Influence of prostaglandins on papillary blood flow and pressure-natriuretic response.

Roman, Richard J.; Lianos, Elias A.

doi:10.1161/01.hyp.15.1.29

Cited by 79 publications

(64 citation statements)

References 30 publications

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“…Our results could therefore be interpreted to mean that prostanoids and PAF do not play a significant role in pressure-natriuresis. In contrast, Roman and Lianos 17 have shown that inhibition of prostaglandin synthesis with indomethacin in rats blunted the pressure-natriuresis response. Karlstrom and colleagues 4 suggested that medullipin is natriuretic, and our previous study 3 also provided indirect evidence supporting this proposition.…”

Section: Discussionmentioning

confidence: 89%

“…15 The vasodilator prostaglandin E 2 is also made in the renal medulla 16 and has been shown to enhance sodium and water excretion from the kidney in response to increased renal perfusion pressure 17 and thus may contribute to the rapid fall in blood pressure after changes in renal perfusion pressure in this model. Furthermore, Ma and Dunham 18 have shown recently that cyclooxygenase products are the major vasodepressor substances produced by rat papillary tissue after incubation in vitro.…”

Section: Discussionmentioning

confidence: 97%

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Mediators of the hypotensive response to increased renal perfusion in rabbits.

1993

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We have previously shown that increasing the renal perfusion pressure by using an extracorporeal circuit in anesthetized rabbits resulted in a progressive fall in systemic arterial pressure. Prior ablation of the renal medulla with 2-bromoethylamine abolished the hypotensive response. In the present study, we investigated whether vasodilator prostanoids or platelet activating factor (PAF), both known to be produced in the renal medulla, were responsible for the hypotensive response to increased renal perfusion pressure. Anesthetized animals were treated with indomethacin (5 mg/kg+0.5 mg/kg per hour), the PAF antagonist WEB 2086 (0.5 mg/kg+0.5 mg/kg per hour), enalaprilat (2 mg/kg+10 /ig/kg per hour), or all three agents. In response to acute elevation of renal artery pressure to 170 mm Hg, systemic mean arterial pressure fell at 0.76±0.17, 0.59±0.08, and 0.76±0.17 mm Hg/min in the indomethacin, WEB 2086, and enalapril groups, respectively. These responses were not significantly different from the rate of 1.00±0.21 mm Hg/min in a control group that received vehicle infusion alone. Renal blood flow and the diuretic and natriuretic responses were also similar in all groups. Thus, increased renal perfusion pressure resulted in a progressive fall in systemic arterial pressure that was not mediated by PAF, prostaglandins, or suppression of renin release and angiotensin II production. T here is increasing evidence that vasodepressor substances from the renal medulla, particularly the yet to be identified "medullipin," 1 are involved in the circulatory responses to arterial hypertension. The strongest evidence comes from studies of the "normalization" of blood pressure after removal of renal artery clips in chronic Goldblatt hypertensive rats. Prior medullectomy of the kidney in these rats with 2-OH-bromoethylamine retards the rate at which arterial pressure returns to normal.2 There is also evidence for the involvement of renal medullary substances in the responses to acute rises in arterial pressure; we have shown recently that the renal medulla releases hypotensive factors in response to acutely increased renal perfusion pressure in dogs and rabbits, 3 and Karlstrom and colleagues 4 have reported similar results in rats. The nature of the hypotensive substance in these latter experiments remains to be elucidated, but several vasoactive substances are known to be produced in the renal medulla, including platelet activating factor (PAF) 5 and prostaglandins 6 ' 7 as well as the putative vasodepressor hormone medullipin.1 The latter is a neutral lipid of unknown chemical structure, 1 and the importance of Received June 19, 1992; accepted in revised form October 7, 1992. this substance in the regulation of blood pressure in vivo is still to be established.The present study was aimed at clarifying the factors responsible for the hypotensive response to acute elevation of renal perfusion pressure. As in our previous study, 3 we perfused the left kidneys of rabbits in situ by using an extracorporeal circuit that allowed...

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 97%

Mediators of the hypotensive response to increased renal perfusion in rabbits.

1993

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“…It is a potent vasodilator in both the peripheral (45) and renal vasculature (46). Moreover, PGE 2 has potent natriuretic effects in the kidney through direct epithelial effects on salt and water transport and as a consequence of its hemodynamic actions to increase renal blood flow (3,8). Accordingly, it has been suggested that inhibition of PGE 2 could explain the actions of NSAID and COX-2 inhibitors to cause edema and hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…For example, infusion of PGE 2 into the kidney commonly causes renal vasodilation (2,3). PGE 2 also modulates renal sodium and water excretion (1,4).…”

