Role of macula densa in renal nerve modulation of renin secretion

1982 ◽  
Vol 242 (3) ◽  
pp. R367-R371 ◽  
Author(s):  
J. L. Osborn ◽  
M. D. Thames ◽  
G. F. DiBona
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Renal Perfusion ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Aortic Constriction ◽  
Renal Nerve ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation

Low-frequency renal nerve stimulation (0.25 Hz) augments the renin secretion response to reduction of renal perfusion pressure to 50 mmHg by aortic constriction. The present experiments determined whether this modulating influence could be demonstrated when the macula densa receptor was inoperative. In 10 anesthetized dogs with a nonfiltering kidney and sectioned renal nerves, aortic constriction to 52 mmHg decreased renal blood flow and increased renin secretion from 126 +/- 94 to 192 +/- 55 ng/min. During low-frequency renal nerve stimulation and aortic constriction to 50 mmHg, renin secretion was not augmented (37 +/- 13 to 81 +/- 42 ng/min). In four anesthetized dogs with nonfiltering kidneys, aortic constriction to 52 mmHg increased renin secretion similarly before (16 +/- 8 to 68 +/- 17 ng/min) and after renal denervation (14 +/- 14 to 78 +/- 18 ng/min). Therefore, the augmentation of the renin secretion response to aortic constriction to 50 mmHg by low-frequency renal nerve stimulation in filtering kidneys does not result from an interaction with the renal vascular baroreceptor or the juxtaglomerular granular cells. Since neural augmentation of renin secretion during aortic constriction was not observed in the nonfiltering kidney where the macula densa is inoperative, we conclude that the macula densa is the probable site for the neural modulation of renin secretion.

Effect of low-level renal nerve stimulation on renin release from nonfiltering kidneys

1981 ◽  
Vol 241 (2) ◽  
pp. F156-F161 ◽  
Author(s):  
H. Holdaas ◽  
G. F. DiBona ◽  
F. Kiil
Keyword(s):  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Low Frequency ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Nerve ◽  
Low Level ◽  
Renal Perfusion Pressure ◽  
Renal Nerve Stimulation

The mechanism whereby renal nerves influence the renin-release response to aortic constriction was examined in a nonfiltering ureter-occluded kidney preparation in anesthetized dogs. The kidney was rendered nonfiltering by a combination of mannitol infusion and ureteral occlusion. Suprarenal aortic constriction reduced renal perfusion pressure to 61 +/- 7 mmHg and increased renin release from 16.7 +/- 4.1 to 26.1 +/- 6.0 U/min. At normal renal perfusion pressure, low-frequency renal nerve stimulation (0.25 Hz) increased renin release by 11.6 +/- 4.2 to 25.1 +/- 7.6 U/min. The effect of combined low-level renal nerve stimulation and aortic constriction on renin release was additive; renin release increased by 24.6 +/- 6.5 to 39.5 +/- 7.3 U/min. Propranolol or metoprolol, administered intrarenally at 2 microgram . min-1 . kg-1, abolished the renin-release response to low-level renal nerve stimulation at normal renal perfusion pressure. These data provide evidence that low-frequency renal nerve stimulation influences the renin-release response to reduction in renal perfusion pressure in a nonfiltering ureter-occluded kidney with an inoperative macula densa receptor mechanism. The neural effect on renin release at normal renal perfusion pressure is mediated via beta 1-adrenoceptors probably located on the juxtaglomerular granular cells.

Effect of catecholamines and the renal nerves on renin secretion in anesthetized dogs

1965 ◽  
Vol 209 (3) ◽  
pp. 659-662 ◽  
Author(s):  
Arthur J. Vander
Keyword(s):  
Nerve Stimulation ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Pressor Activity ◽  
Renal Nerve Stimulation

Intravenous infusion of either epinephrine (5–6 µg/min) or norepinephrine (12–16 µg/min) during maintenance of a constant renal arterial blood pressure by means of suprarenal aortic constriction, or stimulation of the renal nerves produced essentially the same effects on renal function and renal venous plasma renin concentration, the latter being measured indirectly by bioassaying the pressor activity produced by plasma incubation under standardized conditions. Glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion were decreased, and renin concentration was increased. The induction of osmotic diuresis during catecholamine infusion or renal nerve stimulation reversed or prevented the increase in renin secretion but did not alter the changes in GFR or RPF. It is suggested that the increased renin secretion induced by catecholamines and renal nerve stimulation in nondiuretic dogs might be the indirect result of the decrease in filtered sodium produced by these procedures. However, a direct effect of the catecholamines and renal nerves on the renin-secreting cells cannot be ruled out.

