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

Hesse, I.F.A.; Johns, Edward J.

doi:10.1113/jphysiol.1984.sp015308

Cited by 54 publications

(27 citation statements)

References 28 publications

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“…In particular, a direct effect of NE on tubular function in the medulla cannot be discounted, because tubular adrenoceptors are certainly known to directly influence fluid and sodium reabsorption in the kidney. 7,8 On the other hand, our present results are consistent with the large body of work by Cowley 1 showing that treatments that alter MBF, but not those that influence CBF alone, profoundly influence the pressure diuresis/natriuresis response. Cowley has argued that the chief initiating factor in the pressure natriuresis response is increased MBF and that this leads to a rise in renal interstitial hydrostatic pressure, which in turn inhibits tubular sodium reabsorption.…”

Section: Pressure Natriuresissupporting

confidence: 91%

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

et al. 2000

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Abstract-Increasing renal arterial pressure activates at least 3 antihypertensive mechanisms: reduced renin release, pressure natriuresis, and release of a putative renal medullary depressor hormone. To examine the role of renal medullary perfusion in these mechanisms, we tested the effects of the infusion of norepinephrine, either infusion into the renal medullary interstitium or intravenous infusion, on responses to increased renal arterial pressure in pentobarbital-anesthetized rabbits. We used an extracorporeal circuit, which allows renal arterial pressure to be set to any level above or below systemic arterial pressure. With renal arterial pressure initially set at 65 mm Hg, intravenous and medullary interstitial norepinephrine (300 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ) similarly increased mean arterial pressure (by 12% to 17% of baseline) and reduced total renal blood flow (by 16% to 17%) and cortical perfusion (by 13% to 19%), but only medullary norepinephrine reduced medullary perfusion (by 28%). When renal arterial pressure was increased to Ϸ160 mm Hg, in steps of Ϸ65 mm Hg, urine output and sodium excretion increased exponentially, and plasma renin activity and mean arterial pressure fell. Medullary interstitial but not intravenous norepinephrine attenuated the increased diuresis and natriuresis and the depressor response to increased renal arterial pressure. This suggests that norepinephrine can act within the renal medulla to inhibit these renal antihypertensive mechanisms, perhaps by reducing medullary perfusion. These observations support the concept that medullary perfusion plays a critical role in the long-term control of arterial pressure by its influence on pressure diuresis/natriuresis mechanisms and also by affecting the release of the putative renal medullary depressor hormone. Key Words: kidney medulla Ⅲ laser-Doppler flowmetry Ⅲ norepinephrine Ⅲ natriuresis Ⅲ renal circulation I t has been hypothesized that the level of medullary blood flow (MBF) is an important determinant of urinary sodium excretion (U Na ϩ V) and, indeed, may be the key initiating factor in the pressure natriuresis response. 1 In turn, the impact of MBF on the pressure natriuretic mechanism provides an explanation for the effects of chronic changes in MBF on the long-term control of arterial pressure. 1 Thus, in rats, chronic reductions in MBF shift the pressure natriuresis relation toward higher pressures and lead to hypertension in normotensive animals. Conversely, chronic increases in MBF shift the pressure natriuresis relation toward lower pressures and ameliorate hypertension in spontaneously hypertensive rats. 1 From studies using an extracorporeal circuit in anesthetized rabbits, 2 we recently obtained preliminary evidence indicating that influences on the release and/or actions of the putative renal medullary depressor hormone might also contribute to the impact of MBF on the long-term control of arterial pressure. In this model, 3 major renal antihypertensive mechanisms can be studied simultaneously. Thus, when renal arterial ...

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Section: Pressure Natriuresissupporting

confidence: 91%

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

et al. 2000

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“…Findings in the present study indicate that the c^-adrenergic receptor mediates the RNS effects on sodium and water reabsorption in normal rats and are consistent with results reported in the dog 7 and rabbit. 8 Treatment with prazosin for 3 days significantly increased the renal density of a 2 -adrenergic receptors in the rat. Kidneys obtained from these rats still demonstrated an enhanced retention of sodium and water following RNS.…”

Section: Discussionmentioning

confidence: 92%

Renal alpha 2-adrenergic receptors multiply and mediate sodium retention after prazosin treatment.

