Renal sodium excretion and the peritubular capillary physical factors in essential hypertension.

Willassen, Yngvar; Ofstad, J.

doi:10.1161/01.hyp.2.6.771

Cited by 34 publications

(11 citation statements)

References 25 publications

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“…6). That GC-A null mice displayed increased sodium excretion under conditions of low protein volume expansion is consistent with data from many laboratories demonstrating exaggerated natriuresis in both animals and humans with hypertension (23)(24)(25)(26)(27). Various hypotheses for enhanced natriuresis have included an augmented effect of ANP on the kidney (25,28).…”

Section: Resultssupporting

confidence: 86%

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Dubois

Kishimoto

Lillis

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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Disruption of the atrial natriuretic peptide (ANP) receptor [guanylyl cyclase-A (GC-A)] gene yields mice with a salt-resistant form of hypertension, raising fundamental questions on the role of ANP in acute regulation of the kidney. Here, we show that water intake, food consumption, stool weight, urine volume, and sodium excretion are not significantly different between wild-type and GC-A null mice on standard rodent chow (0.7% NaCl) or a high-salt diet (8% NaCl). In conscious mice with an indwelling catheter, the infusion of a physiological saline solution containing 4% BSA resulted in a marked natriuresis͞diuresis in wild-type mice but no response in GC-A null animals. When physiological saline was given by gavage, however, the kidney response of wild-type and null mice was equivalent, raising the possibility that the gastrointestinal tract can directly regulate kidney function. However, administration of 0.9% saline through an intraperitoneal route also resulted in equal kidney responses in wild-type and null mice. When 0.9% NaCl lacking protein was infused i.v., wild-type and null mice both responded at the kidney level. Thus, GC-A appears dispensable for regulation of sodium͞water excretion in response to changes in dietary sodium concentration, but likely becomes critical in volume expansions where the isooncotic pressure remains constant, such as head-out immersion or the initial and correctable stages of congestive heart failure.

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Section: Resultssupporting

confidence: 86%

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Dubois

Kishimoto

Lillis

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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“…Thus, early borderline hypertension is often salt-resistant (70) with minimally decreased renal plasma flow and normal GFR (71), and this corresponds with the renal hemodynamic changes associated with minimal renal arteriolar lesions (42). Younger subjects with short-duration (mean, 3 yr) hypertension also do not show any increase in peritubular capillary hydrostatic pressure with salt-loading, consistent with a normal autoregulatory response (72). In contrast, older hypertensive subjects tend to be salt-sensitive (70), have lower renal blood flow (73), have more prominent renal arteriolar changes (30), and worse renal function (30); some studies suggest that the age-dependent decline in GFR in our population may largely relate to the presence of hypertension (74).…”

Section: Relevance Of Stages Of Hypertension With the Progression Of mentioning

confidence: 74%

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Johnson

Segal

Srinivas

et al. 2005

Journal of the American Society of Nephrology

263

171

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Hypertension and hypertension-associated ESRD are epidemic in society. The mechanisms responsible for renal progression in mild to moderate hypertension and those groups most at risk need to be identified. Historic, epidemiologic, clinical, and experimental studies on the pathogenesis of hypertension and hypertension-associated renal disease are reviewed and an overview/hypothesis for the mechanisms involved in renal progression is presented. There is increasing evidence that hypertension may exist in one of two forms/stages. The first stage, most commonly observed in early or borderline hypertension, is characterized by salt-resistance, normal or only slightly decreased GFR, relatively normal or mild renal arteriolosclerosis, and normal renal autoregulation. This group is at minimal risk for renal progression. The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted renal autoregulation, defines a group at highest risk for the development of microalbuminuria, albuminuria, and progressive renal disease. This second stage is more likely to be observed in blacks, in subjects with gout or hyperuricemia, with low level lead intoxication, or with severe obesity/metabolic syndrome. The two major mechanistic pathways for causing impaired autoregulation at mild to moderate elevations in BP appear to be hyperuricemia and/or low nephron number. Understanding the pathogenetic pathways mediating renal progression in hypertensive subjects should help identify those subjects at highest risk and may provide insights into new therapeutic maneuvers to slow or prevent progression.

