Effect of decreased renal sympathetic nerve activity on renal tubular sodium reabsorption

Prosnitz, Eric H.; DiBona, G. F.

doi:10.1152/ajprenal.1978.235.6.f557

Cited by 48 publications

(35 citation statements)

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“…Both arterial anid renal venous norepinephrine concentrations were significantly higher in the sodiumdepleted animals than in the sodium-replete control group. The calculated rate of renal norepinephrine overflow was significantly higher in the sodiumdlepleted animlals than in the sodium-replete clogs (32,565 vs. 12,758 pg/min, P < 0.01). 48 pg/ml in the normal sodiium dogs; it ranged from 27 to 378 pg/ml and averaged 92 pg/ml in the sodium-depleted animals.…”

Section: Resultsmentioning

confidence: 78%

“…Recent data suggest that the renal adrenergic nervous system may be directly involved in renal tubular reabsorption. Changes in efferent renal sympathetic nerve activity parallel changes in renal tubular sodium reabsorption without altered hemodynamics (31,32). In addition, norepinephrine has been shown to stimulate active sodium reabsorption across isolated epithelial membranes (33).…”

Section: Discussionmentioning

confidence: 99%

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Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Oliver¹,

Pinto²,

Sciacca³

et al. 1980

J. Clin. Invest.

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A B S T R A C T To determine whether vasoactive renal hormones modulate renal blood flow during alterations of sodium balance, simultaneous measurements of arterial and renal venous concentrations of norepinephrine and prostaglandin E2 (PGE2) and of plasma renin activity, as well as renal blood flow and systemic hemodynamics were carried out in 24 sodiumdepleted and 28 sodium-replete anesthetized dogs. The mean arterial blood pressure of the sodium depleted dogs was not significantly different from that of the animals fed a normal sodium diet, but cardiac outptut was significantly lower (3.07±0.18 vs. 3.77±0.17 liters/mim, mean±SEM; P < 0.01). Despite the higher total peripheral vascular resistance in the sodiumdepleted dogs (46.1±2.9 vs. 37.0±2.1 arbitrary resistance U; P < 0.02), the renal blood flow and renal vascular resistance were not significantly different in the two groups. The arterial plasma renin activity and concentration of norepinephrine were higher in the sodium-depleted animals than in the controls; the arterial concentration of PGE2 was e(ual in both groups. The renal venous plasma renin activity was higher in the sodium-depleted dogs. Similarly, the renal venous norepinephrine concentration was higher in the sodium-depleted dogs than in the controls (457±44 vs. 196±25 pg/ml; P <0.01); renal venous PGE2 concentration was also higher in the sodium depleted dogs (92±22 vs. 48±11 pg/ml; P < 0.01). Administration of indomethacin to five sodium-replete dogs had no effect on renal blood flow. In five sodium-depleted dogs indomethacin lowered renal blood flow from 243±19 to 189+30 ml/min (P < 0.05) and PGE2 in renal venous blood from 71±14 to 15±2 pg/ml (P < 0.02). The results indicate that moderate chronic sodium depletion, in addition to enhancing the activity of the renin-angiotensin system, also increases the activity of the renal adrenergic nervous system and increases renal PGE2 synthesis. In sodiumReceived for publication 19 February 1980 and in revised form 4 June 1980. 748 depleted dogs, inhibition of prostaglandin synthesis was associated with a significant decrease in renal blood flow. The results suggest that the renal blood flow is maintained during moderate sodiulm depletion by an effect of the prostaglandins to oppose the vasoconstrictor effects of angiotensin II and the rencal sympathetic nervous system.

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Section: Resultsmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Oliver¹,

Pinto²,

Sciacca³

et al. 1980

J. Clin. Invest.

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“…The mechanisms involved were not elucidated in these studies. As renal sympathetic activity has been shown to influence sodium excretion via both arteriolar vasoconstriction and alterations in tubular sodium reabsorption (12)(13)(14), we hypothesized that renal denervation altered the development of hypertension in the SHR in part through an effect on renal sodium handling. Therefore, the purpose of these experiments was to determine whether renal sympathetic activity contributes to the development and maintenance of hypertension in the SHR by causing enhanced sodium retention.…”

Section: Introductionmentioning

confidence: 99%

Role of the Renal Sympathetic Nerves in the Development and Maintenance of Hypertension in the Spontaneously Hypertensive Rat