Smyth¹,

Umemura²,

Pettinger³

1986

Hypertension

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SUMMARY Renal nerve stimulation-induced antinatriuresis normally is mediated through postsynaptic oti-adrenergic receptors; however, prazosin-induced a,-adrenergic receptor blockade is associated clinically with sodium retention and not natriuresis. To study whether a r adrenergic receptors mediate renal nerve stimulation-induced antinatriuresis after chronic prazosin treatment, Sprague-Dawley rats were pretreated for 3 days with prazosin (3 mg/kg/day i.p. plus 0.15 mg/ml drinking water) or vehicle (untreated). In isolated perfused (Krebs-Henseleit; Ficoll, 3.5 g/dl, + albumin, 1.0 g/dl at 36°C) kidneys from untreated rats, subpressor levels of renal nerve stimulation (~1 Hz, 10 V, 1 msec) decreased (p < 0.05) sodium (from 4.50 ± 0.42 to 1.71 ± .23 /xEq/min) and urinary excretion rate (from 87.2 ± 4.1 to 57.9 ± 3.9 ^il/min). Adding prazosin (30 nM) to the perfusate completely (~90%) reversed this effect (p < 0.05), while a 2 -adrenergic receptor blockade with yohimbine (300 nM) had no effect. In perfused kidneys from prazosin-treated rats, renal nerve stimulation decreased (p < 0.05) sodium (from 3.24 ± .40 to 1.32 ± .27 /u.Eq/min) and urinary excretion rate (from 78.7 ± 5.0 to 54.1 ± 5.3 /xl/min). However, adding prazosin (100 nM) to the perfusate produced only a slight, insignificant reversal of these effects; prazosin plus yohimbine were required to completely reverse the effects. These results suggest that renal nerve stimulation-induced sodium reabsorption was activated by a,-adrenergic receptors in untreated rats and in part by a 2 -adrenerglc receptors in rats pretreated for 3 days with prazosin. Since renal a 2 -adrenergic receptor density increased (p < 0.05) with prazosin therapy, the most likely explanation is that newly formed a 2 -adrenergic receptors occupy the postsynaptic sites at which a,-adrenergic receptors ordinarily predominate. (Hypertension 8: 323-331, 1986) KEYWORDS • renal a 2 -adrenergic receptors • renal nerve stimulation • sodium retention chronic prazosin • postjunctional • a, and a 2 adrenergic receptors • neurogenic sodium transport A CTIVATION of renal a-adrenergic receptors in-/\ duces sodium retention,' and renal denerva-A. \. tion causes sodium and water excretion. 2 -3 Subpressor levels of renal nerve stimulation (RNS) enhance sodium and water reabsorption through acti-

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“…Such an analysis gives no indication of the function of these aadrenoceptors and the question therefore arises as to which subtype(s) of a-adrenoceptor are involved in the increased reabsorption of sodium induced by the adrenergic nervous system. Functional data from this laboratory using the rabbit (Hesse & Johns, 1984a), and from Osborn et al (1983) using the dog, have shown that the increase in sodium reabsorption caused by activation of the renal nerves at low rates is mediated solely by xl-adrenoceptors. However, whether blood borne noradrenaline could induce increases in sodium reabsorption by activation of both a,-and/or a,-adrenoceptors, which may be more accessible to circulating noradrenaline, is not known but might go some way to explaining the differing conclusions arising from radioligand and functional studies.…”

confidence: 99%

The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit

Hesse

Johns

1985

British J Pharmacology

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1 A study was undertaken in the anaesthetized rabbit to classify the a-adrenoceptor subtypes responsible for increasing renal tubular sodium reabsorption and renin secretion. Intrarenal administration of noradrenaline, at doses which did not change renal blood flow or glomerular filtration rate, significantly decreased urine flow, absolute and fractional sodium excretion by between 26% and 29%. These renal responses to noradrenaline were abolished by the selective a,-adrenoceptor antagonist, prazosin, but not by the selective M2-adrenoceptor antagonist, idazoxan. 2 Noradrenaline, given intrarenally, increased renin secretion between two and three fold and this response was not modified by either prazosin or idazoxan. 3 Intrarenal administration of the selective a-adrenoceptor agonists, phenylephrine and methoxamine, at dose rates which did not change renal haemodynamics, significantly reduced urine flow, absolute and fractional sodium excretion by 15% to 33%, but at doses which reduced blood flow and filtration rate, by between 11% and 26%, urine flow, absolute and fractional sodium excretion decreased between 42% and 49%. 4 Infusion of guanabenz (selective M2-adrenoceptor agonist), at doses with no renal haemodynamic action, increased urine flow, absolute and fractional sodium excretion by 11 % to 15%, while at doses which decreased blood flow by 7%, these other variables did not change. 5 Administration of UK 14304 (selective o2-adrenoceptor agonist) reduced blood flow and filtration rate by 3% and 9% respectively but had no other measurable action. At higher doses, which decreased blood flow by 14% and filtration rate by 24%, urine flow, absolute and fractional sodium excretion fell by between 27% and 50%. 6 Renin secretion was significantly increased by the high doses of phenylephrine and UK 14304 but not by the low doses of these drugs. 7 These studies show that adrenergic stimulation of renal tubular sodium reabsorption involves the activation of al-but not M2-adrenoceptors. Further, adrenergic activation of the juxtaglomerular cells to release renin does not appear to involve either al-or M2-adrenoceptors.

show abstract

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

Cited by 54 publications

References 28 publications

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

Renal alpha 2-adrenergic receptors multiply and mediate sodium retention after prazosin treatment.

The role of α‐adrenoceptors in the regulation of renal tubular sodium reabsorption and renin secretion in the rabbit

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