Stress induced hypertension (SIH) is caused by emotional and
psychological stress. Renin angiotensin system plays a role in the control of
blood pressure. In a previous study this group showed that Angiotensin II and
Angiotensin (1-7) in the RVLM increased cardiovascular activities and release
of excitatory amino acids in normal rats. Also when AT1R antagonists are microinjected
into the RVLM, there is an attenuated pressor response.
Hypothesis: Angiotensin II and angiotensin (1-7) in the RVLM
are differently activated in the RVLM
Results/Findings:
1.) Angiotensin II not angiotensin (1-7) activated in SIH.
Also the AT1R pathway is tonically active.
2.) ACE production is increased in SIH suggesting that
angiotensin II production is unregulated
3.) Increased activity of the angiotensin II pathway leads
to increased excitatory and decreased inhibitory amino acid release.
Same here, also finish off your methods and provide the full reference (i.e. authors and journal citation) when you get a chance.
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