Abnormal renal responses to calcium entry blockade in normotensive offspring of hypertensive parents.

Montanari, Alberto; Ragni, G; Guerra, Angela; Colla, Rossana; Novarini, A; Coruzzi, Paolo

doi:10.1161/01.hyp.12.5.498

Cited by 30 publications

(13 citation statements)

References 48 publications

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“…Three subsequent studies, including the present one, that controlled dietary sodium intake and used more precise renal clearance methods to estimate fractional excretion of lithium have found no difference in the fractional excretion of lithium between the normotensive offspring of hypertensive and normotensive parents. 8 ' 20 In our study and that of Stadler and colleagues, 8 the fractional excretion of lithium did not differ between the offspring groups on low-or on high-sodium diet; furthermore, in our study, it did not differ between the groups during acute natriuresis induced by intravenous saline infusion. Judged against these more thorough and carefully controlled investigations, the initial report of Weder may represent a false-positive result.…”

Section: Fig 2 Line Graphs Show Effect Of Intravenous Infusion Of Nosupporting

confidence: 63%

Renal sodium excretion in sons of hypertensive parents.

Turner

Reilly

1993

Hypertension

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The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is increased in normotensive white men with a familial predisposition to develop essential hypertension. We compared 11 normotensive sons of two hypertensive parents (SOHT) with 11 normotensive sons of two normotensive parents (SONT); renal sodium handling was assessed after 1 week of low-sodium diet ( A prevailing hypothesis to explain the familial predisposition to essential hypertension (hy-. pertension) is that inherited factors have effects that impair the kidneys' ability to excrete sodium chloride (sodium).1 Sodium excretion may be impaired either because less sodium is filtered by the kidneys or because more filtered sodium is reabsorbed by the renal tubules. Either alteration might result from an abnormality that is intrinsic to the kidneys or one that is secondary to extrarenal factors. Because plasma sodium concentration and glomerular filtration rate -the determinants of the filtered load of sodium-are not decreased early in the course of uncomplicated hypertension, 2 increased tubular reabsorption of sodium has been the renal alteration most often postulated to impair sodium excretion and contribute to the development of hypertension.Despite compelling arguments presented by Guyton and others that impairment of renal sodium excretion is Received February 15,1993; accepted in revised form April 28, 1993.From the Division of Hypertension, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minn (S.T.T.), and the Department of Human Genetics, University of Michigan, Ann Arbor (S.L.R.).Previously published in abstract form (Hypertension. 1989; 14:345).Correspondence to Stephen T. Turner, MD, Division of Hypertension, Mayo Foundation, Rochester, MN 55905. a sine qua non for hypertension to develop, 3 studies that have assessed renal excretion and tubular reabsorption of sodium in normotensive humans with a familial predisposition to develop hypertension have been inconsistent in their results. For example, the natriuretic response to intravenous saline infusion has been reported to be either decreased or increased in normotensive first-degree relatives of hypertensive patients, 4 " 6 and the fractional excretion of lithium -an inverse indicator of proximal tubular reabsorption of sodiumhas been reported to be either increased or no different in normotensive offspring of hypertensive patients. 7 -8 The reasons for these inconsistencies may include differences between studies in methods used to select subjects with contrasting predispositions to develop hypertension, differences in the level of dietary sodium intake before assessment of renal sodium handling, and differences in the measures used to assess renal sodium handling.We undertook the present study in search of evidence to support the hypothesis that renal excretion of sodium is impaired and that tubular reabsorption of sodium is increased in normotensive white men with a familial predisposit...

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Section: Fig 2 Line Graphs Show Effect Of Intravenous Infusion Of Nosupporting

confidence: 63%

Renal sodium excretion in sons of hypertensive parents.

Turner

Reilly

1993

Hypertension

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“…28 Such a procedure was preferred rather than standard urinary clearance because an unethical bladder catheterization should be necessary to avoid errors in urine collection, potentially of the same order of magnitude as that of measured changes in renal hemodynamics. 16,24 Constant infusion technique already has been shown to detect in humans rapid changes in renal hemodynamics as a result of administration of different substances such as nifedipine, 29 L-NAME 16,24 and Ang II. 30 PAH and inulin concentrations were measured in the infusate, then multiplied for the volume of infused solution per minute.…”

Section: Calculationsmentioning

confidence: 99%

Renal Hemodynamic Control by Endothelin and Nitric Oxide Under Angiotensin II Blockade in Man

