Renal and systemic hemodynamics in sustained essential hypertension.

London, Gérard M.; Me, Safar; Sassard, J; Levenson, J; Simón, A

doi:10.1161/01.hyp.6.5.743

Cited by 63 publications

(23 citation statements)

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“…3,4 Because RBF and cardiac output (CO) are strongly correlated, the ratio of both is a reliable parameter for the assessment of renal perfusion. 24,25 In this study, CO was not measured. However, potential confounding factors such as blood pressure or the size and structure of the heart, which reflect profound alterations in systemic hemodynamics, were similar between the different genotypes in our study population.…”

Section: Discussionmentioning

confidence: 90%

“…Previous studies have reported normal to enhanced renal blood and/or plasma flow in the prehypertensive stage and in borderline hypertension, 2,4,19 -22 whereas in sustained hypertension, the consistently observed pattern of renal hemodynamics is characterized by a decreased renal blood and/or plasma flow and a normal to slightly decreased GFR, resulting in an elevated renal filtration fraction. [23][24][25] Renal hemodynamic changes have been supposed to play an important role in the development of hypertension. Evidence for this hypothesis comes from the observation of an abnormal control of renal circulation in subjects with a positive family history of hypertension in response to mental stress, and Bianchi et al 4 found that normotensive offspring of hypertensive parents were characterized by high renal blood flow (RBF) despite normal cardiac output, suggesting a specific renal vasodilation in the prehypertensive stage.…”

Section: Discussionmentioning

confidence: 99%

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G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

et al. 2001

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Abstract-The C825T polymorphism of the gene encoding the G-protein ␤ 3 subunit (GNB3) is associated with increased intracellular signal transduction and arterial hypertension. The aim of the study was to investigate the impact of this polymorphism on early adaptive processes of the left ventricle and renal hemodynamic changes in young normotensive to mildly hypertensive subjects. Ninety-five white male students with normal or mildly elevated blood pressure were genotyped for the GNB3 C825T polymorphism. In each participant, 24-hour ambulatory blood pressure, left ventricular structure and function (2D-guided M-mode echocardiography), renal plasma flow (para-aminohippurate clearance), glomerular filtration rate (inulin clearance), and 24-hour urinary sodium excretion were determined. The GNB3 825T allele was not associated with casual or ambulatory blood pressure, parameters of left ventricular structure or function, glomerular filtration, or 24-hour urinary sodium excretion. However, in T-allele carriers (CTϩTT), renal plasma flow was higher than in CC subjects (CT/TT: 659Ϯ96 versus CC: 614Ϯ91 mL/min, Pϭ0.019). ANOVA disclosed that renal plasma flow was independently influenced by both genotype and blood pressure, with hypertensives having a higher renal plasma flow than normotensive subjects. This was the fact irrespective of the criteria used for the definition of hypertension (World Health Organization or 24-hour ambulatory blood pressure criteria). The GNB3 825T variant is associated with increased renal perfusion in this study. Because early renal hemodynamic changes play a pivotal role in the pathogenesis of essential hypertension, our data suggest a relevance of increased G-protein activation in the pathogenesis of hypertension. Key Words: G proteins Ⅲ polymorphism Ⅲ genes Ⅲ hypertension, essential Ⅲ hemodynamics T he early course of essential hypertension is characterized by structural and functional changes in the systemic and renal circulation. In addition, early structural changes of the left ventricle (LV) have been reported. Increased concentric remodeling of the LV and impaired diastolic function have been recognized to reflect early changes of the myocardium in early essential hypertension. 1 Renal hemodynamics were shown to be abnormally regulated in a prehypertensive stage, and increased renal perfusion was reported in early hypertension. [2][3][4] It has been proposed that renal vascular changes may not simply be a complication but the cause for blood pressure elevation and thus may play a pivotal role in the pathogenesis of essential hypertension. 5 In the search for mechanisms by which genetic markers contribute to the development of hypertension, recent interest focused on a novel gene polymorphism closely associated with a wellestablished intermediate phenotype, that is, the enhanced Na ϩ /H ϩ exchanger activity in hypertensive subjects. 6 Immortalized lymphoblasts of these patients have been found to respond with enhanced G-protein activation on stimulation. 7 Subsequently, a single nucleo...

