Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat

The renal functional effects of renal mechano- (MR) and chemoreceptor (CR) stimulation were examined in dogs and rats. In dogs increasing ureteral pressure (increases UP) increased ipsilateral (ipsi) renal blood flow and renin secretion rate, decreased contralateral (contra) renal blood flow, but did not affect contra renal excretion or renin secretion rate. Increasing renal venous pressure (increases RVP) increased ipsi renin secretion rate but did not affect contra renal function. Retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect either ipsi or contra renal function. In rats,increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl at unchanged UP did not affect mean arterial pressure, heart rate, contra renal blood flow, or glomerular filtration rate but increased contra urine flow rate and urinary sodium excretion. Increasing ureteral pressure with 0.1 M NaCl increased contra urine flow rate and urinary sodium excretion, whereas retrograde ureteropelvic perfusion with 0.1 M NaCl was without effect. Thus increases UP and retrograde ureteropelvic perfusion with 0.9 M NaCl stimulated renal MR and CR, respectively. The contra diuretic and natriuretic responses to renal MR and CR stimulation were abolished by either ipsi or contra renal denervation. Renal MR and CR stimulation increased ipsi afferent renal nerve activity (RNA) and decreased contra efferent RNA. These results indicate that in dogs renal MR stimulation results in a modest contralateral excitatory renorenal reflex, whereas in rats renal MR and CR stimulation produce a contralateral inhibitory renorenal reflex.

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Central mu opioids mediate differential control of urine flow rate and urinary sodium excretion in conscious rats

Life Sciences ◽

10.1016/0024-3205(95)00065-e ◽

1995 ◽

Vol 56 (14) ◽

pp. PL243-PL248 ◽

Cited By ~ 7

Author(s):

Daniel R. Kapusta ◽

Edward M. Dzialowski

Keyword(s):

Flow Rate ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urine Flow ◽

Urinary Sodium ◽

Urine Flow Rate ◽

Conscious Rats ◽

Mu Opioids ◽

Differential Control

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Blunted natriuresis to atrial natriuretic peptide in chronic sodium-retaining disorders

AJP Renal Physiology ◽

10.1152/ajprenal.1987.252.5.f865 ◽

1987 ◽

Vol 252 (5) ◽

pp. F865-F871 ◽

Cited By ~ 4

Author(s):

J. P. Koepke ◽

G. F. DiBona

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Flow Rate ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urine Flow ◽

Urine Flow Rate ◽

Atrial Natriuretic

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.

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Excretion of endogenous digoxin-like immunoreactive factors in human urine is a function of urine flow rate.

Clinical Chemistry ◽

10.1093/clinchem/34.5.960 ◽

1988 ◽

Vol 34 (5) ◽

pp. 960-964 ◽

Cited By ~ 4

Author(s):

B A Siegfried ◽

R Valdes

Keyword(s):

Urinary Excretion ◽

Flow Rate ◽

Human Urine ◽

Sodium Excretion ◽

Salt Intake ◽

Fractional Excretion ◽

Urinary Sodium Excretion ◽

Urine Flow ◽

Urine Flow Rate ◽

Healthy Humans

Abstract We studied the effect of varying water and salt intake on the renal excretion of endogenous digoxin-like immunoreactive factors (DLIF). DLIF were measured in human urine and serum by competitive displacement of 125I-labeled digoxin from anti-digoxin antibodies. Diuresis was selectively induced in normal healthy humans by acute water ingestion, and natriuresis was preferentially induced by acute saline ingestion. We found the amount of endogenous immunoreactivity excreted in urine to be correlated with urine flow rate but not with urinary sodium excretion. Urinary excretion of DLIF, normalized to creatinine, was 3.6-fold greater at a urine flow rate of 5.5 mL/min than at 0.5 mL/min. On the other hand, saline intake increased urine flow rate 1.9-fold and increased sodium excretion threefold, but did not affect urinary excretion of DLIF. Fractional excretion of DLIF was linearly related to fractional excretion of water. This study demonstrates that normalization of DLIF values to urinary creatinine does not make DLIF excretion independent of urine flow rate and underscores the need for information on urine flow rate when DLIF measurements in urine are being interpreted.