Winternitz¹,

Katholi²,

Oparil³

1980

J. Clin. Invest.

205

113

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A B S T R A C T Neurogenic factors and, in particular, enhanced renal sympathetic tone, have been implicated in the pathogenesis of hypertension in the spontaneously hypertensive rat of the Okamoto strain. To examine the hypothesis that the renal sympathetic nerves contribute to the development and maintenance of hypertension by causing urinary sodium retention, 7-wk-old (early hypertensive) and 18-wk-old (established hypertensive) male spontaneously hypertensive rats were subjected to bilateral renal denervation and compared with sham-operated controls. In 7-wk-old animals renal denervation delayed the onset and slowed the rate of developmentofhypertension. These alterations were associated with a significantly greater fractional excretion of sodium (percentage of sodium intake excreted) during the first 3 wk after denervation. Blood pressure 2 wk after surgery was 169+3.5 (sham) vs. 150+2.4 mm Hg (denervated) (P < 0.001), corresponding to fractional sodium excretions of 65±1.3% (sham) vs. 80+2.3% (denervated) (P < 0.001). By the 5th wk after surgery, at which time an increase in renal norepinephrine content of denervated animals suggested reinnervation, blood pressures in the two groups converged (sham, 199+6.5 mm Hg vs. denervated 180+3.5 mm Hg, NS) and there was no difference in sodium excretion (sham, 77+2.5% vs. denervated 79±2.3%). Plasma and kidney renin activity of denervated animals did not differ significantly from that of sham-operated controls. In 18-wk-old rats renal denervation did not alter blood pressure or urinary sodium excretion. These data indicate that the renal svmpathetic nerves contribute to the development of hypertension in the spontaneously hypertensive rat in Dr. Wintemitz is the recipient of a National Heart, Lung, and Blood Clinical Investigator Award (l-K08 HL00707-01).

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“…Recent studies have suggested that renal tubular sodium reabsorption may be modulated by renal nerve activity (4,5,7,9,27). The kidney is richly innervated by adrenergic nerves and the presence of dopamine-and norepinephrine-containing nerves have been demonstrated (1, 2, 10).…”

Section: Methodsmentioning

confidence: 99%

“…In the adult dog, no consistent specific binding could be demonstrated for plasma membranes obtained from any region of the kidney. These studies indicate that during maturation there is a decrease in alpha-adrenoceptor density and affinity in membranes from the outer cortex of the kidney.Recent studies have suggested that renal tubular sodium reabsorption may be modulated by renal nerve activity (4,5,7,9,27). The kidney is richly innervated by adrenergic nerves and the presence of dopamine-and norepinephrine-containing nerves have been demonstrated (1, 2, 10).…”

mentioning

confidence: 99%

Alpha-Adrenoceptors in the Developing Kidney

et al. 1983

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Summary MATERIALS AND METHODSThe maturation of renal alpha-adrenoceptors was investigated in dogs. Alpha-adrenoceptors were characterized by radioligand binding using the alpha-1-adrenergic antagonist, [3HI-WB-4101. In renal olasma membranes obtained from the outer cortex of neonates,-the binding of the ligand was rapid, reversible, of high affinitv. saturable. and stereoselective. The com~etition studies " , with adrenergic agonists and antagonists were indicative of alphareceptors. In puppies less than 1-w-old, the binding affinity of 13H] -WB-4101 (Ka = 0.638 f 0.17 nM) was greater than 3-5 week-old puppies (Kd 1.573 + 0.315 nm); (P < 0.05), but receptor number was similar (63.75 + 19.1 versus 79.10 + 5.99 fmole/mg protein).N o consistent specific binding could be demonstrated in plasma membranes obtained from inner cortex or medulla. In the adult dog, no consistent specific binding could be demonstrated for plasma membranes obtained from any region of the kidney. These studies indicate that during maturation there is a decrease in alpha-adrenoceptor density and affinity in membranes from the outer cortex of the kidney.Recent studies have suggested that renal tubular sodium reabsorption may be modulated by renal nerve activity (4,5,7,9,27). The kidney is richly innervated by adrenergic nerves and the presence of dopamine-and norepinephrine-containing nerves have been demonstrated (1, 2, 10). The adrenergic nerves have been shown to be in direct contact with basement membrane of the proximal and distal tubules (1). Renal denervation decreases (4) and renal nerve stimulation increases (3) tubular sodium reabsorption. Several pathophysiologic conditions (denervation, salt loading) have been shown to alter norepinephrine and epinephrine levels in the kidney (22). In the rat (24) and dog (33) changes in sodium reabsorption have been related to alterations in alpha-adrenergic activity. In the isolated tubules of rabbits (5, 16) and mouse (26) however, increased sodium and chloride reabsorption (5, 16) in the proximal convoluted tubule, the thick ascending limb of Henle and the collecting duct followed administration of isoproterenol, a beta-adrenergic agonist. In addition, Bello-Reuss (5) showed that the increase in fluid (and presumably sodium) reabsorption in the proximal convoluted tubule induced by norepinephrine can be blocked by propranolol, a beta-adrenergic antagonist, but not by phenoxybenzamine, an alpha-adrenergic antagonist; thus, at least in the rabbit and mouse, betaadrenergic stimulation increases fluid transport. Dopamine, on the other hand, has been shown to decrease sodium reabsorption beyond the superficial distal tubule (25).Recently, specific adrenergic and dopaminergic receptors have been described in the kidney in several animal species (1 1, 12, 17, 18, 20, 21, 31). But no studies have characterized renal tubular alpha-adrenergic receptors in the dog, the species in which much of the physiologic data has been acquired. In order to understand further the role of alpha-adrenergic receptors...

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Effect of decreased renal sympathetic nerve activity on renal tubular sodium reabsorption

Cited by 48 publications

References 0 publications

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.

Role of the Renal Sympathetic Nerves in the Development and Maintenance of Hypertension in the Spontaneously Hypertensive Rat

Alpha-Adrenoceptors in the Developing Kidney

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