Renal neuroadrenergic transmission

Slick, GL; Aguilera, AJ; Ej, Zambraski; DiBona, G. F.; Kaloyanides, GJ

doi:10.1152/ajplegacy.1975.229.1.60

Cited by 93 publications

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“…By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct.…”

mentioning

confidence: 76%

Neural Control of the Kidney

DiBona

2003

Hypertension

158

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Abstract-This article provides a chronological perspective on the development of knowledge concerning the neural control of renal function and is divided into three parts: the past, the present, and the future. The PastResearch in the area of the neural control of renal function was not very active for the first half of the 20th century. This can be attributed to 2 factors. First, the renowned renal physiologist, Homer Smith, rendered an opinion that the renal nerves were of little functional consequence. [1][2][3] This was based on his interpretation of experiments involving renal denervation in anesthetized and surgically operated animals. He criticized this approach, as he believed that the starting level of renal sympathetic nerve activity (RSNA) would be quite elevated, owing to the associated stress, so that "denervation hyperemia and diuresis appear to be a release from enhanced vasoconstriction engendered by anesthesia and traumatic operative procedures." 3 Second, there was a lack of convincing evidence that the renal innervation extended beyond the renal vasculature to either the tubules or the juxtaglomerular apparatus. The demonstration by Luciano Barajas 4 that all segments of the renal tubule (as well as the juxtaglomerular apparatus) were innervated by norepinephrine-containing renal sympathetic nerve terminals that make contact with the renal tubular epithelial cell basement membrane paved the way for increased research activity in this area. This critical observation reconfirmed once again the important relationship between structure and function.Given the powerful influence of changes in renal hemodynamics (ie, arterial pressure, glomerular filtration rate [GFR] and renal blood flow [RBF]) on urinary sodium excretion (U Na V), it was evident that the influence of changes in RSNA on U Na V must be examined in experimental protocols in which these variables remained constant. By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct. 6,7 Subsequent work (reviewed in DiBona and Kopp 8 ) showed that this was owing to the release of norepinephrine from renal sympathetic nerve terminals with stimulation of postsynaptic ␣ 1 -adrenoceptors located on the basolateral membrane of renal tubular epithelial cells throughout the nephron. Subsequent intracellular signaling events resulted in an increase in activity of the sodium pump (Na ϩ ,K ϩ -ATPase), with increased transepithelial sod...

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confidence: 76%

Neural Control of the Kidney

DiBona

2003

Hypertension

158

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“…Administration of drugs to block either the renin-angiotensin system (Zambraski & DiBona, 1976;Johns, 1979Johns, , 1980, or the production ofprostaglandins (DiBona, Zambraski, Aguilera & Kaloyanides, 1977;Kopp, 1980) or renal f8-adrenoceptors (Johns, Lewis & Singer, 1976;DiBona & Osborn, 1981) failed to influence the action of the renal nerves on tubular sodium reabsorption, indicating that the reninangiotensin system,prostaglandins and,-adrenoceptors were unlikely to be involved. By contrast, in studies in which adrenergic neurone blockade was induced with guanethidine, ora-adrenoceptor antagonism was achieved with phenoxybenzamine or phentolamine, the nerve-mediated tubular sodium reabsorption was abolished (Slick, Zambraski, DiBona & Kaloyanides, 1975;Zambraski et al 1976b;DiBona & Johns, 1980), which supported the concept thatac-adrenoceptors were present on the renal tubular cells and could influence the rate of sodium transfer across the tubular epithelium.…”

Section: Introductionmentioning

confidence: 89%

The subtype of alpha‐adrenoceptor involved in the neural control of renal tubular sodium reabsorption in the rabbit.

