Effect of L-arginine on systemic and renal haemodynamics in salt-sensitive patients with essential hypertension

Campese, Vito M.; Amar, Mohamed Ben; Anjali, Chamoli; Medhat, Tarek; Wurgaft, A

doi:10.1038/sj.jhh.1000485

Cited by 44 publications

(29 citation statements)

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“…This putative NO deficit may be responsible for their endothelial dysfunction, which in turn may contribute to SSBP by impeding vasodilation after a salt load. 49 4. The sympathetic nervous system: Several investigators showed that in an SS substrain of SHR, the pressor response to salt was associated with increased levels of plasma and urine catecholamines 50 and renal nerve activity, 51 whereas alterations in hypothalamic norepinephrine turnover with decreased norepinephrine content suggested diminished central sympathetic inhibition of peripheral sympathetic outflow.…”

Section: Elijovich Et Al Salt Sensitivity Of Blood Pressure E11mentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

386

230

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The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 23, 2016, and the American Heart Association Executive Committee on February 23, 2016. A copy of the document is available at http://professional.heart.org/statements by using either "Search for Guidelines & Statements" or the "Browse by Topic" area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@ wolterskluwer.com.The American Heart Association requests that this document be cited as follows: Elijovich F, Weinberger MH, Anderson CAM, Appel LJ, Bursztyn M, Cook NR, Dart RA, Newton-Cheh CH, Sacks FM, Laffer CL; on behalf of the American Heart Association Professional and Public Education Committee of the Council on Hypertension; Council on Functional Genomics and Translational Biology; and Stroke Council. Salt sensitivity of blood pressure: a scientific statement from the American Heart Association. Hypertension. 2016;68:e7-e46. doi: 10.1161/HYP.0000000000000047.Expert peer review of AHA Scientific Statements is conducted by the AHA Office of Science Operations. For more on AHA statements and guidelines development, visit http://professional.heart.org/statements. Select the "Guidelines & Statements" drop-down menu, then click "Publication Development."Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.heart.org/HEARTORG/General/CopyrightPermission-Guidelines_UCM_300404_Article.jsp. A link to the "Copyright Permissions Request Form" appears on the right side of the page. Figure 2 shows the major effect of aging in increasing the prevalence of SSBP in both normotensive and hypertensive subjects. An important and encouraging observation is that the multiple phenotypic characteristics described in pure SS strains of rodents reproduce those observed in humans, indicating that the phenotypic cluster of SSBP can be brought out in humans by the current techniques used in carefully controlled research. Additionally, despite the unquestionable influence of environmental factors in the determination of SSBP in humans, estimates of its heritability have been as high as 74% in blacks 9 and 50% in Chinese subjects, 10 both higher than those for hypertension. Salt Sensitivity of Blood PressureAn important issue is the clinical significance of the SSBP phenotype. There was increasing understanding that it represents an abnormality. The reasons w...

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Section: Elijovich Et Al Salt Sensitivity Of Blood Pressure E11mentioning

confidence: 99%

Salt Sensitivity of Blood Pressure

Elijovich¹,

Weinberger²,

Anderson³

et al. 2016

Hypertension

386

230

View full text Add to dashboard Cite

show abstract

“…Infusion of L-arginine, the substrate for NOS, evokes a blunted renal vasodilatory response in patients with salt-sensitive versus salt-resistant hypertension and controls. 35 This implies the existence of a specific renal NO defect in salt sensitivity. Although the issue of salt sensitivity was not specifically addressed, Cardillo et al 36 observed reduced NO-dependent vasodilator activity in the forearm circulation during mental stress in blacks.…”

Section: Discussionmentioning

confidence: 99%

Effects of aging and alterations in dietary sodium intake on total nitric oxide production

