Direct effects of prostaglandin on renal function and renin release in anesthetized dog

Vander, AJ

doi:10.1152/ajplegacy.1968.214.2.218

Cited by 189 publications

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“…First, a direct action of prostaglandins (of the E series) on tubular function was thought unlikely because in isolated high resistance epithelial tissues prostaglandins stimulate rather than inhibit active sodium transport (Barry & Hall, 1969;Lipson & Sharp, 1971). Secondly, a causal link was assumed because, in the anaesthetized animal, both haemodynamic and urinary changes are apparent following intravenous administration of prostaglandin E (Vander, 1968) or stimulation (Bolger, Eisner, Ramwell & Slotkoff, 1976) or inhibition (Aiken & Vane, 1973) of renal prostaglandin synthesis. However, in the anaesthetized dog the haemodynamic and urinary changes produced by exogenous prostaglandins have been separated.…”

Section: Dtscussionmentioning

confidence: 99%

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Haylor¹,

Lote²

1980

The Journal of Physiology

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SuMMARY1. Conscious rats, with implanted carotid arterial cannulae, received a saline infusion (5.8 ml./hr) via a tail vein for a 6 hr period. The urinary excretion of water, sodium, potassium, urea and the osmolal output were monitored, together with the systemic blood pressure. Glomerular filtration rate (inulin clearance) and effective renal plasma flow (p-aminohippurate clearance) were also measured. Four hours after the start of the infusion, indomethacin (10 mg/kg body weight) in buffered saline, or buffered saline alone, was a inistered via the tail vein.2. Following indomethacin administration, urine flow, sodium output and osmolal output were markedly reduced (P < 0.01). However, there were no measurable changes in the systemic blood pressure, glomerular filtration rate, or effective renal plasma flow.3. It is concluded that the changes in urinary excretion observed after indomethacin are not dependent on changes in effective renal plasma flow or glomerular filtration, and it is suggested that indomethacin inhibits the synthesis of endogenous prostaglandins which directly influence renal tubular function.

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Section: Dtscussionmentioning

confidence: 99%

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Haylor¹,

Lote²

1980

The Journal of Physiology

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“…These results may seem surprising because the intrarenal infusion of PGE or PGA results in a natriuresis (1,2). Yet, the infusion of either of these agents causes hemodynamic alterations (i.e.…”

Section: Re Sultsmentioning

confidence: 99%

“…Prostaglandins of either the A (PGA)1 or E (PGE) series, when infused into the renal artery, cause an increase in urinary sodium excretion (1,2). Therefore, it has been suggested that the endogenous release of these lipids might be a potent natriuretic stimulus and serve an important role in the regulation of sodium balance (1).…”

Section: Introductionmentioning

confidence: 99%

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

Kirschenbaum¹,

Stein²

1976

J. Clin. Invest.

115

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A B S T R A C T Studies were performed to determine the effect of decreased endogenous release of renal prostaglandins on urinary sodium excretion. Two structurally dissimilar inhibitors of prostaglandin synthesis were employed, and studies were performed in conscious dogs allowed to recover from prior surgical instrumentation. Either meclofenamate (2 mg/kg) or the competitive prostaglandin inhibitor RO 20-5720 (1 mg/kg) was given to seven unanesthetized dogs undergoing a water diuresis. The administration of either prostaglandin inhibitor did not alter glomerular filtration rate, renal plasma flow, urinary volume, or potassium excretion. Sodium excretion, however, increased from 32 to 130 ueq/min (P <0.02). Essentially, the entire increase in sodium excretion was due to an increase in urinary sodium concentration from 7.7 to 28.3 meq/liter (P < 0.02). On a different day, the same animals were studied before and after administration of the diluent of the prostaglandin inhibitor. No change was noted in sodium excretion or any other parameter.Thus, these findings suggest that prostaglandin inhibition in the conscious dog is associated with a natriuresis without a change in urinary volume or potassium excretion during water diuresis. This may indicate that the natriuresis was due to diminished sodium reabsorption beyond the distal tubule.