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“…6 - 7 The increase of plasma volume (PV) during saline infusion was computed from the decrease of hct using the following equation:…”

Section: Analytical Procedures and Calculationsmentioning

confidence: 99%

“…4 -5 In previous studies 6 - 7 we have examinted the postglomerular capillary physical forces in humans by estimating the peritubular capillary hydrostatic pressure from the intrarenal venous (wedged) pressure (IRVP), 8 and by estimating the colloid osmotic forces from the systemic oncotic pressure and the filtration fraction. Our results indicate that the peritubular capillary physical factors are normal in uncomplicated essential hypertension (EH) both in antidiuresis and during saline volume expansion.…”

mentioning

confidence: 99%

“…Our results indicate that the peritubular capillary physical factors are normal in uncomplicated essential hypertension (EH) both in antidiuresis and during saline volume expansion. 7 In the present study we have applied an identical experimental protocol to study the relationship between the peritubular physical forces and the sodium excretion in the renal hypertension of chronic glomerulonephritis (GN) in different stages of the disease.…”

mentioning

confidence: 99%

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Intrarenal pressure and sodium excretion in hypertension of chronic glomerulonephritis in humans.

Willassen¹,

Ofstad²

1983

Hypertension

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SUMMARY The relationship between the fractional excretion of filtered sodium (FE^) and the peritubular capillary physical factors (PCPF) in the hypertension (HT) of chronic glomerulonephritis (GN) was examined in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% net increase of body weight) in 32 GN patients (16 with HT), and compared with our previous findings in 20 normal individuals (NORM) and 19 patients with essential hypertension (EH). Fourteen GN patients (seven with HT) had a 75% reduction of glomerular filtration rate (GFR), the others (nine with HT) had normal or near normal GFR. The PCPF were estimated from the intrarenal venous (wedged) pressure (IRVP) and the calculated efferent arteriolar protein concentration (EAPC).In C, IRVP correlated to GFR (r = 0.682, p < 0.001) and (FE^,,) (r = -0.357, p < 0.05), but IRVP and EAPC were similar in HT and normotension at comparable levels of GFR. The increase of FE Na during E (AFE N> ) was exaggerated in all HT groups even at reduced levels of GFR, and could not be related to changes in renal hemodynamics or PCPF. AFE^ correlated with mean arterial pressure in C both in GN (r, = 0.702, p < 0.01) and in the combined NORM/EH group (r 2 = 0.478, p < 0.01), with r, > r 2 (p < 0.005). The findings indicate that the pathogenesis of hypertension of chronic glomerulonephritis is independent of changes in the PCPF, and are compatible with the idea that humoral factors are the main mediators of the altered sodium excretion during saline volume expansion in the HT of both chronic GN and EH. (Hypertension 5:375-384, 1983) KEY WORDS • renal hypertension • renal sodium excretion • renal hemodynamics intrarenal pressure • glomerulonephritis R ETENTION of sodium is considered to be an important pathogenetic factor in the hypertension of primary, nonvascular renal disease. The mechanism of sodium retention as well as the hypertensive mode of action of the sodium ion is, however, still not clear. Changes in the hydrostatic and oncotic pressures in the peritubular microcirculation have been shown to modify the tubular reabsorption of sodium in different experimental animals.1 " 3 By inference, these physical factors have been implicated as mediators of altered tubular sodium transport in phys- Received July 19, 1982; revision accepted October 8, 1982. iological and pathological conditions in man, including hypertension. 4 -5 In previous studies 6 -7 we have examinted the postglomerular capillary physical forces in humans by estimating the peritubular capillary hydrostatic pressure from the intrarenal venous (wedged) pressure (IRVP), 8 and by estimating the colloid osmotic forces from the systemic oncotic pressure and the filtration fraction. Our results indicate that the peritubular capillary physical factors are normal in uncomplicated essential hypertension (EH) both in antidiuresis and during saline volume expansion. 7In the present study we have applied an identical experimental protocol to study the relationship between the peritubular ph...

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Renal sodium excretion and the peritubular capillary physical factors in essential hypertension.

Cited by 34 publications

References 25 publications

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

A genetic model defines the importance of the atrial natriuretic peptide receptor (guanylyl cyclase-A) in the regulation of kidney function

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Intrarenal pressure and sodium excretion in hypertension of chronic glomerulonephritis in humans.

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