Why the study?
Does captopril given in drinking fluid reduce blood pressure and fluid intake in a rat model of DOC-salt hypertension?
Does captopril given in drinking fluid reduce blood pressure and fluid intake in a rat model of DOC-salt hypertension?
Answers are grounded in this paper and cite their sources.
Captopril does not prevent DOC-salt hypertension in rats but reduces fluid intake, suggesting central renin-angiotensin system involvement in fluid intake regulation.
UNLABELLED: 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). CONCLUSION: 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.
No takes yet. Share an insight, caveat, or question.
Basso et al. (1985) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: