Effects of renal denervation on renin release in response to tilting and furosemide

1977 ◽  
Vol 232 (5) ◽  
pp. H500-H507 ◽  
Author(s):  
A. Stella ◽  
A. Zanchetti
Keyword(s):  
Renal Denervation ◽  
Early Period ◽  
Bilateral Adrenalectomy ◽  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Stimulation Of

In anesthetized cats head-up tilting for 30 min and infusion of furosemide at 0.75 mg/kg in 30 min significantly raised renin release from the innervated kidney (increments of 90.7 +/- 21.4 ng/min on tilting and 105.4 +/- 26.4 ng/min after furosemide); a small and inconstant increase from the contralateral denervated kidney (increments of 16.8 +/- 16.0 and 16.3 +/- 17.7 ng/min, respectively) was abolished by acute bilateral adrenalectomy. Larger doses of furosemide (6.0 mg/kg) could release renin from the denervated kidney also, but the response was still more marked on the innervated side especially in the early period of infusion (increments of 132.7 +/- 23.8 and 33.7 +/- 23.8 ng/min of innervated and denervated sides at 10 min). The response of the denervated kidney to 6.0 mg furosemide/kg was not affected by adrenalectomy. Stimulation of juxtaglomerular cells by tilting is entirely due to sympathoadrenergic activation; stimulation by furosemide is also entirely neural when the diuretic drug is given in moderate doses, but is partly independent of innervation when larger doses are administered.

scholarly journals Osmotic stimulation of renin release from single mouse juxtaglomerular cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Ole Skott ◽  
Boye L. Jensen ◽  
Kirsten Madsen ◽  
Finn Jorgensen ◽  
Pernille B. Hansen ◽  
...  
Keyword(s):  
Renin Release ◽  
Juxtaglomerular Cells ◽  
Osmotic Stimulation ◽  
Stimulation Of

scholarly journals Role of the heart in blood pressure lowering during chronic baroreflex activation: insight from an in silico analysis

2018 ◽  
Vol 315 (5) ◽  
pp. H1368-H1382 ◽  
Author(s):  
John S. Clemmer ◽  
W. Andrew Pruett ◽  
Robert L. Hester ◽  
Radu Iliescu ◽  
Thomas E. Lohmeier
Keyword(s):  
Blood Pressure ◽  
Mathematical Model ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Lowering ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Pressure Lowering ◽  
Renal Sympathetic ◽  
Stimulation Of

Electrical stimulation of the baroreflex chronically suppresses sympathetic activity and arterial pressure and is currently being evaluated for the treatment of resistant hypertension. The antihypertensive effects of baroreflex activation are often attributed to renal sympathoinhibition. However, baroreflex activation also decreases heart rate, and robust blood pressure lowering occurs even after renal denervation. Because controlling renal sympathetic nerve activity (RSNA) and cardiac autonomic activity cannot be achieved experimentally, we used an established mathematical model of human physiology (HumMod) to provide mechanistic insights into their relative and combined contributions to the cardiovascular responses during baroreflex activation. Three-week responses to baroreflex activation closely mimicked experimental observations in dogs including decreases in blood pressure, heart rate, and plasma norepinephrine and increases in plasma atrial natriuretic peptide (ANP), providing validation of the model. Simulations showed that baroreflex-induced alterations in cardiac sympathetic and parasympathetic activity lead to a sustained depression of cardiac function and increased secretion of ANP. Increased ANP and suppression of RSNA both enhanced renal excretory function and accounted for most of the chronic blood pressure lowering during baroreflex activation. However, when suppression of RSNA was blocked, the blood pressure response to baroreflex activation was not appreciably impaired due to inordinate fluid accumulation and further increases in atrial pressure and ANP secretion. These simulations provide a mechanistic understanding of experimental and clinical observations showing that baroreflex activation effectively lowers blood pressure in subjects with previous renal denervation. NEW & NOTEWORTHY Both experimental and clinical studies have shown that the presence of renal nerves is not an obligate requirement for sustained reductions in blood pressure during chronic electrical stimulation of the carotid baroreflex. Simulations using HumMod, a mathematical model of integrative human physiology, indicated that both increased secretion of atrial natriuretic peptide and suppressed renal sympathetic nerve activity play key roles in mediating long-term reductions in blood pressure during chronic baroreflex activation.