Hesse¹,

Johns²

1984

The Journal of Physiology

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SUMMARY1. A study was undertaken in pentobarbitone anaesthetized rabbits, undergoing a saline diuresis, to determine the subtype of a-adrenoceptor mediating renal tubular sodium reabsorption.2. Stimulation of the renal nerves at low rates, to cause an 11 % fall in renal blood flow, did not change glomerular filtration rate but significantly reduced urine flow rate, and absolute and fractional sodium excretions by approximately 40 %. These responses were reproducible in different groups of animals and with time.3. Renal nerve stimulation during an intra-renal arterial infusion of prazosin, to block a1-adrenoceptors, had no effect on the renal haemodynamic response but completely abolished the reductions in urine flow rate, and absolute and fractional sodium excretion.4. During intra-renal. arterial infusion of yohimbine, to block renal a2-adrenoceptors, stimulation of the renal nerves to cause similar renal haemodynamic changes resulted in significantly larger reductions in urine flow rate, and absolute and fractional sodium excretion of about 52-58 %.5. These results indicate that in the rabbit a1-adrenoceptors are present on the renal tubules, which mediate the increase in sodium reabsorption caused by renal nerve stimulation. They further suggest the presence of presynaptic a2-adrenoceptors on those nerves innervating the renal tubules.

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“…16 -" Taken together, the findings of these studies have led to the hypothesis that, when DS are placed on a high sodium intake, small increases in body fluid volumes do not result in appropriately decreased renal sympathetic outflow. In the presence of a high sodium intake without reduced renal nerve activity, the DS would be unable to efficiently excrete the increased sodium chloride load, therefore leading to elevation of extracellular fluid volume, cardiac output, and arterial pressure.…”

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confidence: 99%

Renal nerves and the development of Dahl salt-sensitive hypertension.

1988

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SUMMARY Several experimental forms of hypertension require intact renal innervation for the development or maintenance (or both) of the elevated arterial pressure. We determined the relationships between urinary sodium and water excretion and arterial pressure in Dahl salt-sensitive rats (DS) with innervated (n = 6) and denervated (n = 7) kidneys after switching from a low to a high sodium diet. Arterial pressure significantly increased in both groups within 48 hours after they began to eat an 8% sodium chloride diet. This hypertension increased to 188 ± 9 and 190 ± 7 mm Hg, respectively, in rats with innervated and denervated kidneys after 12 days. Mean arterial pressures were not significantly different between groups on any day. The rise in arterial pressure of DS placed on a high sodium intake was associated with an elevation of urine flow rate and urinary sodium excretion in rats with either innervated or denervated kidneys. Urine flow rates and urinary sodium excretions were greater in denervated than in innervated rats on Days 4 through 7 after beginning the high sodium diet. This diuresis and natriuresis in rats with denervated kidneys were associated with greater water and sodium intakes on Days 4 to 7 of the high sodium diet when compared with rats with innervated kidneys. These results demonstrate that, following exposure to a high sodium intake, DS have increased arterial pressure within 24 hours. The development of this arterial hypertension is not dependent on intact renal innervation. In conscious DS, the renal innervation does participate in the regulation of urinary sodium excretion by promoting renal sodium and water reabsorption. However, DS with either innervated or denervated kidneys maintained sodium balance and rapidly became hypertensive when fed a high salt diet. Thus, elevation of sodium intake in DS results in arterial hypertension independent of measurable renal neurogenic alterations in salt and water balance. 1 " 7 In these studies, renal denervation was shown to either abolish 2 ' 6i 7 or reduce the magnitude 13 " 5 of the hypertension. Alterations in the development of hypertension by renal denervation may result from interruption of renal afferent or renal efferent sympathetic pathways. Stimulation of renal afferent pathways has been reported to be important in the development of hypertension during ipsilateral renal artery stenosis 8 or during intrarenal infusion of adenosine.9 Activation of renal efferent nerve fibers either by direct electrical stimulation or by reflex activation of sympathetic outflow increases renal vascular resistance, tubular sodium reabsorption, and renin release. 10 These factors could elevate arterial pressure through the vasoconstrictor effects of subsequent increases in circulating angiotensin II or by expansion of the extracellular fluid volume through increased sodium and water reabsorption (or by both mechanisms).Abnormalities in neural control mechanisms of hypertensive animals have been reported, including prehypertensive Dahl salt-sensitive rat...

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Renal neuroadrenergic transmission

Cited by 93 publications

References 0 publications

Neural Control of the Kidney

Neural Control of the Kidney

The subtype of alpha‐adrenoceptor involved in the neural control of renal tubular sodium reabsorption in the rabbit.

Renal nerves and the development of Dahl salt-sensitive hypertension.

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