Effect of furosemide on renal function in the stenotic and contralateral kidneys of patients with renovascular hypertension.

Ruilope, L. M.; García-Robles, Reggie; Sancho-Rof, J; Payá, Carlos V.; Rodicio, José L.; Strong, Cameron G.; Knox, Franklyn G.; Romero, J. Carlos

doi:10.1161/01.hyp.5.6_pt_3.v43

Cited by 14 publications

(9 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, in the present study UPGE2V of the clipped kidney was significantly lower than the control value. The same re sults were also reported in human RVH [16,17], Since ischemia in the clipped kidney is reduced by a high perfusion pressure during progress of hypertension [23] and PRA in this experiment was at a low level, renal PGE2 synthesis might not be stimulated so highly as that in the early phase. On the other hand, renal PGs production in the nonclipped kidney was reported to increase in the early phase which might be mediated by circulating an giotensin II stimulation [2,[13][14][15][16][17][18]20,21].…”

Section: Discussionsupporting

confidence: 85%

Role of Sodium and Renal Prostaglandin E2 in the Maintenance of Hypertension in the Chronic Phase of Two-Kidney One-Clip Renovascular Hypertension in Rabbits

Machida

Ueda

Yoshida

et al. 1988

Nephron

View full text Add to dashboard Cite

To study the role of sodium and renal prostaglandin E₂ in the chronic phase of two-kidney one-clip renovascular hypertension, urinary excretion rates of sodium and prostaglandin E₂ were measured in rabbits with hypertension induced by left renal artery constriction during alteration in sodium intake. The arterial blood pressure, the increasing rate of body weight and sodium balance during alteration in sodiurm intake were directly proportional to the amount of sodium intake in the hypertensive rabbits, but not in the control ones. Plasma renin activity and plasma aldosterone concentration, which had no significant difference between hypertensive and control rabbits, were inversely proportional to the amount of sodium intake in both rabbits. Urinary excretion rates of sodium in the clipped kidneys of the hypertensive rabbits were significantly lower than the control values in all dietary regimens (p < 0.01). Urinary excretion rates of sodium in the nonclipped kidneys were not significantly higher and in the total kidneys were significantly lower than the corresponding control values during sodium load (p < 0.01). Urinary excretion rates of prostaglandin E₂ were inversely proportional to the amount of sodium intake in both groups. Urinary excretion rates of prostaglandin E₂ in the clipped kidneys were significantly lower than the control values in all dietary regimens (p < 0.001). Urinary excretion rates of prostaglandin E₂ in the nonclipped kidneys were significantly higher during sodium restriction (p < 0.01) but not during sodium load than the control values. Furthermore, urinary excretion rates of prostaglandin E₂ in the total kidneys were significantly lower than the control values in all dietary regimens (p < 0.01). These results suggest that two-kidney one-clip renovascular hypertension in rabbits seems to be partly sodium-dependent in the chronic phase because the nonclipped kidney fails to excrete sodium sufficiently. There may also be disorders of renal prostaglandin E₂ metabolism influencing these disorders of sodium in the nonclipped kidneys.

show abstract

Section: Discussionsupporting

confidence: 85%

Role of Sodium and Renal Prostaglandin E2 in the Maintenance of Hypertension in the Chronic Phase of Two-Kidney One-Clip Renovascular Hypertension in Rabbits

Machida

Ueda

Yoshida

et al. 1988

Nephron

View full text Add to dashboard Cite

show abstract

“…Urinary prostaglandins E 2 (PGEJ and 6-keto-F, a (6-keto-PGF,J were measured by radioimmunoassay according to the method previously described. 13 Analysis of variance for randomized block design was used to test the null hypothesis, that there were no changes with each maneuver. The Newman-Keuls test was used to determine significant differences between maneuvers.…”

