Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Fadem, Stephen Z.; Hernandez-Llamas, Guillermo; Patak, Ram V.; Rosenblatt, Steven G.; Lifschitz, Meyer D.; Stein, Janice Gross

doi:10.1172/jci110487

Cited by 57 publications

(24 citation statements)

References 12 publications

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“…9 The present study demonstrated that the ANF induced natriuresis is not dependent on a redistribution of RBF to the juxtamedullary cortex.…”

Section: Discussionsupporting

confidence: 55%

“…Others have shown that acetylcholine, a vasodilator, produces a natriuretic effect accompanied by an increase in medullary blood flow 9 - 18 and that secretin, a vasodilator, fails to produce natriuresis or increase medullary blood flow. 9 The present study demonstrated that the ANF induced natriuresis is not dependent on a redistribution of RBF to the juxtamedullary cortex.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 1988

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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-

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“…9 The present study demonstrated that the ANF induced natriuresis is not dependent on a redistribution of RBF to the juxtamedullary cortex.…”

Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

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

et al. 1988

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“…8 The important role of PPF in the regulation of sodium excretion is further supported by a recent study demonstrating that increased PPF is associated with increased sodium excretion after administration of acetylcholine and bradykinin. 7 Our present study, however, failed to demonstrate any association between increased sodium excretion and alteration of medullary blood flow after acute elevation of renal perfusion pressure. The PPF was unchanged despite a significant rise in MAP.…”

contrasting

confidence: 98%

“…Recently, several studies have demonstrated a significant role of papillary plasma flow 7 and papillary tissue tonicity*- 9 in the regulation of sodium excretion. The blood flow to the inner medulla of the kidney is poorly autoregulated, according to some investigators.…”

mentioning

confidence: 99%

Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat.

Chen¹,

Caldwell²,

Hsu³

1984

Hypertension

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SUMMARY We studied the role of renal papillae in the mechanism of increased sodium excretion during acute increase in mean arterial pressure (MAP). Sodium excretion increased dramatically in normal rats after acute increase in MAP by epinephrine (E) infusion (0.4 ^g/min/100g). Glomerular filtration rate (GFR), renal blood flow (RBF), and papillary plasma flow (PPF) remained unchanged after the E administration. To define the role of the medulla in the mechanism of pressure-induced natriuresis, experiments were performed in a group of rats 8 to 12 days after the development of papillary necrosis induced by bromoethylamine hydrobromide. Urinary sodium and fractional sodium excretions were 2.00 ± 0.34 /iEq/ min and 2.37 ± 0.53% (n = 7), respectively, in papillary necrosis rats infused with saline. Administration of E to papillary necrosis rats, however, failed to increase both urinary sodium (2.89 ± 0.61 /xEq/min) and fractional sodium (FE Nl , 2.82 ± 0.63%, n = 6) excretions despite a marked increase in MAP (129 vs 150 mm Hg, p < 0.01). The RBF increased slightly after E infusion (4.42 vs 3.24 ml/min/100 g, p < 0.05), but the GFR was not different between the control (0.39 ± 0.05 ml/min/100 g, n = 7) and the Etreated rats (0.43 ± 0.06, n = 6). Failure to increase sodium excretion during acute increase in MAP was not due to the decreased GFR, since control rats with bilateral partial nephrectomy were able to increase sodium excretion from 1.92 ± 0.33to7.76 ± 1.63/xEq/min(p< 0.01) after E infusion. These findings, therefore, suggest that renal papillae play a major role in the mechanism of natriuresis during acute increase in MAP. T HE mechanism of natriuresis that accompanies acute elevation of renal perfusion pressure has been studied extensively; however it remains undetermined. Previous studies have indicated that acute increase in perfusion pressure is associated with an increase in intratubular pressure and a decrease in fractional sodium reabsorption in the proximal tubule.

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“…Clearance studies have shown that infusion of kinins into the renal artery produces natriuresis and diuresis (1)(2)(3)(4). Micropuncture and tissue-tonicity studies have further suggested that bradykinin-induced redistribution of blood flow toward the medulla and the resulting medullary washout could, at least in part, account for these effects (5,6). On the other hand, recent enzymatic and anatomic data suggest an action of the kallikrein-kinin system within the cortex.…”

Section: Introductionmentioning

confidence: 99%

Interactions of lysyl-bradykinin and antidiuretic hormone in the rabbit cortical collecting tubule.

Schuster¹,

Kokko²,

Jacobson³

1984

J. Clin. Invest.

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Abstract. Although intrarenal infusions of kinins produce diuresis, it is not clear to what extent this response is due to hemodynamically mediated medullary washout and/or to direct epithelial effects ofkinins. Recent evidence has shown that bradykinin binds to collecting tubules in vitro. We therefore examined the interactions of lysyl-bradykinin and antidiuretic hormone (ADH) with respect to hydraulic conductivity (L,) in the rabbit cortical collecting tubule perfused in vitro. To ensure adequate substrate for prostaglandin synthesis, the bath contained 2.5 qM arachidonic acid. Arachidonic acid produced no change in base-line lp and had no effect on the subsequent response to a supramaximal dose of ADH (100 ,U/ml).Therefore, all subsequent experiments were done in the presence of arachidonic acid. added to either the lumen or bath had no effect on baseline Lp. Collecting tubules which were exposed for 1 h to bath lysyl-bradykinin (10-9 M) had a significantly diminished subsequent Lp in response to ADH (P < 0.02).In tubules exposed to bath lysyl-bradykinin plus indomethacin (5 pM), the subsequent ADH response was normal. Lysyl-bradykinin (10-9 M) added to the lumen had no effect on subsequent ADH response.We conclude that lysyl-bradykinin from the basolateral side inhibits the hydroosmotic response ofthe cortical collecting tubule to ADH, and that this inhibition is probably prostaglandin-mediated. Lysyl-bradykinin does not affect water flow from the luminal surface. These Dr.

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Studies on the Mechanism of Sodium Excretion during Drug-induced Vasodilatation in the Dog

Cited by 57 publications

References 12 publications

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

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

Role of renal papillae in the regulation of sodium excretion during acute elevation of renal perfusion pressure in the rat.

Interactions of lysyl-bradykinin and antidiuretic hormone in the rabbit cortical collecting tubule.

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