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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Physiol 2016 ; 594 (21): 6079-103 Nephropedia Template TP
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Pivotal role of ?2 Na+ pumps and their high affinity ouabain binding site in cardiovascular health and disease #MMPMID27350568
J Physiol 2016[Nov]; 594 (21): 6079-103 PMID27350568show ga
Reduced smooth muscle (SM)?specific ?2 Na+ pump expression elevates basal blood pressure (BP) and increases BP sensitivity to angiotensin II (Ang II) and dietary NaCl, whilst SM??2 overexpression lowers basal BP and decreases Ang II/salt sensitivity. Prolonged ouabain infusion induces hypertension in rodents, and ouabain?resistant mutation of the ?2 ouabain binding site (?2R/R mice) confers resistance to several forms of hypertension. Pressure overload?induced heart hypertrophy and failure are attenuated in cardio?specific ?2 knockout, cardio?specific ?2 overexpression and ?2R/R mice. We propose a unifying hypothesis that reconciles these apparently disparate findings: brain mechanisms, activated by Ang II and high NaCl, regulate sympathetic drive and a novel neurohumoral pathway mediated by both brain and circulating endogenous ouabain (EO). Circulating EO modulates ouabain?sensitive ?2 Na+ pump activity and Ca2+ transporter expression and, via Na+/Ca2+ exchange, Ca2+ homeostasis. This regulates sensitivity to sympathetic activity, Ca2+ signalling and arterial and cardiac contraction.