Intrarenal Prostaglandins E&lt;sub&gt;2&lt;/sub&gt; and F&lt;sub&gt;2&lt;/sub&gt;&lt;sub&gt;α&lt;/sub&gt; in Experimental Renovascular Hypertension

Soejima, Hidehisa; Nomura, Yoshio; Tsuruta, Kazuma; Ikegami, Keiichi

doi:10.1159/000280407

Cited by 4 publications

(9 citation statements)

References 16 publications

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“…In our study split UPGE:V as a reflection of renal PGE2 synthesis [19], which is a factor in influencing renal sodium excretion [12], was investigated. In the early phase of 2K-1C RVH, it was reported that the synthesis of renal PGs is increased in the clipped kidney, which might be mediated by the reduction of perfusion pressure as well as increased local and circulating angiotensin II [13,18,20,21]. However, in the present study UPGE2V of the clipped kidney was significantly lower than the control value.…”

Section: Discussioncontrasting

confidence: 73%

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

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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.

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Section: Discussioncontrasting

confidence: 73%

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

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“…These data indicate that the ele vation of urinary PGE2 in the acute and intermediate phases may be a reasonable response to the elevated angiotensin II. However, as other reports suggested [5][6][7][8][9][10][11], the elevated renal PGE2 may partially act as a defensive factor for renal function and hypertension by promoting urinary sodium excretion.…”

Section: Discussionmentioning

confidence: 98%

“…There have been some studies on the course of twokidney, one-clip renovascular hypertension in dogs, rats, and rabbits [8,11,13,24,25]. Brown et al [11] divided the course of this hypertension into three phases: the initial acute phase, in which hypertension was mainly depend ent on angiotensin II, the second intermediate phase, in which the effect of angiotensin II was weakened and some other factors such as sodium retention and in creased arteriolar responsiveness to vasoconstrictors seemed to be involved, and the third maintenance phase, in which the role of angiotensin II was no longer obvious.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that angiotensin II stimulates the produc tion of renal PGE2 [30,31] which has diuretic and natriu retic actions. Then some workers supposed a protective effect of PGE2 on renal function in the acute phase of hypertension [6][7][8][9][10][11]. Romero and Strong [5] demonstrated that the inhibition of the PG production by indomethacin induced renal failure, oliguria, and malignant hyperten sion in rabbits with hypertension produced by unilateral renal artery constriction.…”

Section: Discussionmentioning

confidence: 99%

“…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%

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

Yoshida¹,

Soejima²,

Ueda³

et al. 1986

Nephron

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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.

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Role of eicosanoids of the contralateral kidney in maintenance of two-kidney, one-clip renovascular hypertension in rats

Kalaitzis

Giannakopoulos

Pantazis

et al. 2007

Scandinavian Journal of Urology and Nephrology

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In the chronic phase of two-kidney, one-clip renovascular hypertension, the contralateral kidney of post-Goldblatt hypertensive and post-Goldblatt normotensive rats excretes more vasoconstrictive thromboxane in comparison to controls, whereas excretion of vasodilatory prostaglandin is not elevated. However, increased TXB(2) excretion and the absence of an increase in PGE(2) excretion from the contralateral kidney do not appear to be important for the maintenance of high blood pressure in this model of renovascular hypertension.

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Intrarenal Prostaglandins E<sub>2</sub> and F<sub>2</sub><sub>α</sub> in Experimental Renovascular Hypertension

Cited by 4 publications

References 16 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 Renal Prostaglandin E<sub>2</sub> in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

Role of eicosanoids of the contralateral kidney in maintenance of two-kidney, one-clip renovascular hypertension in rats

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