Sympathetic regulation of the NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats.

Sympathetic regulation of the NCC in norepinephrine-evoked salt-sensitive hypertension in Sprague-Dawley rats. Am J Physiol Renal Physiol. 2019 Oct 14;: Authors: Frame AA, Puleo F, Kim K, Walsh KR, Faudoa E, Hoover RS, Wainford RD Abstract Salt sensitivity of blood pressure is characterized by inappropriate sympathoexcitation and renal sodium reabsorption during high salt intake. In salt-resistant animal models, exogenous norepinephrine infusion promotes salt-sensitive hypertension and prevents dietary sodium-evoked suppression of the sodium chloride cotransporter (NCC). Studies of the adrenergic signaling pathways that modulate NCC activity during norepinephrine infusion have yielded conflicting results implicating α1- and/or β-adrenoceptors and a downstream kinase network that phosphorylates and activates the NCC, including with- no-lysine kinases (WNKs), STE20/SPS1-related proline alanine-rich kinase (SPAK), and oxidative stress response 1 (OxSR1). In these studies, we used selective adrenoceptor antagonism in norepinephrine-infused male Sprague-Dawley rats to investigate the differential roles of α1- and β-adrenoceptors in sympathetically-mediated NCC regulation. Norepinephrine infusion evoked salt-sensitive hypertension and prevented dietary sodium-evoked suppression of NCC mRNA, protein expression, phosphorylation, and in vivo activity. Impaired NCC suppression during high salt intake in norepinephrine-infused rats was para...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research