Intrarenal Pressure and Exaggerated Natriuresis in Essential Hypertension

Lowenstein, Jerome; Beranbaum, Elliott R.; Chasis, Herbert; Baldwin, David S.

doi:10.1042/cs0380359

Cited by 118 publications

(53 citation statements)

References 24 publications

(30 reference statements)

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“…Lowenstein et al ' found an elevated intrarenal venous pressure (IRVP) in patients with essential hypertension, and also observed that the augmented natriuretic response to saline volume expansion was associated with an exaggerated increase in IRVP in these patients. 8 These findings have been considered as evidence for an increased peritubular capillary hydrostatic pressure in human essential hypertension compensating for the postulated sodium retaining mechanisms and partly explaining the "resetting" of the pressure natriuresis. 8 " 11 We have not been able to confirm the findings of Lowenstein et al that saline volume expansion increases the IRVP in normal man, 1* and our preliminary observations in patients with essential hypertension 1 ' did not suggest any abnormality of IRVP.…”

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“…8 These findings have been considered as evidence for an increased peritubular capillary hydrostatic pressure in human essential hypertension compensating for the postulated sodium retaining mechanisms and partly explaining the "resetting" of the pressure natriuresis. 8 " 11 We have not been able to confirm the findings of Lowenstein et al that saline volume expansion increases the IRVP in normal man, 1* and our preliminary observations in patients with essential hypertension 1 ' did not suggest any abnormality of IRVP. In our present study we examine the IRVP in antidiuresis and during sustained volume expansion in essential hypertension to assess the hydrostatic and oncotic forces acting in the postglomerular capillaries in these experimental conditions.…”

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confidence: 99%

“…At normal BP, sodium is therefore retained until the BP has increased enough to establish sodium and water balance. 8 ' The mediators of this abnormal relationship between kidney perfusion pressure and the renal excretion of sodium -commonly referred to as "resetting" of the pressure natriuresis -have not yet been identified. The hypothesis presupposes factors causing sodium retention as a primary event as well as natriuretic mechanisms associated with the development of hypertension.…”

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

Willassen¹,

Ofstad²

1980

Hypertension

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SUMMARY Peritubular capillary hydrostatic and oncotic forces and their relationship to the renal excretion of sodium (U Na V) were examined in 19 patients with moderate and uncomplicated essential hypertension (HT) and compared with data from 20 normotensire subjects (NT). Observations were made in hydropenia (C) and during sustained isotonlc saline volume expansion (E; 3% increase in body weight). 1 ' a The hypothesis states that this relationship is altered in essential hypertension so that a higher BP is needed for the renal excretion of a given quantity of sodium. At normal BP, sodium is therefore retained until the BP has increased enough to establish sodium and water balance.8 ' The mediators of this abnormal relationship between

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

Willassen¹,

Ofstad²

1980

Hypertension

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“…18 Also, they have pharmacological evidence that the progression of glomerulosclerosis can be retarded by lowering intraglomerular pressure in rats. 19 -20 Lowenstein et al 21 found that wedged renal vein pressure is increased in hypertensive patients. This observation suggests that increased systemic arte- rial pressure is transmitted through the glomerulus to the renal vein.…”

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Long-term improvement in renal function after short-term strict blood pressure control in hypertensive nephrosclerosis.

et al. 1989

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Seventy-nine hypertensive nephrosclerosis patients i entered a prospective randomized singleblind study to 1) establish the pattern of decay of renal function in this population and the variability therein and 2) to determine if strict diastolic blood pressure (DBP) control (<80 mm Hg) is more effective than conventional levels (90-95 mm Hg) in conserving renal function. Because of unexpected significant improvement in renal function in patients from both groups, which changed the perspectives on the course of this disease as described herein, this report is being published before completion of the trial. The selection criteria were 1) serum creatinine concentration of 1.6-7.0 mg/dl, 2) glomerular filtration rate of less than 70 ml/min/1.73 m 2 , and 3) absence of diseases (other than hypertension) known to destroy renal function. Renal function was assessed by glomerular filtration rate ([ l2S I]iothalamate clearance) and serum creatinine concentration. Before randomization, DBP was aggressively treated to reduce it to less than 80 mm Hg. Twenty-two subjects (14 in the strict DBP control group and eight in the conventional DBP control group) have been enrolled in the study for 36 months. In contrast to results from previous studies in humans and rats, renal function improved in both patient groups. Thus, irrevocable progression of renal damage after onset of renal failure from high blood pressure does not necessarily occur, and in fact, long-term improvement of renal function resulted from the effects of the study itself. The study design involving the 2-4-month initial period of aggressive DBP control at 80 mm Hg or less followed by control of DBP at less than 90 mm Hg was associated with long-term improvement in renal function. (Hypertension 1989; 13:766-772)

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“…4 The main focus of the Renal Laboratory in the Department of Medicine was to investigate the role of the kidney in the pathogenesis of essential hypertension. With evidence that renal artery stenosis was characterized by excessive sodium reabsorption, 5,6 Baldwin and others in the laboratory sought to determine whether the abnormalities in the renal excretion of sodium might be a feature of essential hypertension.…”

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