Key result
Captopril treatment increased angiotensin II immunoreactive material in the subfornical organ of spontaneously hypertensive rats, but decreased it in normotensive Wistar-Kyoto rats.
Why the study?
Does captopril treatment affect angiotensin II content in the subfornical organ of spontaneously hypertensive rats?
Does captopril treatment affect angiotensin II content in the subfornical organ of spontaneously hypertensive rats?
Captopril treatment increases angiotensin II immunoreactivity in the subfornical organ of spontaneously hypertensive rats, suggesting an interaction between hypertension and captopril treatment in the brain.
Answers are grounded in this paper and cite their sources.
Suggests differential central responses to captopril by hypertension status in rats; leaves open relevance to human therapy.
We studied the effects of spontaneous high blood pressure and the captopril treatment on the subfornical organ (SFO) of rats. The brains of control Wistar-Kyoto rats (WKY), WKY rats treated with captopril (WKY-T), spontaneously hypertensive rats (SHR) and SHR rats treated with captopril (SHR-T) were processed immunohistochemically using anti-angiotensin II as primary antibody. Immunorective material (IRM) for angiotensin II was observed in a group of neurons and some cells of the ependymal layer of the SFO in WKY rats. The angiotensin II immunoreactive (AGII-ir) in the SHR rats was decreased, showing positive reaction only in a few neurons, while captopril treatment induced an increase in immunoreactive material in hypertensive rats, but contrarily, the expression of AGII-ir in the WKY-T group was scarce. The variations of the angiotensin II observed in the SFO could be owing to an interaction between the hypertension and its captopril treatment.
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Carmona-Calero et al. (2005) studied Hypertension. Captopril vs. No captopril was evaluated on Angiotensin II content in the subfornical organ (SFO). Captopril treatment increased angiotensin II immunoreactive material in the subfornical organ of spontaneously hypertensive rats, but decreased it in normotensive Wistar-Kyoto rats.
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