Interactions among renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin release

1984 ◽  
Vol 247 (5) ◽  
pp. F706-F713 ◽  
Author(s):  
J. L. Osborn ◽  
U. C. Kopp ◽  
M. D. Thames ◽  
G. F. DiBona
Keyword(s):  
Arterial Pressure ◽  
Prostaglandin E2 ◽  
Low Frequency ◽  
Urinary Sodium Excretion ◽  
Macula Densa ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Aortic Constriction ◽  
Renal Nerve

To examine the interactions among the renal nerves, prostaglandins, and renal arterial pressure in the regulation of renin secretion, experiments using low-frequency renal nerve stimulation (LFRNS; supramaximal voltage, 0.5 ms, 0.5 Hz) were performed in anesthetized dogs. LFRNS, which did not affect renal hemodynamics or urinary sodium excretion, increased renin secretion rate before (79 +/- 16 ng/min) but significantly less after renal arterial administration of indomethacin or meclofenamate (26 +/- 7 ng/min). In a separate group of dogs, LFRNS increased both renin secretion rate (266 +/- 139 ng/min) and renal prostaglandin E2 secretion rate (2,080 +/- 635 ng/min). LFRNS does not alter input stimuli to the renal vascular baroreceptor or tubular macula densa receptor mechanisms for renin secretion and represents a direct neural stimulus for renin secretion; this also increases renal prostaglandin E2 secretion rate, which contributes to the increase in renin secretion rate. The renin secretion rate response of innervated and denervated kidneys to reduction in renal arterial pressure to 50 mmHg was examined before and after indomethacin/meclofenamate administration. The observation that indomethacin/meclofenamate decreased but did not abolish the renin secretion rate response to aortic constriction in innervated kidneys suggests the presence of a prostaglandin-independent mechanism that is mediated by an interaction between the renal nerves and the tubular macula densa receptor, as indomethacin/meclofenamate essentially abolished the renin secretion rate response to aortic constriction in denervated kidneys.

Mechanisms of antinatriuresis during low-frequency renal nerve stimulation in anesthetized dogs

1985 ◽  
Vol 249 (3) ◽  
pp. R360-R367
Author(s):  
J. L. Osborn ◽  
R. J. Roman ◽  
R. W. Harland
Keyword(s):  
Sodium Bicarbonate ◽  
Nerve Stimulation ◽  
Low Frequency ◽  
Acid Base Balance ◽  
Renal Nerve ◽  
Bicarbonate Reabsorption ◽  
Anesthetized Dogs ◽  
Renal Nerve Stimulation ◽  
Bicarbonate Infusion ◽  
Sodium Bicarbonate Infusion

The influence of 1.0 Hz renal nerve stimulation (RNS) on the renal excretion of sodium and bicarbonate was determined in anesthetized dogs before and during inhibition of renal bicarbonate reabsorption. RNS decreased both urinary sodium and bicarbonate excretion without changing arterial pressure, renal blood flow, or glomerular filtration rate. Pharmacological blockade of bicarbonate reabsorption with acetazolamide prevented RNS-induced decreases in bicarbonate excretion and reduced the antinatriuretic response. Physiological blockade of tubular bicarbonate reabsorption with intrarenal sodium bicarbonate infusion (1 M) abolished both the antinatriuretic response to RNS and the decrease in bicarbonate excretion. This physiological blockade of neurogenic antinatriuresis resulted from alkalinization of the urine and/or peritubular blood rather than an increase in filtered sodium load, because during intrarenal infusion of 1 M sodium chloride RNS concomitantly decreased sodium and urinary bicarbonate excretion. Since antinatriuretic responses and the decrease in bicarbonate excretion response to RNS were significantly decreased by blockade of bicarbonate reabsorption (with acetazolamide and intrarenal sodium bicarbonate infusion), antinatriuresis during RNS is partly mediated by a mechanism dependent on intact bicarbonate reabsorption. The data suggest that renal nerve activity may participate in the normal regulation of acid-base balance via changes in bicarbonate excretion.

Renal opiate receptor mediation of renin secretion to renal nerve stimulation in the dog

1986 ◽  
Vol 250 (6) ◽  
pp. R973-R979
Author(s):  
S. Koyama ◽  
H. Hosomi
Keyword(s):  
Nerve Stimulation ◽  
High Frequency ◽  
Opiate Receptor ◽  
Renal Hemodynamics ◽  
Renin Secretion ◽  
High Frequency Stimulation ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Frequency Stimulation ◽  
Renal Nerve Stimulation