Section: Methodsmentioning

confidence: 99%

Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

et al. 1988

Self Cite

View full text Add to dashboard Cite

SUMMARY Tbe natriuretk response to the intrarenal administration of atrial natriuretic factor (ANF)is accompanied by an increase in tbe synthesis of prostaglandins and by a redistribution of renal blood flow from the superficial to the deep cortex. This study was undertaken to define whether prostaglandins mediate the ANF-induced redistribution of renal blood flow and if prostaglandins and renal blood flow redistribution contribute to the natriuretic actions of ANF. In anesthetized dogs, the Intrarenal administration of indomethadn (10 jtg/kg/min) or the intravenous administration of meclofenamate (5 mg/kg) completely prevented the sixfold and twofold increments in urinary prostaglandin E 2 and 6-keto-prostaglandin F l a excretion, respectively; it also abolished the redistribution of renal blood flow to the deep cortex. However, ANF induced a similar natriuresis before (from 53 ± 17 to 281 ± 48 /tEq/min) and after (from 45 ± 13 to 273 ± 60 /iEq/min) the administration of prostaglandin synthesis inhibitors. It is concluded that the ANF-induced redistribution of renal blood flow to the deep cortex is prostaglandinmediated but that neither redistribution nor increased prostaglandin synthesis Is an important mediator of ANF's natriuretic action. (Hypertension 12: 274-278, 1988) KEY WORDS • atrial natriuretic factor • intrarenal blood flow distribution • prostaglandin synthesis inhibitors • sodium excretionW E have recently found that the natriuretic response to the intrarenal infusion of atrial natriuretic factor (ANF) at doses that do not alter mean arterial pressure (MAP), renal blood flow (RBF), or glomerular filtration rate (GFR) is accompanied by a significant increase in urinary excretion of prostaglandins and by a redistribution of RBF from the superficial to the juxtamedullary cortex.1 Previous studies have shown that enhanced prostaglandin synthesis or selective prostaglandin infusion increases juxtamedullary cortical flow.2 -5 Others have shown that blockade of prostaglandin synthesis decreases juxtamedullary cortical flow more than superficial cortical flow. 5 -7 Increases in medullary flow have been shown to produce natriuresis, 8 -9 as has increased prostaglan-

show abstract

“…It is well known that renal prostaglandins (PGs) have vasodilatory, natriuretic, and diuretic effects [1,2], and synthesis and release of them augment in various renal pathological conditions [2][3][4], In experimental renovas cular hypertension produced by constriction of the unila teral renal artery, some participations of renal PGs in the development and maintenance of hypertension have also been suggested [5][6][7][8][9][10]. In experimental renovascular hy pertension, the initial rise of blood pressure is mainly caused by vasoconstriction due to increased angiotensin II, but the mechanism of the maintenance of hyperten sion has not been obvious [11,12].…”

Section: Introductionmentioning

confidence: 99%

Role of Renal Prostaglandin E2 in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

Yoshida¹,

Soejima²,

Ueda³

et al. 1986

Nephron

View full text Add to dashboard Cite

To investigate the role of renal prostaglandin E₂ (PGE₂) in renovascular hypertension, urinary PGE₂ was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypetension (1 week after the constriction), urinary excretions of PGE₂ and sodium were significantly increased without correlations with changes in the systemic blood pressure (ΔBP). In this phase, ΔBP was directly proportional to plasma renin activity and plasma aldosterone concentration (p < 0.001). In the intermediate phase (5 weeks), ΔBP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p < 0.01). In the maintenance phase (10 weeks), ΔBP showed inverse correlations (p < 0.01) with both PGE₂ and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE₂ excretion in the acute phase was significantly elevated (p < 0.02), and both sodium and PGE₂ excretions were significantly decreased (p < 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE₂ and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, ΔBP showed inverse correlation (p < 0.01) with both PGE₂ and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases. The present data suggest that the renin-angiotensin system chiefly contributes to the development of hypertension in the acute phase. However, elevated renal PGE₂ may also partially act as a defensive factor by promoting urinary sodium excretion. In the maintenance phase, the reduced level of urinary sodium excretion in the nonclipped kidney, which has significant correlation with the reduced level of PGE₂, may play an important role to maintain hypertension instead of the renin-angiotensin system.

show abstract

Effect of furosemide on renal function in the stenotic and contralateral kidneys of patients with renovascular hypertension.

Cited by 14 publications

References 24 publications

Role of Sodium and Renal Prostaglandin E<sub>2</sub> in the Maintenance of Hypertension in the Chronic Phase of Two-Kidney One-Clip Renovascular Hypertension in Rabbits

Role of Sodium and Renal Prostaglandin E<sub>2</sub> in the Maintenance of Hypertension in the Chronic Phase of Two-Kidney One-Clip Renovascular Hypertension in Rabbits

Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

Role of Renal Prostaglandin E<sub>2</sub> in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

Contact Info

Product

Resources

About