss of body sodium. It was not clear whether the thirst for water and the desire for salt were due to effects of captopril in the CNS or were secondary to increased excretion of salt and water.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D004326:Drinking / Q000187:drug effects*; D006973:Hypertension / Q000378:metabolism; D008297:Male; D011392:Proline / Q000031:analogs & derivatives*; D051381:Rats; D011919:Rats, Inbred Strains / Q000378:metabolism / Q000502:physiology*; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000008:administration & dosage
D012965:Sodium Chloride; D011392:Proline; D002216:Captopril; D012964:Sodium