Zarei, M., Heshmatian, B., Sarihi, A. (2010). The effect of reversible inactivation of the central amygdaloid nucleus on cardiovascular responses in rats with renal hypertension. Iranian Journal of Pharmaceutical Research, Volume 3(Supplement 1), 77-77.
M Zarei; B Heshmatian; A Sarihi. "The effect of reversible inactivation of the central amygdaloid nucleus on cardiovascular responses in rats with renal hypertension". Iranian Journal of Pharmaceutical Research, Volume 3, Supplement 1, 2010, 77-77.
Zarei, M., Heshmatian, B., Sarihi, A. (2010). 'The effect of reversible inactivation of the central amygdaloid nucleus on cardiovascular responses in rats with renal hypertension', Iranian Journal of Pharmaceutical Research, Volume 3(Supplement 1), pp. 77-77.
Zarei, M., Heshmatian, B., Sarihi, A. The effect of reversible inactivation of the central amygdaloid nucleus on cardiovascular responses in rats with renal hypertension. Iranian Journal of Pharmaceutical Research, 2010; Volume 3(Supplement 1): 77-77.
The effect of reversible inactivation of the central amygdaloid nucleus on cardiovascular responses in rats with renal hypertension
The brain rennin-angiotensin system (RAS) has an important role in the regulation of cardiovascular function. The aim of the present study was to determine the effect of reversible inactivation of the central amygdaloid nucleus (Ace) in normotensive rats and rats with renal hypertension (2K-1C). Two groups of normotensive rats were selected for this study. In one group, hypertension was induced by Goldblatt method and the other group subjected to a sham procedure. After 6 weeks, tests were performed on anesthetized rats with urethane (1 g/Kg). To perform bilaterally reversible inactivation, lidocaine (2%) was injected into Ace. Then, direct measurements of femoral blood pressure and heart rate were recorded just before and 5, 10, 20, 40, and, 60 min after injection of lidocaine. The degree of change was determined in relation to baseline. Our results revealed that sham group with Ace inactivation had a significant increase of blood pressure at 5 min after injection (P<0.05). There was also no significant difference between blood pressure at different times before and after injection in hypertensive group. The percentage of change had also a significant increase at 5 min following inactivation in sham-operated group as compared to 2K-1C rats (P<0.05). However, concerning heart rate there was no differences between groups. It seems that the tonic inhibitory effect of amygdala on blood pressure has disappeared due to hypertension. Thus, inactivation of Ace has no effect on blood pressure in hypertensive rats. It can be concluded that the change in Ace activity during induction of hypertension is due to the change in RAS activity.
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