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Effect of a kinin antagonist on renal function and haemodynamics during alterations in sodium balance in conscious normotensive rats

Clinical Science ◽

10.1042/cs0780165 ◽

1990 ◽

Vol 78 (2) ◽

pp. 165-168 ◽

Cited By ~ 6

Author(s):

Paolo Madeddu ◽

Nicola Glorioso ◽

Aldo Soro ◽

Paolo Manunta ◽

Chiara Troffa ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Renal Function ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Filtration Rate ◽

Sodium Intake ◽

Urinary Sodium Excretion

1. To evaluate whether sodium intake can modulate the action of endogenous kinins on renal function and haemodynamics, a receptor antagonist of bradykinin was infused in conscious normotensive rats maintained on either a normal or a low sodium diet. 2. The antagonist inhibited the hypotensive effect of exogenously administered bradykinin. It did not change the vasodepressor effect of acetylcholine, dopamine or prostaglandin E2. 3. The antagonist did not affect mean blood pressure, glomerular filtration rate, renal blood flow or urinary sodium excretion, in rats on sodium restriction. It did not change mean blood pressure, glomerular filtration rate or urinary sodium excretion, but decreased renal blood flow, in rats on a normal sodium intake. 4. The kallikrein–kinin system has a role in the regulation of renal blood flow in rats on a normal sodium diet.

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Interaction between neural and nonneural mechanisms controlling renin secretion rate

AJP Renal Physiology ◽

10.1152/ajprenal.1984.246.5.f620 ◽

1984 ◽

Vol 246 (5) ◽

pp. F620-F626 ◽

Cited By ~ 7

Author(s):

U. C. Kopp ◽

G. F. DiBona

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Neural Mechanisms ◽

Secretion Rate ◽

The Other ◽

Renin Secretion ◽

Renal Nerves ◽

The Right

The interaction between the neural and nonneural mechanisms in the control of renin secretion rate was studied in anesthetized vagotomized dogs at renal arterial pressures of 170, 130, 90, and 50 mmHg. Left renal nerves were stimulated (RNS) at either 0.075, 0.3, or 0.7 Hz and the right kidney was denervated. At spontaneous renal arterial pressure RNS at 0.075, 0.3, and 0.7 Hz decreased renal blood flow 0, 1 +/- 0, and 2 +/- 1%, respectively, and urinary sodium excretion 0, 2 +/- 1, and 22 +/- 3%, respectively. RNS at 0.075 Hz augmented renin secretion rate at 50 mmHg by 1,806 +/- 505 ng/min; there was no augmentation at 90, 130, and 170 mmHg. RNS at 0.3 Hz augmented renin secretion rate at 50 and 90 mmHg by 2,635 +/- 824 and 1,197 +/- 289 ng/min, respectively; there was no augmentation at 130 and 170 mmHg. RNS at 0.7 Hz augmented renin secretion rate at 50, 90, and 130 mmHg by 1,421 +/- 287, 747 +/- 172, and 273 +/- 163 ng/min, respectively; there was no augmentation at 170 mmHg. RNS at 0.075 Hz to one kidney and 0.7 Hz to the other kidney in the same dog demonstrated that the renin secretion rate was greater with RNS at 0.7 Hz than with 0.075 Hz at 50 and 90 mmHg but not at 130 and 170 mmHg. We conclude that the nonneural and neural mechanisms interact in the control of renin secretion rate. The degree of interaction depends on the level of renal arterial pressure and the intensity of RNS.

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Role of renal alpha-adrenoceptors mediating renin secretion

AJP Renal Physiology ◽

10.1152/ajprenal.1982.242.6.f620 ◽

1982 ◽

Vol 242 (6) ◽

pp. F620-F626 ◽

Cited By ~ 2

Author(s):

