Role of angiotensin receptors in the medial amygdaloid nucleus in autonomic, baroreflex and cardiovascular changes evoked by chronic stress in rats

Abstract

This study investigated the role of AT1, AT2 and Mas angiotensinergic receptors within the MeA in autonomic, cardiovascular and baroreflex changes evoked by a 10‐day (1 hr daily) repeated restraint stress (RRS) protocol. Analysis of cardiovascular function after the end of the RRS protocol indicated increased values of arterial pressure, without heart rate changes. Arterial pressure increase was not affected by acute MeA treatment after the RRS with either the selective AT1 receptor antagonist losartan, the selective AT2 receptor antagonist PD123319 or the selective Mas receptor antagonist A‐779. Analysis of heart rate variability indicated that RRS increased the sympathetic tone to the heart, which was inhibited by MeA treatment with either losartan, PD123319 or A‐779. Baroreflex function assessed using the pharmacological approach via intravenous infusion of vasoactive agents revealed a facilitation of tachycardia evoked by blood pressure decrease in chronically stressed animals, which was inhibited by MeA treatment with losartan. Conversely, baroreflex responses during spontaneous fluctuations of blood pressure were impaired by RRS, and this effect was not affected by injection of the angiotensinergic receptor antagonists into the MeA. Altogether, the data reported in the present study suggest an involvement of both angiotensinergic receptors present in the MeA in autonomic imbalance evoked by RRS, as well as an involvement of MeA AT1 receptor in the enhanced baroreflex responses during full range of blood pressure changes. Results also indicate that RRS‐evoked increase in arterial pressure and impairment of baroreflex responses during spontaneous variations of arterial pressure are independent of MeA angiotensinergic receptors.

Sodium Hydrosulfide Reverts Chronic Stress–Induced Cardiovascular Alterations by Reducing Oxidative Stress

“…4 Our results show that CRS induced an increase in blood pressure, as previously shown. 51–53 This rise in blood pressure during chronic stress could be attributed, among other mechanisms, to (1) impairments in baroreflex and sympathetic responses 53 ; (2) elevated NE levels 12 ; (3) vascular oxidative stress 54 ; and (4) vascular dysfunction. 52 Notably, we found that the treatment with NaHS restored blood pressure to physiological levels in animals with chronic stress.…”

“…4 Our results show that CRS induced an increase in blood pressure, as previously shown. [51][52][53] This rise in blood pressure during chronic stress could be attributed, among other mechanisms, to (1) impairments in baroreflex and sympathetic responses 53 ;…”

Lateral hypothalamus involvement in control of stress response by bed nucleus of the stria terminalis endocannabinoid neurotransmission in male rats

“…One day before the trial, rats were anesthetized with tribromoethanol (250 mg/kg, i.p. ), and a catheter (Clay Adams, Parsippany, NJ, USA) filled with a solution of heparin (50UI/ml, Hepamax-S, Blausiegel, Cotia, SP, Brazil) diluted in saline (0.9% NaCl) was inserted into the abdominal aorta through the femoral artery for cardiovascular recording, according to procedures previously described by our group 13 , 57 , 59 , 60 . After the surgery, the non-steroidal anti-inflammatory flunixin meglumine (0.5 mg/ml/kg, s.c.) was administered for post-operation analgesia.…”

Angiotensinergic Neurotransmissions in the Medial Amygdala Nucleus Modulate Behavioral Changes in the Forced Swimming Test Evoked by Acute Restraint Stress in Rats

“…All rats were allowed at least 60 min to adapt to the sound and illumination conditions of the room (25 °C and acoustically isolated) before starting the experiment. Afterwards, animals randomly received bilateral microinjections into the MeA of the selective AT 1 receptor antagonist losartan (1 nmol/100 nL, n = 9), the selective MAS receptor antagonist A-779 (0.1 nmol/100 nL, n = 10), the selective AT 2 receptor antagonist PD12319 (0.5 nmol/100 nL, n = 8) or vehicle (NaCl 0.9%, 100 nL, n = 21) [ 42 , 51 , 52 , 53 ]. Ten minutes after the drug microinjection into the MeA, the animals underwent the 60 min session of restraint stress.…”