et al. 2002

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Abstract-To investigate whether endothelin-A receptors and nitric oxide modulate renal hemodynamics in man under angiotensin II receptor-1 blockade, 6 healthy volunteers, on a 240 mmol Na diet, underwent 4 separate renal hemodynamic measurements, in 3 of which endothelin-A blocker BQ-123 0.2 nmol ⅐ kg ⅐ min Ϫ1 was infused for 90 minutes after pretreatment with either placebo, telmisartan 1 mg ⅐ kg ⅐ day Ϫ1 for 3 days, or telmisartan as well, but with co-infusion of both BQ-123 and N G -nitro-L-arginine methylester 0.5 g ⅐ kg ⅐ min Ϫ1 . A fourth infusion was made with N G -nitro-L-arginine methylester alone. No change followed infusion of either N G -nitro-L-arginine methylester alone or BQ-123 alone. With BQ-123 after telmisartan, renal blood flow rose from 916Ϯ56 mL ⅐ min Ϫ1 ⅐ 1.73 m 2 to 1047Ϯ51.2 (PϽ0.001), and renal vascular resistances fell from 89Ϯ7 mm Hg ⅐ min ⅐ L Ϫ1 to 74Ϯ4 (PϽ0.001). These changes were fully abolished by the co-infused N G -nitro-L-arginine methylester. Infusion of BQ-123, devoid of renal hemodynamic effects at baseline, produces significant renal vasodilation when angiotensin II receptors are blocked, indicating an increasing renal hemodynamic role of endothelin-A-receptor activity. Because such a vasodilation is prevented by nonvasoconstricting microdoses of N G -nitro-L-arginine methylester, nitric oxide-endothelin balance controls substantially renal hemodynamics under angiotensin II blockade. These findings are consistent with a rationale of the association of endothelin-A blockers with angiotensin II blockers or angiotensin-converting enzyme inhibitors in treating nitric oxide-deficient conditions such as arterial hypertension, heart failure, and chronic renal diseases. Key Words: angiotensin II Ⅲ nitric oxide Ⅲ endothelin Ⅲ kidney Ⅲ hemodynamics Ⅲ L-NAME Ⅲ receptors, endothelin H emodynamic control in both systemic circulation and kidney results physiologically from a balance of opposing vasodilator systems such as nitric oxide (NO) and prostaglandins, and vasoconstrictor systems. 1 These latter include, besides sympathetic nervous system, the 2 potent peptide vasoconstrictors angiotensin II (Ang II) and endothelin-1 (ET-1), 1 this latter being the predominant isoform of endothelin family expressed in human vasculature. 2 Vasoactive properties of ET-1 are mediated by 2 receptor subtypes, ET A and ET B , both leading to vasoconstriction in vascular smooth muscle cells, whereas activation of ET B in endothelial cells may cause vasodilation through the release of prostacyclin and NO. 2,3 At the kidney level, however, studies in both dogs 4,5 and humans 6,7,8 have indicated the ET A receptor as the main mediator of the vasoconstrictor effect of ET-1.A considerable body of evidence has shown that ET-1, although it is the most potent endogenous vasoconstrictor, assumes a major hemodynamic role and contributes to the end-organ damage, mainly under experimental and clinical pathophysiological conditions. 2,3 Furthermore, a number of interactions have been recognized between Ang II and ET...

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“…15 These publications suggest that an abnormal renal vasoconstriction exists in the prehypertensive state. Offspring of hypertensive parents have shown an exaggerated renal vasodilation in response to calcium channel blockers 16 - 17 and converting enzyme inhibitors. 18 ' 19 This vasodilation suggests the existence of functional renal vasoconstriction in subjects at risk of developing hypertension.…”

Section: Renal Hemodynamics In the Prehypertensive State In Humansmentioning

confidence: 99%

Are renal hemodynamics a key factor in the development and maintenance of arterial hypertension in humans?

Ruilope¹,

Lahera²,

Rodicio³

et al. 1994

Hypertension

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The kidney plays a key role in the control of body fluids and blood pressure. Evidence has shown that impairment of renal function can lead to the development of arterial hypertension. The regulation of renal blood flow appears to be a key element in the pathophysiology of the hypertensive process, because multiple evidence suggests the existence of a functional enhancement of renal vascular tone in this disorder. The existence of renal vasoconstriction and of an inherited defect in the regulation of renal blood flow has been proposed in the prehypertensive stage. The mechanisms responsible for this alteration include a lack of modulation of the renal vasculature to angiotensin II, increased sympathetic activity, or suppressed renal dopaminergic activity. Established hypertension is characterized by elevated renal vascular resistance, decreased renal blood flow, sustained glomerular filtration rate, and increased filtration fraction. The increase in renal vascular resistance is initially due to elevations in renal vascular tone and is reversible, whereas later it becomes irreversible because of structural changes involved in nephrosclerosis. Antihypertensive drugs are able to decrease blood pressure and to prevent the development of further renal vascular damage independently of variable effects on renal hemodynamics. (Hypertension. 1994^3 -3 -9.)Key Words • hemodynamics • glomerular filtration rate • sodium • hypertension, arterial • antihypertensive agents I t has long been known that the kidney plays a central role in the control of body fluids and blood pressure and that a derangement of renal function could lead to the development of hypertension.1 Furthermore, several theories have been proposed as to which specific hemodynamic or tubular alterations could induce an elevation of blood pressure.2 " 8 In this review, the clinical studies investigating changes in renal function accompanying the development and maintenance of essential hypertension are critically examined. The studies indicate that the common manifestation of hypertension is an increase of intrarenal vascular resistance; however, the manner in which this single alteration could trigger all the pathophysiological alterations responsible for hypertension is not completely known. Renal Hemodynamics in the Prehypertensive State in HumansThe role of the kidney in the development of essential hypertension has been examined in studies of control and experimental subjects with a family history of hypertension.9 These studies have revealed conflicting results. Bianchi et al 10 -11 found that renal blood flow and glomerular filtration rate were elevated in offspring of hypertensive parents, whereas filtration fraction remained normal. glomerular filtration rate were normal in the offspring of both normotensive and hypertensive parents; however, renal vascular resistance was increased.13 Van Hooft et al 14 reported that renal blood flow was reduced and renal vascular resistance and filtration fraction were elevated in young people at risk for hy...

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Abnormal renal responses to calcium entry blockade in normotensive offspring of hypertensive parents.

Cited by 30 publications

References 48 publications

Renal sodium excretion in sons of hypertensive parents.

Renal sodium excretion in sons of hypertensive parents.

Renal Hemodynamic Control by Endothelin and Nitric Oxide Under Angiotensin II Blockade in Man

Are renal hemodynamics a key factor in the development and maintenance of arterial hypertension in humans?

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