Role of nitric oxide in regulation of long-term pressure-natriuresis relationship in Dahl rats

Hu, Lufei; Manning, R. Davis

doi:10.1152/ajpheart.1995.268.6.h2375

Cited by 73 publications

(92 citation statements)

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“…The first evidence that basal NO production played an important role in determining arterial blood pressure arose from observations that chronic oral or intravenous administration of NOS inhibitors such as L-NAME or N G -monomethyl-L-arginine (L-NMMA) produced hypertension (28,32,55,123). It was unclear, however, whether the observed hypertension was primarily a result of generalized systemic vasoconstriction, an effect of NO reduction in brain, or a primary consequence of reduced renal excretory function.…”

Section: Importance Of Medullary No Production In the Long-term Contrmentioning

confidence: 99%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

175

202

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. Role of renal NO production in the regulation of medullary blood flow. Am J Physiol Regul Integr Comp Physiol 284: R1355-R1369, 2003 10.1152/ajpregu.00701.2002The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormoneinduced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of L-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure. renal medulla; Dahl salt-sensitive rats; hypertension; L-arginine THE RENAL MEDULLARY CIRCULATION is now recognized to be of importance for reasons that extend far beyond providing the economy of countercurrent exchange to concentrate large volumes of filtrate to produce small volumes of concentrated urine. It is now recognized that medullary blood flow (MBF) can play an important role in determining long-term levels of arterial pressure and that 15-30% reductions of blood flow to the renal medulla in the face of imperceptibly small changes of total renal blood flow can lead to the development of hypertension (16,21). Evidence is reviewed showing that nitric oxide (NO) plays a unique role in the acute and chronic regulation of renal MBF, sodium homeostasis, and arterial pressure. More specifically, the role of NO in the regulation of MBF, in linking tubular metabolic needs with delivery of nutrients and as a counterregulatory system to protect the medulla from the consequences of underperfusion, are the focus of this review. The influence of NO on the renal cortex and such issues that relate to pressure-natriuresis, autoregulation of total renal blood flow, tubuloglomerular feedback, and glomerular filtration rate (GFR) regulation are important subjects of renal function that either have been reviewed by others (2,29,43,55,96) or are beyond the scope of this relatively brief review.

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Section: Importance Of Medullary No Production In the Long-term Contrmentioning

confidence: 99%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

175

202

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“…[7][8][9][10][11][12][13]38 Reduced NO levels may result from decreased production as well as from increased inactivation. Superoxide ions are known to reduce NO bioavailability.…”

Section: Nad(p)h Polymorphisms Cardiovascular Risk Factors and Cardimentioning

confidence: 99%

“…[2][3][4] Increased activity of the NAD(P)H oxidase system is expected to be associated with reduced NO levels, vascular dysfunction, hypertension and salt sensitivity. [4][5][6] The latter, is known to be associated with reduced NO bioactivity [7][8][9][10][11][12][13] and increased superoxide production. 5,6 Consequently, genetic and/or disease-induced changes in NADPH oxidase activity and superoxide formation may play an important role in the pathogenesis of saltsensitive hypertension.…”

Section: Introductionmentioning

confidence: 99%

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

et al. 2006

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Mutations in the NAD(P)H oxidase gene may be associated with abnormal superoxide generation, nitric oxide (NO) availability and cardiovascular diseases. We investigated the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism, and its possible association with blood pressure, NO production, salt sensitivity and cardiovascular risk factors in Hispanics. Genotype frequencies were as follows: CC, 52.9%; CT, 40.3%; and TT, 6.8%. There were no significant differences in systolic blood pressure, diastolic blood pressure, age, weight, fasting and post-load glucose levels, LDL and HDL cholesterol, triglyceride and urinary albumin levels in subjects with CC, CT or the TT genotypes. Presence of the T allele was associated with increased salt sensitivity in women, but not in men.NO metabolite excretion was markedly decreased both in women and men with the TT genotype (CC: 868779 lmol/day; CT: 839775 lmol/day; TT: 5347 78 lmol/day; Po0.05). In conclusion, the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism in Venezuelans was comparable to that of Caucasians, but different from that of Chinese and Japanese. Although the T allele was not associated with cardiovascular risk factors, hyperinsulinaemia or hypertension, in women, it appeared to be a genetic susceptibility factor for salt sensitivity. Both in women and men, the p22phox gene may play a role in the genetic control of NO levels.

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“…1,[38][39][40] Experimental evidence indicates that NO plays a key role in endothelial health and salt sensitivity. 41 In genetic models of salt sensitivity and in human subjects, salt sensitivity appears linked to impaired NO production, [2][3][4][5][6] an effect reversed by administration of the NO precursor, L-arginine. 42,43 Despite numerous evidences supporting the role for NO in salt sensitivity, prior to this work no studies had been conducted on the relationships between eNOS polymorphisms and salt sensitivity.…”

Section: Ethnicity and Enos Polymorphismsmentioning

confidence: 99%

“…In animal models and in human subjects, salt sensitivity has been shown to be linked to impaired NO production. [2][3][4][5][6] Therefore, and because of the well-known role of NO on BP control, salt-sensitive hypertension and vascular function, mutations in the genes encoding for the NO synthesizing enzymes might be associated with salt sensitivity and cardiovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Endothelial nitric oxide synthase polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

et al. 2004

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Mutations in the endothelial nitric oxide synthase (eNOS) gene may be associated with abnormal nitric oxide (NO) production and cardiovascular diseases. In this study, we investigated the prevalence of two eNOS polymorphisms, the Glu298Asp variant on exon 7, and the 4a/b variable number of tandem repeats (VNTR) on intron 4, and their association with blood pressure (BP), NO production, salt sensitivity and cardiovascular risk factors in healthy Venezuelans. The prevalence of both polymorphisms in Venezuelans was comparable to that described for Caucasians, but significantly different from that known for African-Americans and Japanese. The 4a/b genotype was associated with reduced levels of NO metabolites (25% decrease), larger BP lowering in response to salt restriction (9.0 vs 4.8 mmHg, Po0.05), greater prevalence of salt sensitivity (39% in 4a/b and 27% in 4b/b; Po0.05) and with higher LDL-cholesterol levels. The Glu298T polymorphism did not affect NO production, nor it was associated with salt sensitivity. Glu298Asp polymorphism was positively associated with higher weight, triglycerides and LDL-cholesterol. Neither polymorphism was associated with changes in fasting or postload serum glucose, BP, obesity and albuminuria. In conclusion, the prevalence of eNOS polymorphisms is strongly determined by ethnic factors. The 4a/b gene polymorphism could be a genetic susceptibility factor for the BP response to salt intake and for the genetic control of NO production. The reduced NO production in subjects with the 4a/b genotype may be responsible for the increased sensitivity of their BP to salt.

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Role of nitric oxide in regulation of long-term pressure-natriuresis relationship in Dahl rats

Cited by 73 publications

References 0 publications

Role of renal NO production in the regulation of medullary blood flow

Role of renal NO production in the regulation of medullary blood flow

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

Endothelial nitric oxide synthase polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

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