Schmidt

Beierwaltes

Baylis

2001

American Journal of Kidney Diseases

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Animal studies suggest that nitric oxide (NO) deficiency is linked to salt-sensitive hypertension and that NO activity decreases during normal aging. This study investigates the impact of increasing age and manipulations in dietary salt intake on biochemical indices of the NO system in healthy humans. We measured NO 2 + NO 3 (NO X ; stable oxidation products of NO) and cyclic guanosine monophosphate (cGMP; major second messenger) in plasma and urine of 30 healthy subjects aged 22 to 77 years. Subjects were maintained on controlled low NO X and low-, normal-, or high-salt diets for 3 days. Salt sensitivity of blood pressure was seen only in the oldest subjects. Plasma renin activity was suppressed by a high salt intake in all age groups, and baseline values declined with advancing age. Neither age nor salt intake correlated with indices of NO activity over the third 24-hour period of controlled salt intake. In a subgroup of subjects aged 33 ± 4 years challenged with ultrahigh sodium intake (400 mEq/24 h), again there was no increase in NO 2 + NO 3 or cGMP measures. In contrast to animal studies, there is no correlation in humans between either salt intake or age and total NO production and activity, indicated by NO 2 + NO 3 and cGMP measures. This does not preclude undetected alterations occurring in NO production and/or activity in strategic locations in the kidney and cardiovascular system. Limitations of blood and urine measurements of NO 2 + NO 3 and cGMP as indices of NO activity are discussed. Index WordsSodium excretion; blood pressure (BP); salt-sensitive hypertension; cyclic guanosine monophosphate (cGMP); NO 2 + NO 3 (NO X ); nitric oxide (NO) With Advancing Age, the kidney is less able to either conserve sodium in response to dietary restriction or remove sodium after excess intake. 1,2 Both aging rats and humans have a blunted ability to excrete an acutely administered sodium load, 1,3,4 and pressure natriuresis is attenuated in the old rat. 5,6 According to Guyton et al, 7 impaired pressure natriuresis leads to salt-sensitive hypertension, and the incidence of salt-sensitive hypertension increases substantially in humans with increasing age, 8 reflected by an increased frequency of low-renin essential hypertension. 9 Increased nitric oxide (NO) production occurs in response to high dietary salt intake in normal rats, and chronic NO synthase (NOS) inhibition combined with high dietary salt intake can lead to volume-dependent hypertension. [10][11][12][13] In addition, the genetically salt-sensitive hypertension in the Dahl rat is associated with defective NO production in the face of high sodium intake. 14,15 NO directly inhibits sodium transport in several parts of the tubule. NO is NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript also a powerful renal vasodilator, and in NO deficiency experimentally induced by NOS inhibition, pressure natriuresis is attenuated. 16,17 It therefore is widely held that an appropriate increase in NO production in the kidney and perip...

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“…High salt intake initially stimulates NO production (to maintain normotension despite increase in blood volume caused by increased salt intake) to maintain blood flow, and only when the enhanced salt intake continues for a long time, NO synthesis is decreased (possibly because of the exhaustion of the eNOS activity), which leads to the development of hypertension (Nakanishi et al, 2002). On the other hand, supplementation of L-arginine reduces high salt intakeinduced hypertension (Campese et al, 1997;Bayorh et al, 1999). Vasodilation to acetylcholine increases with potassium chloride supplementation, in patients with hypertension (Taddei et al, 1994), which explains its mild to moderate antihypertensive action.…”

Section: No and Hypertensionmentioning

confidence: 99%

Long-chain polyunsaturated fatty acids interact with nitric oxide, superoxide anion, and transforming growth factor-β to prevent human essential hypertension

Das¹

2004

Eur J Clin Nutr

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Patients with uncontrolled essential hypertension have elevated concentrations of superoxide anion (O 2 ÀK ), hydrogen peroxide (H 2 O 2 ), lipid peroxides, endothelin, and transforming growth factor-b (TGF-b) with a simultaneous decrease in endothelial nitric oxide (eNO), superoxide dismutase (SOD), vitamin E, and long-chain polyunsaturated fatty acids (LCPUFAs). Physiological concentrations of angiotensin II activate NAD(P)H oxidase and trigger free radical generation (especially that of O 2 ÀK ). Normally, angiotensin II-induced oxidative stress is abrogated by adequate production and release of eNO, which quenches O 2 ÀK to restore normotension. Angiotensin II also stimulates the production of endothelin and TGF-b. TGF-b enhances NO generation, which in turn suppresses TGF-b production. Thus, NO has a regulatory role on TGF-b production and is also a physiological antagonist of endothelin. Antihypertensive drugs suppress the production of O 2 ÀK and TGF-b and enhance eNO synthesis to bring about their beneficial actions. LCPUFAs suppress angiotensin-converting enzyme (ACE) activity, reduce angiotensin II formation, enhance eNO generation, and suppress TGF-b expression. Perinatal supplementation of LCPUFAs decreases insulin resistance and prevents the development of hypertension in adult life, whereas deficiency of LCPUFAs in the perinatal period results in raised blood pressure later in life. Patients with essential hypertension have low concentrations of various LCPUFAs in their plasma phospholipid fraction. Based on this, it is proposed that LCPUFAs serve as endogenous regulators of ACE activity, O 2 ÀK , eNO generation, and TGF-b expression. Further, LCPUFAs have actions similar to statins, inhibit (especially o-3 fatty acids) cyclooxygenase activity and suppress the synthesis of proinflammatory cytokines, and activate the parasympathetic nervous system, all actions that reduce the risk of major vascular events. Hence, it is proposed that availability of adequate amounts of LCPUFAs during the critical periods of growth prevents the development of hypertension in adulthood.

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Effect of L-arginine on systemic and renal haemodynamics in salt-sensitive patients with essential hypertension

Cited by 44 publications

References 2 publications

Salt Sensitivity of Blood Pressure

Salt Sensitivity of Blood Pressure

Effects of aging and alterations in dietary sodium intake on total nitric oxide production

Long-chain polyunsaturated fatty acids interact with nitric oxide, superoxide anion, and transforming growth factor-β to prevent human essential hypertension

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