The brain renin-angiotensin system and the development of DOC-salt hypertension.
The effect of captopril, given in the drinking fluid, on the development of DOC-salt hypertension was analyzed. Although captopril did not prevent an increase in blood pressure (BP) elicited by DOC-salt, captopril did diminish BP in both DOC-salt and control animals. From the first week of treatment DOC-salt rats increased their fluid intake (FI). At the end of the experiment, captopril reduced this increment (655% to 357%). At the same time plasma angiotensinogen was diminished (-35%; p less than 0.001) and cerebrospinal fluid (CSF) substrate concentration increased (+33%; p less than 0.02) in DOC-salt rats, captopril did not modify these changes. In control rats captopril did not alter FI, depleted plasma angiotensinogen, (-73%; p less than 0.001), did not change the central prohormone and increased plasma renin activity (PRA) (+260%; p less than 0.001).


CONCLUSIONS
CSF angiotensinogen concentration changes as previously found in CNS while a clear dissociation between plasma and CSF angiotensinogen was found in DOC-salt rats. In these animals the hypertension was not clearly affected by captopril treatment. However the effect of the converting enzyme inhibitor suggests that the central renin-angiotensin system could participate in the increase in FI.
D000808:Angiotensinogen / Q000097:blood / Q000134:cerebrospinal fluid; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001921:Brain / Q000503:physiopathology*; D002216:Captopril / Q000494:pharmacology; D003900:Desoxycorticosterone; D004326:Drinking / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects; D012965:Sodium Chloride
D000808:Angiotensinogen; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D002216:Captopril; D012083:Renin