The Eagle Biosciences Noradrenaline (Norepinephrine) Sensitive ELISA was used in a recent study. This highly sensitive assay kit is part of our veterinary and neurobiology product lines. It is intended for the detection of noradrenaline (norepinephrine) in biological samples including serum, plasma, tissue, and cell culture samples of mice and rats.
Abstract
Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension & renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response. Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension and renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response.
Raikwar, NS;Braverman, C;Snyder, PM;Fenton, RA;Meyerholz, DK;Abboud, FM;Harwani, SC; (2019). Renal Denervation and CD161a Immune Ablation Prevent Cholinergic Hypertension and Renal Sodium Retention. Am. J. Physiol. Heart Circ. Physiol.. doi:10.1152/ajpheart.00234.2019.
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