scholarly journals LOW-INTENSITY FOCUSED ULTRASOUND ON RENAL SYMPATHETIC NERVE PREVENT MYOCARDIAL INFARCTION INDUCED SYMPATHETIC NEURAL ACTIVATION AND VENTRICULAR ARRHYTHMIAS IN CANINES

2021 ◽  
Vol 77 (18) ◽  
pp. 303
Author(s):  
Mingxian Chen ◽  
Songyun Wang ◽  
Zhuo Wang ◽  
Xin Lai ◽  
Shenghua Zhou
Keyword(s):  
Myocardial Infarction ◽  
Sympathetic Nerve ◽  
Ventricular Arrhythmias ◽  
Focused Ultrasound ◽  
Neural Activation ◽  
Low Intensity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

α2-Adrenergic stimulation is protective against ischemia-reperfusion-induced ventricular arrhythmias in vivo

2002 ◽  
Vol 283 (6) ◽  
pp. H2606-H2611 ◽  
Author(s):  
John J. Cai ◽  
Donald A. Morgan ◽  
William G. Haynes ◽  
James B. Martins ◽  
Hon-Chi Lee
Keyword(s):  
Sympathetic Nerve ◽  
Ventricular Arrhythmias ◽  
Ischemia Reperfusion ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Adrenergic Antagonist ◽  
Renal Sympathetic

We previously reported that α2-adrenergic receptor (α2-AR) stimulation in Purkinje fibers in vitro prolongs action potential duration and suppresses β-adrenergic-induced delayed afterdepolarizations and sustained triggered activities. We examined the effects of α2-AR stimulation on reperfusion-induced ventricular arrhythmias [ventricular tachycardia/ventricular fibrillation (VT/VF)] in vivo. Arterial blood pressure, heart rate, surface electrocardiogram, and renal sympathetic nerve activities were recorded simultaneously in Sprague-Dawley rats. The incidence of VT/VF was 87.5% for controls, 50% for the β-blocker group, 72% for the α1-blocker group, and 12.5% for the α1 + β-blockers group (unopposed α2-adrenergic activation). Direct α2-AR stimulation with UK-14304 also prevented VT/VF. These effects were reversed by the α2-adrenergic antagonist yohimbine. Increases in renal sympathetic nerve activity were associated with left anterior descending coronary artery ligation and reperfusion (33 ± 1.5 and 62 ± 1.7% over baseline, respectively) in controls. Similar patterns were observed among all experimental groups irrespective of the incidence of VT/VF on reperfusion. We conclude that α2-AR stimulation has a potent antiarrhythmic effect on ischemia-reperfusion-induced VT/VF in vivo and that this effect is not centrally mediated.

Effects of l-carnosine on renal sympathetic nerve activity and DOCA-salt hypertension in rats

2002 ◽  
Vol 97 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Akira Niijima ◽  
Tomoko Okui ◽  
Yasuo Matsumura ◽  
Toshihiko Yamano ◽  
Nobuo Tsuruoka ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Salt Hypertension ◽  
Renal Sympathetic

Suppression of renal sympathetic nerve activity during portal vein infusion of hypertonic saline

1998 ◽  
Vol 274 (1) ◽  
pp. R97-R103 ◽  
Author(s):  
Yasuhiro Nishida ◽  
Isao Sugimoto ◽  
Hironobu Morita ◽  
Hiroshi Murakami ◽  
Hiroshi Hosomi ◽  
...  
Keyword(s):  
Portal Vein ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Venous Infusion ◽  
Portal Vein Infusion ◽  
Renal Sympathetic

Sodium ions absorbed from the intestine are postulated to act on the liver to reflexly suppress renal sympathetic nerve activity (RSNA), resulting in inhibition of sodium reabsorption in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venous NaCl infusion involves an action of arginine vasopressin (AVP) at the area postrema, we examined the effects of portal venous infusion of hypertonic NaCl on RSNA before and after lesioning of the area postrema (APL) or after pretreatment with an AVP V1 receptor antagonist (AVPX). Rabbits were chronically instrumented with portal and femoral venous catheters, femoral arterial catheters, and renal nerve electrodes. Portal venous infusion of 9.0% NaCl (0.02, 0.05, 0.10, and 0.15 ml ⋅ kg−1 ⋅ min−1of 9.0% NaCl for 10 min) produced a dose-dependent suppression of RSNA (−12 ± 3, −34 ± 3, −62 ± 5, and 80 ± 2%, respectively) that was greater than that produced by femoral vein infusion of 9.0% NaCl (2 ± 3, −3 ± 2, −12 ± 4, and −33 ± 3%, respectively). The suppression of RSNA produced by portal vein infusion of 9.0% NaCl was partially reversed by pretreatment with AVPX (−9 ± 3, −20 ± 3, −41 ± 4, and −55 ± 4%, respectively) and by APL (−11 ± 2, −25 ± 2, −49 ± 3, and −59 ± 6%, respectively). There were no significant differences between the effects of AVPX and APL, and the effect of APL was not augmented by AVPX. These results indicate that the suppression of RSNA due to portal venous infusion of 9.0% NaCl involves an action of AVP via the area postrema.

scholarly journals Electroacupuncture and Moxibustion Decrease Renal Sympathetic Nerve Activity and Retard Progression of Renal Disease in Rats

2012 ◽  
Vol 35 (5) ◽  
pp. 355-364 ◽  
Author(s):  
Josne C. Paterno ◽  
Cássia T. Bergamaschi ◽  
Ruy R. Campos ◽  
Elisa M.S. Higa ◽  
Maria Fernanda Soares ◽  
...  
Keyword(s):  
Renal Disease ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Progression Of Renal Disease ◽  
Renal Sympathetic
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