Electrical stimulation of the renal arterial nerves does not unmask the blindness of renal denervation procedure in swine

2014 ◽  
Vol 176 (3) ◽  
pp. 1061-1063 ◽  
Author(s):  
Dimitris Tsiachris ◽  
Costas Tsioufis ◽  
Kyriakos Dimitriadis ◽  
Athanasios Kordalis ◽  
Costas Thomopoulos ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Renal Denervation ◽  
Stimulation Of

scholarly journals Calcium-dependent phosphodiesterase 1C inhibits renin release from isolated juxtaglomerular cells

2009 ◽  
Vol 297 (5) ◽  
pp. R1469-R1476 ◽  
Author(s):  
M. Cecilia Ortiz-Capisano ◽  
Tang-Dong Liao ◽  
Pablo A. Ortiz ◽  
William H. Beierwaltes
Keyword(s):  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Renin Release ◽  
Calcium Sensing Receptor ◽  
Calcium Dependent ◽  
Calcium Sensing ◽  
Inhibitory Modulation ◽  
Camp Formation ◽  
Stimulation Of

Renin release from the juxtaglomerular (JG) cell is stimulated by the second messenger cAMP and inhibited by calcium. We previously showed JG cells contain a calcium sensing receptor (CaSR), which, when stimulated, decreases cAMP formation and inhibits renin release. We hypothesize CaSR activation decreases cAMP and renin release, in part, by stimulating a calcium calmodulin-activated phosphodiesterase 1 (PDE1). We incubated our primary culture of JG cells with two selective PDE1 inhibitors [8-methoxymethil-IBMX (8-MM-IBMX; 20 μM) and vinpocetine (40 μM)] and the calmodulin inhibitor W-7 (10 μM) and measured cAMP and renin release. Stimulation of the JG cell CaSR with the calcimimetic cinacalcet (1 μM) resulted in decreased cAMP from a basal of 1.13 ± 0.14 to 0.69 ± 0.08 pM/mg protein ( P < 0.001) and in renin release from 0.89 ± 0.16 to 0.38 ± 0.08 μg ANG I/ml·h−1·mg protein−1 ( P < 0.001). However, the addition of 8-MM-IBMX with cinacalcet returned both cAMP (1.10 ± 0.19 pM/mg protein) and renin (0.57 ± 0.16 μg ANG I/ml·h−1·mg protein−1) to basal levels. Similar results were obtained with vinpocetine, and also with W-7. Combining 8-MM-IBMX and W-7 had no additive effect. To determine which PDE1 isoform is involved, we performed Western blot analysis for PDE1A, B, and C. Only Western blot analysis for PDE1C showed a characteristic band apparent at 80 kDa. Immunofluorescence showed cytoplasmic distribution of PDE1C and renin in the JG cells. In conclusion, PDE1C is expressed in isolated JG cells, and contributes to calcium's inhibitory modulation of renin release from JG cells.

Stimulation of renin release in perfused kidney by low calcium and high magnesium

1977 ◽  
Vol 232 (4) ◽  
pp. F377-F382 ◽  
Author(s):  
J. S. Fray
Keyword(s):  
Sodium Excretion ◽  
Calcium Concentration ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Sodium Concentration ◽  
Renin Release ◽  
Isolated Perfused Rat Kidney ◽  
Low Calcium ◽  
Perfused Rat Kidney ◽  
Stimulation Of

These experiments were designed to test whether changing perfusate calcium or magnesium concentrations affected renin release in the isolated perfused rat kidney, and whether kidneys removed from sodium-loaded or sodium-deprived rats released the same amount of renin in response to identical stimuli. Kidneys were perfused with Kreb-Henseleit solution containing albumin. Renin release was inversely related to perfusate calcium concentration, whereas renin release was directly related to perfusate magnesium. Although a low calcium medium or low perfusion pressure (50 mmHg) stimulated renin release, the release was substantially greater in the sodium-deprived rats. Increasing the perfusate sodium concentration from 85 to 206 mM increased excretion, but did not alter renin release. It is concluded that a) low perfusate calcium and high magnesium concentrations stimulate renin release, b) kidneys removed from sodium-deprived rats released substantially more renin thatn those from sodium-loaded rats, and c) changing perfusate sodium concentration alters sodium excretion, but does not affect renin release.

