The ability of baroreflex activation to improve blood pressure and resistance vessel function in spontaneously hypertensive rats is dependent on stimulation parameters

Low intensity stimulation of aortic baroreceptor afferent fibers as a potential therapeutic alternative for hypertension treatment

“…When stimulated acutely in resistant hypertensive patients, device-based unilateral carotid baroreflex activation was previously shown to evoke more than 20 mmHg reduction in MAP at 4 – 7 V, 20 – 100 Hz, 0.48 ms 10 . In conscious SHRs, an approximate 30 mmHg drop in MAP was reported with electrical stimulation of the left carotid sinus nerve at 3 V, 30 Hz and 1 ms 29 . On the other hand, left ADN stimulation at 1 mA, 5 Hz and 2 ms produced an approximate 25 mmHg drop in MAP in conscious L-NAME-induced hypertensive rats, with stimulations beyond 5 Hz resulting in excessive reflex hypotensive responses 19 .…”

“…However, success of conscious longitudinal baroreflex studies using the ADN in rats is currently low and hampered by (1) inherent anatomical challenges given the small diameter of the nerve and the relative ease to sustain a damage to it during dissection and manipulation; and (2) the use of unrefined electrode design and nerve stimulation protocols that can ensure long-term viability of the nerve. To our knowledge, current studies reporting hemodynamic responses to ADN stimulation in conscious rats are typically run within 24 h after surgical implantation of the electrodes 18 , 29 , 36 . It is therefore possible that reported measures by those studies may, to a great extent, be confounded by issues related to surgical stress and inadequate animal recovery.…”

Heart rate variability in male rats

“…In in vivo experiments involving awake or freely moving animals, baseline values are used from sham groups, when the animals, in addition to the implantation of electrodes for continuous ECG recording, are also subjected to other surgical procedures as preparation for the further course of the experiment, but without subsequent targeted experimental intervention. For example, preparation for coronary or femoral artery occlusion (Aires et al, 2017; De La Fuente et al, 2013; Nobre et al, 2006), catheterization (Beckers et al, 2006; Blanco et al, 2015; Fiorino et al, 2012; Krüger et al, 1997, 2000; Mostarda et al, 2009; Müller‐Ribeiro et al, 2017; Quagliotto et al, 2015; Ramaekers et al, 2002; Ribeiro et al, 2021; Sallam et al, 2016, 2017; Shi et al, 2020; Simoes et al, 2016), ligation (Lima et al, 2018; Maida et al, 2017; Ruiz et al, 2014; Wang et al, 2016), bile duct ligation (Haddadian et al, 2013), cannulation (Beltrán et al, 2020; Da Silva et al, 2002; Neto et al, 2017; Sant'Ana et al, 2011), implantation of stimulators (Dai et al, 2020; Domingos‐Souza et al, 2021), or if they have already been administered substances beforehand (Lo Giudice et al, 2002).…”

Update on Hypertension Research in 2021

“…This finding may have critical implications for cardiovascular event occurrence at low ambient temperatures. In addition, Domingos-Souza et al showed that the ability of baroreflex activation to modulate hemodynamics and induce lasting vascular adaptation is critically dependent on the electrical parameters and duration of carotid sinus stimulation in spontaneously hypertensive rats (SHRs) [ 195 ], proposing a rationale for improving baroreflex activation therapy in humans. Although only normotensive and hypertensive rats were used in these two studies, without comparing the two strains, previous studies have shown that neuronal function and activity in the cardiovascular sympathoregulatory nuclei, including the nucleus tractus solitarius and rostral ventrolateral medulla, which are involved in baroreflex regulation, are different between normotensive and hypertensive rats [ 196 , 197 ].…”