◀ Back to NOS1

NOS1 — REN

Text-mined interactions from Literome

Wagner et al., Pflugers Arch 2000 (Hypertension, Renal) : These observations suggest that neither eNOS nor nNOS is essential for up- or downregulation of renin expression
Ollerstam et al., Acta Physiol Scand 2001 : This suggests that inhibition of nNOS stimulates renin release but that this stimulatory effect in the long run might be depressed by the increase in blood pressure
Deng et al., Kidney Int 2002 : We studied renal hemodynamics during early TGF resetting with attention to the importance of renin suppression and NOS I activation
Paliege et al., American journal of physiology. Renal physiology 2004 : To further explore the role of nNOS and COX-2 in renin secretion, we determined plasma renin activity in mice deficient in nNOS or COX-2
Yabuki et al., Exp Anim 2006 (Diabetes Mellitus, Type 2...) : Neuronal nitric oxide synthase (nNOS) and cyclooxygenase-2 (COX-2) regulate the tubuloglomerular feedback ( TGF ) and renin-angiotensin system (RAS) in the kidney
Sällström et al., Am J Hypertens 2008 : This study was conducted to further elucidate the role of neuronal nitric oxide synthase (nNOS) in blood pressure regulation and renin release in relation to different sodium loads ... Our results show that nNOS is necessary for stimulation of renin in response to sodium restriction
Kompanowska-Jezierska et al., Am J Physiol Regul Integr Comp Physiol 2008 : It was hypothesized that renal sympathetic nerve activity ( RSNA ) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading ( NaLoad ) and that RSNA participates in the regulation of arterial blood pressure ( MABP ) ... However, neither renal denervation nor nNOS inhibition affects either the renin down-regulation or the natriuretic response to acute sodium loading ... Acute sodium-driven renin regulation seems independent of RSNA and nNOS under the present conditions
Sällström et al., Am J Hypertens 2010 : Administration of milrinone caused a more pronounced PRC increase in nNOS? ( / ) ?, resulting in normalized renin levels , whereas PDE5 inhibition did not affect PRC in any genotype
el Karib et al., Clin Exp Hypertens 1993 : The central effects of a nitric oxide synthase inhibitor ( N omega-nitro-L-arginine ) on blood pressure and plasma renin
Beierwaltes et al., Am J Physiol 1997 : Although selective NOS inhibition by 7-NI did not affect BP, RBF, or renin in control rats on a normal diet, chronic 7-NI reversed the stimulation of renin induced by dietary sodium restriction