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

et al. 2001

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“…5 Indeed, this increased resistance to blood flow is distributed throughout all tissues, 6 and Pickering observed that the so-called "minimum vascular resistance" (the resistance to blood flow after maximal vasodilation) remained increased in hypertensive patients. 7 Furthermore, Doyle and Black 8 showed that hypertension is associated with an increased "reactivity" of the forearm, i.e., infusion of agonists caused greater pressor responses in forearms of essential hypertensive patients.…”

Section: Essential Hypertensionmentioning

confidence: 99%

Small artery structure in hypertension. Dual processes of remodeling and growth.

Heagerty¹,

Aalkjær²,

Bund³

et al. 1993

Hypertension

607

363

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“…- 40 The decrease in renal blood flow and the renal fraction of cardiac output with hypertension was found to be reversible with administration of centrally acting sympatholytic agents. 26 - 28 However, structural processes in the renal vascular bed also appeared to be responsible for the age-related fall in renal perfusion, because age per se reduced the vasodilator response to administration of acetylcholine and sodium load. 41 Furthermore, a close negative relation between renal blood flow and the severity of arteriolar nephrosclerosis was noted in a series of more than 100 renal biopsies.…”

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confidence: 99%

Accelerated decline in renal perfusion with aging in essential hypertension.

1994

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The present cross-sectional study was designed to assess the effect of the severity of hypertensive cardiovascular disease and age on renal hemodynamics. In a homogeneous population of 157 white men (aged 15 to 87 years), we assessed renal and systemic hemodynamics by measuring mean arterial pressure invasively, renal blood flow by 131 Ipara-aminohippuric acid clearance, and cardiac output by the indocyanine dye dilution technique. Stepwise multiple regression analysis revealed the following independent determinants of renal blood flow: age (/3=-.42, P<.001), height O = + .14, P<.03), mean arterial pressure (/3= -.15, P<.02), and cardiac output (/3=+.19, P<.008). Renal blood flow corrected for height correlated inversely with age in all three groups. However, the renal fraction of cardiac output S tructural changes in the vascular bed of the kidneys caused by arterial hypertension, termed arteriolar nephrosclerosis, have been found to correlate with similar changes in the retina, pancreas, and salivary glands but nevertheless do occur more frequently and extensively in the kidneys than in any other organ.1 Studies of end-stage renal disease showed that hypertension accounted for 15% to 20% of all cases of renal failure in the United States, a percentage that increased to 30% of cases of renal failure in minority populations. 24 In a previous report on the natural history of essential hypertension (at a time when high blood pressure frequently remained untreated), 18% of 350 patients had evidence of impaired renal function that led to end-stage renal disease in 12%. 5At necropsy, 68% to 97% of patients with well-established hypertension had histologicalry proven renal arteriosclerosis.6 -7 The severity of arteriolar renal involvement appeared to be determined by the severity of hypertensive disease. 6 The degree of the renal vascular involvement, either structural or functional, was closely correlated with the reduction in renal blood flow. 8 ' 9 A subsequent study using selective renal arteriography confirmed a good corReceived July 14, 1993; accepted in revised form December 3, 1993.From the Department of Medicine IV, University of ErlangenNurnberg (Germany) (R.E.S.); the Department of Medicine, University of Bonn, Bonn-Venusberg, Germany (H.S.); and the Department of Internal Medicine, Section on Hypertensive Diseases, Ochsner Clinic and Alton Ochsner Medical Foundation, New Orleans, La (F.H.M.).This manuscript, in which one of the authors (F.H.M.) is from the Alton Ochsner Medical Foundation, was sent to the previous Hypertension editorial office at the University of Iowa for review by expert referees, for editorial decision, and for final disposition.Reprint requests to Dr Roland E. Schmieder, 4. Medizinische Klinik/Nephrologie, University of Erlangen-Nurnberg, Kontumazgarten 14-18, D-8500 Nurnberg 80, FRG.did not correlate with age in borderline hypertension (r=.17, P=NS) and in normotension (r=.12, P=NS), suggesting a parallel decline in renal blood flow and cardiac output with aging. In contrast,...

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Renal and systemic hemodynamics in sustained essential hypertension.

Cited by 63 publications

References 60 publications

G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

Small artery structure in hypertension. Dual processes of remodeling and growth.

Accelerated decline in renal perfusion with aging in essential hypertension.

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Renal and systemic hemodynamics in sustained essential hypertension.

Cited by 63 publications

References 60 publications

G-Protein β 3 Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

G-Protein β 3 Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

Small artery structure in hypertension. Dual processes of remodeling and growth.

Accelerated decline in renal perfusion with aging in essential hypertension.

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G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension

G-Protein β ₃ Subunit Gene (GNB3) 825T Allele Is Associated With Enhanced Renal Perfusion in Early Hypertension