Role of renal prostaglandins in the control of renin release.

Freeman, Ronald H.; Davis, James O.; Villarreal, Daniel

doi:10.1161/01.res.54.1.1

Cited by 75 publications

(31 citation statements)

References 79 publications

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“…Considering the PGE 2 -mediated stimulation of renin secretion, our data point toward EP4 receptor as the transducing protein. Prostaglandins are thought to stimulate renin secretion and renin gene expression via increase of intracellular cAMP concentration (39). Among the EP receptors, EP2 and EP4 stimulate cAMP formation through G s␣ .…”

Section: Discussionmentioning

confidence: 99%

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nüsing

Treude

Weißenberger

et al. 2005

Journal of the American Society of Nephrology

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Increased formation of prostaglandin E 2 (PGE 2 ) is a key part of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), a renal disease characterized by NaCl wasting, water loss, and hyperreninism. Inhibition of PGE 2 formation by cyclo-oxygenase inhibitors significantly lowers patient mortality and morbidity. However, the pathogenic role of PGE 2 in HPS/aBS awaits clarification. Chronic blockade of the Na-K-2Cl co-transporter NKCC2 by diuretics causes symptoms similar to HPS/aBS and provides a useful animal model. In wild-type (WT) mice and in mice lacking distinct PGE 2 receptors (EP1 In summary, these findings demonstrate that the EP4 receptor mediates PGE 2 -induced renin secretion and that EP1, EP3, and EP4 receptors all contribute to enhanced PGE 2 -mediated salt and water excretion in the HPS/aBS model.

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Section: Discussionmentioning

confidence: 99%

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nüsing

Treude

Weißenberger

et al. 2005

Journal of the American Society of Nephrology

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“…coworkers 2 as distinct and parallel. This hypothesis has received both a healthy dose of responsible criticism, 3 as well as a substantial degree of experimental support (infra vide). The study by Imanishi et al 1 provides the first clear corroboration of the "prostaglandin" hypothesis in humans.…”

Section: Relation Between Renin Release and Blood Pressure Response Tmentioning

confidence: 99%

Relation between renin release and blood pressure response to nonsteroidal anti-inflammatory drugs in hypertension.

Jackson

1989

Hypertension

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“…The mechanisms involved in prenatal renin synthesis and secretion, however, are less well understood. An article in this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology by Mertz and colleagues (14) provides important new data regarding the interaction of prostaglandins and the RAS during fetal development in lambs.Renal effects of prostaglandins were described more than 20 years ago (3,7,16). However, the mechanisms by which prostaglandins modulate renal function are still not completely understood.…”

mentioning

confidence: 99%

“…Renal effects of prostaglandins were described more than 20 years ago (3,7,16). However, the mechanisms by which prostaglandins modulate renal function are still not completely understood.…”

mentioning

confidence: 99%

“…This is further substantiated by studies demonstrating that various stimuli for renin expression, such as ANG I-converting enzyme inhibition (18), ANG II AT 1 receptor blockade (12,18), salt restriction (8), and renal artery clipping (9), are all associated with increased COX-2 expression. Thus, in addition to a role of prostaglandins for the stimulation of renin synthesis and release (3,7,16), there is also a role of renin for stimulation of prostaglandin synthesis via induction of COX-2. In addition to COX-2-derived prostaglandins, COX-1-derived prostaglandins also seem to be important for the modulation of renin synthesis and release in response to other stimuli.…”

mentioning

confidence: 99%

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Interaction of prostaglandins with the renin-angiotensin system

Stauss

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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IN ADDITION TO ITS PARAMOUNT ROLE in the regulation of fluid and electrolyte homeostasis, the renin-angiotensin system (RAS) is also involved in renal development (1,17). In adulthood, renal perfusion pressure, sodium chloride concentration at the site of the macula densa, and ␤-adrenergic receptor stimulation control release of renin. The mechanisms involved in prenatal renin synthesis and secretion, however, are less well understood. An article in this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology by Mertz and colleagues (14) provides important new data regarding the interaction of prostaglandins and the RAS during fetal development in lambs.Renal effects of prostaglandins were described more than 20 years ago (3,7,16). However, the mechanisms by which prostaglandins modulate renal function are still not completely understood. Recently, Cheng et al. (4) reported that the potentiating effects of prostaglandins on angiotensin-converting enzyme inhibitor-induced renin synthesis and release are mediated by the inducible cyclooxygenase isoform (COX-2), rather than the constitutively expressed cyclooxygenase (COX-1). This conclusion is based on experiments in adult mice with genetic deletion of the COX-1 gene. Captopril treatment increased plasma renin activity, renal renin mRNA expression, and renal renin concentration equally in wild-type and homozygous COX-1-deficient mice. The selective COX-2 inhibitor SC-58236 abolished these effects of the angiotensin-converting enzyme inhibitor. However, in a different study, stimulation of renocortical renin expression by the ANG II AT 1 receptor antagonist candesartan could not be blocked by the COX-2 inhibitor celecoxib (12). Inasmuch as COX-2 mRNA and renin mRNA levels were similarly increased after AT 1 receptor blockade, the authors concluded that ANG II is not required to stimulate COX-2 expression and that COX-2 activity is not required to stimulate renin expression. However, renocortical expression of renin and COX-2 appears to be highly coordinated. This is further substantiated by studies demonstrating that various stimuli for renin expression, such as ANG I-converting enzyme inhibition (18), ANG II AT 1 receptor blockade (12, 18), salt restriction (8), and renal artery clipping (9), are all associated with increased COX-2 expression. Thus, in addition to a role of prostaglandins for the stimulation of renin synthesis and release (3,7,16), there is also a role of renin for stimulation of prostaglandin synthesis via induction of COX-2. In addition to COX-2-derived prostaglandins, COX-1-derived prostaglandins also seem to be important for the modulation of renin synthesis and release in response to other stimuli. The increase in plasma renin activity and renocortical renin mRNA levels in response to a low-salt diet could be blunted with a COX-1 selective antagonist but not with the COX-2 selective inhibitor rofecoxib (11). Thus, depending on the physiological stimulus, both COX-1-and COX-2-derived prostaglandins seem...

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Role of renal prostaglandins in the control of renin release.

Cited by 75 publications

References 79 publications

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Relation between renin release and blood pressure response to nonsteroidal anti-inflammatory drugs in hypertension.

Interaction of prostaglandins with the renin-angiotensin system

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