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confidence: 99%

Role of Microsomal Prostaglandin E Synthase 1 in the Kidney

François

Facemire

Kumar

et al. 2007

Journal of the American Society of Nephrology

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Prostaglandin E 2 (PGE 2 ) is one of the most ubiquitous prostanoids in the kidney, where it may influence a wide range of physiologic functions. PGE 2 is generated through enzymatic metabolism of prostanoid endoperoxides by specific PGE synthases (PGES). Several putative PGES have been identified and cloned, including the membrane-associated, inducible microsomal PGES1 (mPGES1), which is expressed in the kidney. To evaluate the physiologic role of mPGES1 in the kidney, mice with targeted disruption of mPges1 gene were studied, with a focus on responses where PGE 2 has been implicated, including urinary concentration, regulation of blood pressure, and response to a loop diuretic. The absence of mPGES1 was associated with a 50% decrease in basal excretion of PGE 2 in urine (P < 0.001). In female but not male mPGES1-deficient mice, there was a reciprocal increase in basal excretion of other prostanoids. Nonetheless, urinary osmolalities were similar in mPges1 ؉/؉ and mPges1 ؊/؊ mice at baseline and after 12 h of water deprivation. Likewise, there were no differences in blood pressure between mPGES1-deficient and wild-type mice on control or high-or low-salt diets. The furosemide-induced increase in urinary PGE 2 excretion that was seen in wild-type mice was attenuated in mPGES1-deficient mice. However, furosemide-associated diuresis was reduced only in male, not female, mPGES1-deficient mice. Stimulation of renin by furosemide was not affected by mPGES1 deficiency. These data suggest that mPGES1 contributes to basal synthesis of PGE 2 , but there are other pathways that lead to renal PGE 2 synthesis. Moreover, there are significant gender differences in physiologic contributions of mPGES1 to control kidney function.

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“…Atrial natriuretic peptide 2728 and the calcium channel blocker nisoldipine 29 can increase papillary blood flow in rats without altering cortical blood flow. In addition, cyclooxygenase inhibitors 30 and a kinin antagonist 15 have been reported to reduce papillary blood flow preferentially.…”

Section: Discussionmentioning

confidence: 99%

Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

et al. 1991

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The role of angiotensin II and kinins on the renal cortical and papillary hemodynamic and on the sodium and water excretory responses to converting enzyme inhibition with captopril was examined in euvolemic Munich-Wistar rats. Cortical and papillary blood flows were measured using a laser Doppler flowmeter. Cortical blood flow increased 28% after blockade of angiotensin II receptors with DuP 753 (2 mg/kg i.v., n=6). Captopril (2 mg/kg i.v., n=6) had no effect on cortical blood flow in rats pretreated with the angiotensin II antagonist DuP 753 had no effect on papillary blood flow, nor did it prevent the rise in papillary blood flow produced by captopril (2 mg/kg, n=6). Infusion of a kinin receptor antagonist, r>Arg,[Hyp 3 ,Thi M , D-Phe 7 ]-bradykinin (2.5 /tg/min i.v.), reduced basal papillary blood flow by 15% and blocked the rise in papillary blood flow produced by captopril. Renal blood flow rose by 11% after DuP 753 (2 mg/kg, n=6), and subsequent administration of captopril and the kinin antagonist had no effect on renal blood flow. Urine flow and sodium excretion increased after DuP 753, but captopril produced additional increases in urine flow and sodium excretion of 68% and 46%, respectively. Fractional sodium excretion rose from 0.85±0.15% to 1.56±0.14% after captopril. Infusion of the kinin antagonist returned sodium and water excretion to control levels, but fractional sodium excretion was not significantly altered.' Giomenilar filtration rate was not altered by DuP 753 or captopril; however, it fell from 1.6±0.1 to 1.2±0.1 ml/min/g kidney wt during infusion of the kinin antagonist This fall in giomenilar filtration rate was associated with a 30% fall in the ultrafiltration coefficient These results indicate that captopril alters renal hemodynamics through mechanisms other than blockade of the renin-angiotensin system. In particular, its effects on papillary blood flow and giomenilar dynamics may be due to alterations in the intrarenal levels of kinins. (Hypertension 1991;17:1038-1044) C onverting enzyme inhibitors (CEIs) are antihypertensive agents that promote sodium excretion at lower levels of arterial pressure. However, the mechanisms underlying the natriuretic and antihypertensive actions of CEIs remain uncertain. It generally is thought that these drugs act by blocking the renin-angiotensin system in the kidney and the peripheral vasculature. However, CEIs lower arterial pressure in nephrectomized animals, as well as in rats pretreated with angiotensin (Ang) II antagonists.

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Influence of prostaglandins on papillary blood flow and pressure-natriuretic response.

Cited by 79 publications

References 30 publications

Mediators of the hypotensive response to increased renal perfusion in rabbits.

Mediators of the hypotensive response to increased renal perfusion in rabbits.

Role of Microsomal Prostaglandin E Synthase 1 in the Kidney

Effect of an angiotensin II and a kinin receptor antagonist on the renal hemodynamic response to captopril.

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