The present study was designed to evaluate renal opiate receptor mediation of the renin secretion response to electrical stimulation of the renal nerves in the pentobarbital sodium-anesthetized dog by use of the opiate agonist leucine-enkephalin (Leu-enk) and the opiate antagonist naloxone. In all animals studied, left kidneys were pump perfused at a constant renal blood flow. Renal perfusion pressure (RPP) and glomerular filtration rate (GFR) were unaltered at a stimulation frequency of 1.0 Hz; however, renin secretion rate (RSR) increased significantly in the nontreated group. High-frequency renal nerve stimulation (10 Hz) increased RPP and decreased GFR. RSR at the high-frequency stimulation was significantly augmented in the nontreated group. Renal arterial infusion of either Leu-enk (25 micrograms X kg-1 X min-1) or naloxone (7 micrograms X kg-1 X min-1) did not alter base-line levels of renal hemodynamics and RSR and did not produce significant changes in these variables even when renal nerves were stimulated at the low frequency; however, Leu-enk inhibited RPP and RSR responses to the high-frequency stimulation, and naloxone augmented these responses. Phentolamine (13 micrograms X kg-1 X min-1) prevented renal hemodynamic responses to the renal nerve stimulation, whereas RSR responses to the stimulation were unaffected. Propranolol (8 micrograms X kg-1 X min-1) resulted in decreases in RSR at the renal nerve stimulation despite the presence of changes in renal hemodynamics similar to the other groups. The results indicate that intrarenal opiate receptors may participate in inhibiting renal secretion of renin mediated by the renal nerves when renal vasoconstriction and reduction of GFR occurred at the high-frequency stimulation.

Effect of renal nerve stimulation on responsiveness of the rat renal vasculature

2002 ◽  
Vol 283 (5) ◽  
pp. F1056-F1065 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Nerve Stimulation ◽  
Low Frequency ◽  
Rectangular Pulse ◽  
Signal Frequency ◽  
Renal Nerves ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Vasoconstriction ◽  
Low Frequency Oscillations ◽  
Renal Nerve Stimulation

When the renal nerves are stimulated with sinusoidal stimuli over the frequency range 0.04–0.8 Hz, low (≤0.4 Hz)- but not high (≥0.4 Hz)-frequency oscillations appear in renal blood flow (RBF) and are proposed to increase responsiveness of the renal vasculature to stimuli. This hypothesis was tested in anesthetized rats in which RBF responses to intrarenal injection of norepinephrine and angiotensin and to reductions in renal arterial pressure (RAP) were determined during conventional rectangular pulse and sinusoidal renal nerve stimulation. Conventional rectangular pulse renal nerve stimulation decreased RBF at 2 Hz but not at 0.2 or 1.0 Hz. Sinusoidal renal nerve stimulation elicited low-frequency oscillations (≤0.4 Hz) in RBF only when the basal carrier signal frequency produced renal vasoconstriction, i.e., at 5 Hz but not at 1 Hz. Regardless of whether renal vasoconstriction occurred, neither conventional rectangular pulse nor sinusoidal renal nerve stimulation altered renal vasoconstrictor responses to norepinephrine and angiotensin. The RBF response to reduction in RAP was altered by both conventional rectangular pulse and sinusoidal renal nerve stimulation only when renal vasoconstriction occurred: the decrease in RBF during reduced RAP was greater. Sinusoidal renal nerve stimulation with a renal vasoconstrictor carrier frequency results in a decrease in RBF with superimposed low-frequency oscillations. However, these low-frequency RBF oscillations do not alter renal vascular responsiveness to vasoconstrictor stimuli.

Neural and vascular interaction in renin response to graded renal nerve stimulation

1982 ◽  
Vol 242 (5) ◽  
pp. R552-R562 ◽  
Author(s):  
W. S. Ammons ◽  
S. Koyama ◽  
J. W. Manning
Keyword(s):  
Nerve Stimulation ◽  
Control Level ◽  
Low Frequency ◽  
Adrenergic Blockade ◽  
Renal Nerve ◽  
Beta Adrenergic ◽  
Renal Vasoconstriction ◽  
Alpha Adrenergic Receptors ◽  
Alpha Receptors ◽  
Renal Nerve Stimulation

The effect of a 1-min period of renal nerve stimulation was studied in alpha-chloralose-anesthetized cats, whose left kidneys were pump perfused. Renal hemodynamics and filtration parameters were unaltered at stimulation frequencies of 2.0 Hz or less; however, renin secretion rates (RSR) increased with frequency reaching 3 times the control level. At higher frequencies renal vasoconstriction occurred and glomerular filtration rate (GFR) fell. RSR was increased but little more than at 2.0 Hz. The RSR response plots were similar to constant-flow and constant-pressure perfused preparations. beta-Adrenergic blockade with propranolol abolished low-frequency responses and resulted in progressive decreases in RSR at higher frequencies. alpha-Adrenergic blockade with phentolamine prevented renal vascular and GFR changes, whereas RSR continually increased up to 12.0 Hz (13.5 times control). Papaverine treatment, to prevent vascular-GFR changes without blocking alpha-receptors, resulted in similar renin responses. The results indicate that the beta-adrenergic receptor mediates increases in RSR in proportion to frequency when vascular-GFR factors are constant. When renal vasoconstriction occurs at high frequencies the beta-receptor mechanism interacts with an inhibiting mechanism indirectly mediated by alpha-adrenergic receptors.

Sign in / Sign up

Export Citation Format

Share Document