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“…system (RAS) (21,36,38,41). Interactions of the COX isoforms with the RAS system have been revealed by several expression studies; however, critical uncertainties remain.…”

mentioning

confidence: 99%

Augmented cyclooxygenase-2 effects on renal function during varying states of angiotensin II

Green

Rodríguez

Navar

2010

American Journal of Physiology-Renal Physiology

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Green T, Rodriguez J, Navar LG. Augmented cyclooxygenase-2 effects on renal function during varying states of angiotensin II. Am J Physiol Renal Physiol 299: F954 -F962, 2010. First published July 28, 2010 doi:10.1152/ajprenal.00609.2009.-Nonsteroidal anti-inflammatory drug usage has long revealed renoprotective prostaglandin actions on the renal microvasculature during increased pressor hormone influence, but whether increased cyclooxygenase (COX)-2 expression supports prostaglandin vasodilatory influence by interfering with the actions of ANG II remains unresolved. Therefore, we tested the hypothesis that COX-2 inhibition causes hemodynamic and excretory effects that are increased in proportion to ANG II activity. In anesthetized Sprague-Dawley rats having augmented cortical COX-2 expression but different ANG II activity, we conducted renal clearance experiments during acute inhibition of COX-2 with nimesulide (NMSLD) and inhibition of COX-1 with SC-560. In one series of experiments, acute captopril [acute angiotensin-converting enzyme (ACE) inhibitor (aACEi)] was administered alone (n ϭ 13) or in combination with chronic captopril [chronic ACEi (cACEi)] pretreatment (n ϭ 19). In another series of experiments, rats were fed a normal-sodium [0.4% (NS), n ϭ 12] or a low-sodium [0.03% (LS), n ϭ 18] diet. NMSLD did not alter mean arterial blood pressure in any group but, in the LS and cACEi groups, decreased renal plasma flow (from 3.99 Ϯ 0.33 to 2.85 Ϯ 0.26 and from 4.30 Ϯ 0.19 to 3.22 Ϯ 0.21 ml·min Ϫ1 ·g Ϫ1 ), cortical blood flow (Ϫ12 Ϯ 8% and Ϫ13 Ϯ 4%), and glomerular filtration rate (from 0.88 Ϯ 0.04 to 0.65 Ϯ 0.05 and from 0.95 Ϯ 0.07 to 0.70 Ϯ 0.05 ml·min Ϫ1 ·g Ϫ1 ). In contrast, medullary blood flow (MBF) was significantly decreased by COX-2 inhibition in NS (Ϫ24 Ϯ 5%), LS (Ϫ27 Ϯ 8%), aACEi (Ϫ16 Ϯ 3.8%), and cACEi (Ϫ24 Ϯ 4.2%) groups. Absolute and fractional sodium excretion rates were unchanged by NMSLD, except in the LS group (0.75 Ϯ 0.05 eq/min and 0.43 Ϯ 0.15% and 0.51 Ϯ 0.06 eq/min and 0.26 Ϯ 0.10%). SC-560 did not augment the effects of NMSLD. These results demonstrate an augmented COX-2-mediated vasodilation that is not contingent on ANG II, in contrast to COX-2-mediated augmented sodium excretion, where ANG II activity is requisite. Furthermore, the COX-2 effects on MBF are not contingent on ANG II or changes in cortical microvascular responses. These results reflect COX-2 continual regulation of MBF and adaptive opposition to ANG II prohypertensinogenic effects on renal plasma flow, cortical blood flow, glomerular filtration rate, and absolute and fractional sodium excretion.angiotensin-converting enzyme inhibition; sodium restriction; medullary blood flow THE DYNAMIC PROSTAGLANDIN biosynthetic capacity in the kidney relies on the catalysis of the rate-limiting step by the cyclooxygenase (COX) isoforms COX-1 and COX-2 (25). Adaptive renal responses to reduced sodium intake involve augmented COX activity, along with activation of the renin-angiotensin system (RAS) (21,36,38,41). Interactions of th...

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Direct effects of prostaglandin on renal function and renin release in anesthetized dog

Cited by 189 publications

References 0 publications

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

Renal function in conscious rats after indomethacin. Evidence for a tubular action of endogenous prostaglandins.

The effect of inhibition of prostaglandin synthesis on urinary sodium excretion in the conscious dog.

Augmented cyclooxygenase-2 effects on renal function during varying states of angiotensin II

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