Angiotensin II acting in the brain has been implicated in the pathogenesis of hypertension. The site at which angiotensin acts to maintain increased AP in hypertensive rats is unknown (at the time this paper was written). It is thought that the RVLM could play a role for a number of reasons, one of which is the high concentration of angiotensin receptors (AT1 receptors). The RVLM may also play a role in the effects of changes in dietary salt intake on cardiovascular regulation.
This study tested the hypothesis that activation of RVLM AT1 receptors contributes to the increased AP in rats fed a diet high in sodium. The role of the PVN in the maintenance of resting AP was also examined.
All rats were initially fed a diet containing 0.3% NaCl for at least 4 weeks and then some were switched to a high salt diet (8% NaCl) 4 weeks prior to experiments. Rats were anesthetized and prepared for measuring AP and HR. The RVLM was identified with glutamate injections before ANG II injections followed by valsartan (binds to AT1 receptors and inhibits ANG II action) injections. For PVN experiments, rats were first tested with injections of bicuculline (GABA receptor antagonist) followed by injections of muscimol (GABA receptor agonist).
It was found that injection of valsartan into the RVLM or injection of muscimol into the PVN produced a significant decrease in MAP in the high-salt diet hypertensive rats, whereas these treatments had little effect on MAP in low-salt diet rats. These results suggest that RVLM AT1 receptors are tonically activated in hypertensive rats. Additionally, they suggest that the PVN may contribute to the maintenance of baseline AP by way of a tonically active angiotensin-mediated input to the RVLM.
-BH
No comments:
Post a Comment