Regulation of Plasma Renin in Developing Piglets

Jl, Osborn; Jb, Hook; Bailie,

doi:10.1159/000455539

Cited by 17 publications

(7 citation statements)

References 19 publications

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“…As described previously [52], in the control period, the piglet PRA of 1.49 + 0.35 ng angiotensin I/ml per hour was significantly greater than the adult PRA (0.36 + 0.15 ng angiotensin I/ml per hour). Intrarenal infusion of L-NAME did not significantly change PRA in the adult pig from control levels.…”

Section: No and Renin Release In The Developing Kidneysupporting

confidence: 73%

Nitric oxide in the developing kidney

Solhaug

Ballèvre

Guignard

et al. 1996

Pediatric Nephrology

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Although nitric oxide (NO) has a well-established role in regulating renal function in the adult, recent studies point to perhaps an even more critical role for NO in maintaining basal renal blood flow (RBF) and glomerular filtration rate (GFR) in the developing kidney. The immature kidney has enhanced renal hemodynamic and functional responses to stimulation and inhibition of NO synthesis when compared with the adult, and these increased responses are not mediated by prostaglandins. Increased intrarenal activity of NO in the developing kidney counter-regulates the highly activated renin angiotensin system by modulating the angiotensin II-mediated vasoconstriction of the developing renal vasculature, the angiotensin II effects on GFR, as well as renin release. Localization studies demonstrate that NO acts on neonatal RBF and stabilization of GFR through an intrarenal distribution of the synthesizing enzyme, nitric oxide synthase, that is different from that of the adult. The developing kidney is dependent on NO to maintain RBF and GFR during periods of hypoxemia, protecting against renal injury, such as acute renal failure. In summary, NO is vital in the developing kidney to maintain normal physiological function and to protect the immature kidney during pathophysiological stress.

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Section: No and Renin Release In The Developing Kidneysupporting

confidence: 73%

Nitric oxide in the developing kidney

Solhaug

Ballèvre

Guignard

et al. 1996

Pediatric Nephrology

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show abstract

“…Despite reports by Thompson and Weiner that indicate adaptations in the sensitivity of vascular smooth muscle to NO increases after birth (24), renal blood flow remains low in the newborn due to the enhanced vasoconstrictor response of the RAS (8-11). To counter-balance the elevated RAS of the newborn and to maintain adequate RBF and GFR, studies have demonstrated a crucial enhanced role of NO in the neonate's renal hemodynamic state.…”

Section: Discussionmentioning

confidence: 91%

“…Studies involving various species have suggested RVR is further enhanced in the afferent arterioles of the newborn kidney causing functional decreases in RBF, GFR, and filtration fraction, thus highlighting the hemodynamic significance of enhanced vascular resistance in the newborn's afferent arterioles (1,6,7). The major vasoactive agent that causes the newborn's elevated RVR is the renin-angiotensin system (RAS) (8-11). Many components of the RAS are developmentally regulated in the immature preglomerular resistance vessels.…”

Section: Introductionmentioning

confidence: 99%

“…Various studies have shown that NO plays a much more pronounced role in the neonate's renal hemodynamics, than in the adult's, and NO counter-balances the highly activated RAS protecting the immature kidney from the deleterious effects of adverse perinatal events that lead to vasomotor acute renal failure (8,15,17-20). In whole kidney models, developmental patterns of eNOS and nNOS are different, suggesting the isoforms have different regulatory factors and functional contributions in the immature kidney (15,16).…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II Regulates NOS Expression in Afferent Arterioles of the Developing Porcine Kidney

et al. 2010

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NO protection is crucial against angiotensin II (ANG II) mediated vasoconstriction in postnatal preglomerular resistance vessels. Although whole kidney NOS is developmentally regulated, NOS regulation in developing renal resistance vessels is unknown. The hypothesis was NOS expression and function in developing afferent arterioles are regulated by ANG II through AT1 and AT2 receptors. Afferent arterioles from porcine kidneys, ages newborn, 7, 21 d, and adult, were dissected using a polybead perfusion technique. Dissected afferent arterioles were treated with ANG II and with either the AT1 receptor inhibitor candesartan or the AT2 receptor inhibitor PD 123319 and evaluated for NOS isoform expression and NOS enzymatic activity. Although NOS activity and neuronal NOS (nNOS) expression were greater in the newborn than in the adult, endothelial NOS (eNOS) expression was greater in the adult. ANG II increased NOS activity and eNOS expression at all ages, but nNOS expression only in developing afferents. AT1 and AT2 receptor blockade significantly attenuated NOS activity and eNOS expression at all ages, but nNOS expression only in developing afferents. ANG II regulates nNOS and eNOS expression and NOS activity in afferent arterioles of the developing kidney via AT1 and AT2 receptors.

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“…Previous studies have indicated the primary vasoactive factor that effects neonate RVR is the renin-angiotensin system (RAS) [17,[21][22][23][24][25][26][27]. The major components of the RAS, including renin, angiotensin II (ATII), and both ATII receptor subtypes (AT1 and AT2), are highly present in the immature kidney, but their anatomical distribution and activities are quite different than those seen in the adult kidney [21,[28][29][30][31][32][33][34].…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide synthase and renin–angiotensin gene expression and NOS function in the postnatal renal resistance vasculature

et al. 2009

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Nitric oxide (NO), produced by nitric oxide synthase (NOS), critically counteracts angiotensin-II-enhanced vascular resistance in the immature kidney, perhaps due to the developmental regulation of NOS expression and function in the postnatal preglomerular resistance vessels (PRV). Our experiments measured the messenger ribonucleic acid (mRNA) gene expression of neuronal NOS (nNOS), endothelial NOS (eNOS), and components of the renin-angiotensin system (renin, AT1 and AT2 receptors), by real-time RT-PCR, as well as NOS enzymatic activity by citrulline assay in PRVs (afferent, interlobular, and arcuate arterioles) obtained from swine ages newborn, 7 and 21 days, and adult. NOS enzymatic activity was upregulated in PRVs immediately after birth but decreased to adult levels with maturation. Neuronal NOS, renin, and AT2 receptor expression in PRVs were upregulated in the newborn and decreased with age to lowest levels in the adult. In contrast, eNOS and AT1 receptor expression were downregulated at birth but increased to the highest levels in the adult. Upregulated NOS enzymatic activity in newborn PRVs supports the critical neonatal role for NO renal vascular vasodilation. Upregulated nNOS gene expression, concomitant with downregulated eNOS gene expression in neonatal PRVs, suggests that the nNOS isoform may be responsible for counteracting angiotensin II increased vascular resistance in immature porcine PRVs.

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Regulation of Plasma Renin in Developing Piglets

Cited by 17 publications

References 19 publications

Nitric oxide in the developing kidney

Nitric oxide in the developing kidney

Angiotensin II Regulates NOS Expression in Afferent Arterioles of the Developing Porcine Kidney

Nitric oxide synthase and renin–angiotensin gene expression and NOS function in the postnatal renal resistance vasculature

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