J. L. Osborn ◽

G. F. DiBona ◽

M. D. Thames

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Renin Secretion ◽

Renal Nerve ◽

Alpha Adrenoceptors ◽

Alpha Adrenoceptor

The increase in renin secretion resulting from low-frequency renal nerve stimulation (0.5 Hz) occurs in the absence of changes in urinary sodium excretion or renal blood flow and is apparently derived from a direct effect of renal sympathetic nerves on juxtaglomerular granular cells. We sought to determine the role of renal alpha-adrenoceptors in this neurally evoked renin secretion. The neurally evoked renin secretion was unaffected by renal alpha-adrenoceptor blockade with phentolamine or prazosin; however, two dose levels of phenoxybenzamine equally inhibited the renin secretion. The renal vasoconstrictor response to graded renal nerve stimulation was similarly diminished by phentolamine, prazosin, and the higher phenoxybenzamine dose, whereas the lower phenoxybenzamine dose was significantly less effective. Renal alpha-adrenoceptor stimulation with methoxamine infusion at doses that were just subthreshold for altering renal blood flow and urinary sodium excretion or at doses that just reduced urinary sodium excretion also did not change renin secretion. Higher doses of methoxamine that decreased both renal blood flow and sodium excretion increased renin secretion. Based on the inability of phentolamine and prazosin to prevent neurally mediated renin secretion and on the dose-response relationship between methoxamine and changes in renin secretion, renal blood flow, and urinary sodium excretion, we conclude that renal alpha-adrenoceptors do not mediate renin secretion elicited by direct neural activation of the juxtaglomerular granular cells. The data suggest that phenoxybenzamine inhibits neurally mediated renin secretion by a mechanism other than renal alpha-adrenoceptor blockade.

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Central α2-receptor mechanisms contribute to enhanced renal responses during ketamine-xylazine anesthesia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.6.r1867 ◽

1998 ◽

Vol 275 (6) ◽

pp. R1867-R1874 ◽

Cited By ~ 4

Author(s):

Antonio De Melo Cabral ◽

Daniel R. Kapusta ◽

Velga A. Kenigs ◽

Kurt J. Varner

Keyword(s):

Flow Rate ◽

Intravenous Infusion ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urine Flow ◽

Urinary Sodium ◽

Urine Flow Rate ◽

Vasopressin Release ◽

Adrenoceptor Antagonist ◽

Anesthetized Rats

We have recently developed an experimental approach to study central opioid control of renal function in anesthetized rats. This model system uses the intravenous infusion of the α2-agonist xylazine to enhance basal levels of urine flow rate and urinary sodium excretion in ketamine-anesthetized rats. This study examined the contribution of central and peripheral α2-adrenergic receptor mechanisms in mediating the enhanced renal excretory responses produced by xylazine. In ketamine-anesthetized rats, the enhanced levels of urine flow rate and urinary sodium excretion produced by the intravenous infusion of xylazine were reversed by the intravenous bolus injection of the α2-adrenoceptor antagonist yohimbine but not by the α1-adrenoceptor antagonist terazosin. In separate animals the intracerebroventricular administration of yohimbine only reduced urine flow rate by ∼50% but did not alter urinary sodium excretion. The decrease in urine flow rate produced by intracerebroventricular yohimbine was reversed by the intravenous injection of a selective V2-vasopressin receptor antagonist. In a separate group of ketamine- and xylazine-anesthetized rats, the bilateral microinjection of yohimbine into the hypothalamic paraventricular nucleus (PVN) also significantly decreased urine flow rate by 54% without altering urinary sodium excretion. The microinjection of the β-adrenoceptor antagonist propranolol into the PVN did not alter either renal excretory parameter. These results suggest that during intravenous infusion, xylazine increases urine flow rate by activating α2-adrenergic receptors in the PVN, which in turn decrease vasopressin release. The ability of α-adrenergic mechanisms in the PVN to selectively influence the renal handling of water, but not sodium, may contribute to the reported dissociation of the natriuretic and diuretic responses of α2-adrenoceptor agonists.

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Renal blood flow, early distal sodium, and plasma renin concentrations during osmotic diuresis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.279.4.r1268 ◽

2000 ◽

Vol 279 (4) ◽

pp. R1268-R1276 ◽

Cited By ~ 20

Author(s):

Paul P. Leyssac ◽

Niels-Henrik Holstein-Rathlou ◽

Ole Skøtt

Keyword(s):

Blood Flow ◽

Renal Blood Flow ◽

Sodium Excretion ◽

Plasma Renin ◽

Urine Flow ◽

Sodium Reabsorption ◽

Osmotic Diuresis ◽

Nacl Concentration ◽

Proximal Tubular ◽

Distal Tubules

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.

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