Endothelin Inhibits cAMP-Induced Renin Release from Isolated Renal Juxtaglomerular Cells

1995 ◽  
Vol 26 ◽  
pp. S135-137 ◽  
Author(s):  
Michael Ackermann ◽  
Theresia Ritthaler ◽  
Günter Riegger ◽  
Armin Kurtz ◽  
Bernhard K. Krämer
Keyword(s):  
Renin Release ◽  
Juxtaglomerular Cells

Stimulation of renin release by prostaglandin E2 is mediated by EP2 and EP4 receptors in mouse kidneys

2004 ◽  
Vol 287 (3) ◽  
pp. F427-F433 ◽  
Author(s):  
Frank Schweda ◽  
Jürgen Klar ◽  
Shuh Narumiya ◽  
Rolf M. Nüsing ◽  
Armin Kurtz
Keyword(s):  
Vascular Tone ◽  
Threshold Concentration ◽  
Renin Release ◽  
Receptor Subtypes ◽  
Wild Type ◽  
Adrenoceptor Agonist ◽  
Functional Relevance ◽  
Renal Vascular ◽  
Renal Vascular Tone ◽  
Stimulation Of

PGE2 is a potent stimulator of renin release. So far, the contribution of each of the four PGE2 receptor subtypes (EP1–EP4) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP1−/−, EP2−/−, EP3−/−, EP4−/−, and wild-type mice. PGE2 concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP1−/−, EP2−/−, EP3−/−, and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP4−/− mice. Moreover, the maximum stimulation of RSR by PGE2 at 1 μM was significantly reduced in EP4−/− (12.8-fold of control) and EP2−/− (15.9-fold) compared with wild-type (20.7-fold), EP1−/− (23.8-fold), and EP3−/− (20.1-fold). In contrast, stimulation of RSR by either the loop diuretic bumetanide or the β-adrenoceptor agonist isoproterenol was similar in all strains. PGE2 exerted a dual effect on renal vascular tone, inducing vasodilatation at low concentrations (1 nmol/) and vasoconstriction at higher concentrations (100 nmol/) in kidneys of wild-type mice. In kidneys of EP2−/− as well as EP4−/− mice, vasodilatation at low PGE2 concentrations was prevented, whereas vasoconstriction at higher concentrations was augmented. In contrast, the vasodilatatory component was pronounced in kidneys of EP1 and EP3 knockout mice, whereas in both genotypes the vasoconstriction at higher PGE2 concentrations was markedly blunted. Our data provide evidence that PGE2 stimulates renin release via activation of EP2 and EP4 receptors, whereas EP1 and EP3 receptors appear to be without functional relevance in juxtaglomerular cells. In contrast, all four receptor subtypes are involved in the control of renal vascular tone, EP1 and EP3 receptors increasing, and EP2 as well as EP4 receptors, decreasing it.

Prostaglandins and renin release in vitro

1981 ◽  
Vol 240 (6) ◽  
pp. E609-E614
Author(s):  
C. S. Lin ◽  
H. Iwao ◽  
S. Puttkammer ◽  
A. M. Michelakis
Keyword(s):  
Arachidonic Acid ◽  
Renal Cortex ◽  
The Other ◽  
Renin Release ◽  
Eicosatetraenoic Acid ◽  
Juxtaglomerular Cells ◽  
Prostaglandin F2 Alpha ◽  
Prostaglandin System

The present studies were undertaken to explore further the role of prostaglandins in the release of renin from the renal cortex. To provide the best assessment of renin release, renin was determined by a radioimmunoassay for the direct measurement of renin. Slices of mouse renal cortex were incubated at 37 degrees C with arachidonic acid (AA), 5,8,11,14-eicosatetraenoic acid (ETA), indomethacin, prostaglandins, and synthetic prostaglandin endoperoxide analogue (EPA). Our results showed that AA at 1.5 X 10(-8) M significantly increased renin release at 10 and 30 min of incubation. This renin increase ws abolished by either ETA or indomethacin. Prostaglandin F2 alpha (PGF2 alpha) also significantly stimulated renin release at 10 and 60 min. PGE2 and 16,16-dimethyl PGE2 (DMPGE2) showed much less renin release-stimulating activity. EPA and PGI2 on the other hand very strongly stimulated renin release. However, at higher concentrations the stimulating effect of PGI2 and EPA disappeared and even became inhibitory in the case of EPA. Other prostaglandins were found to have no effect on renin release. The results suggest that the prostaglandin system directly affects renin release from the juxtaglomerular cells independent of systemic neurogenic and hemodynamic influences.

Renin secretion and loop of Henle chloride reabsorption in the adrenalectomized rat

1985 ◽  
Vol 249 (4) ◽  
pp. F596-F602
Author(s):  
W. J. Welch ◽  
C. E. Ott ◽  
G. P. Guthrie ◽  
T. A. Kotchen
Keyword(s):  
Sodium Chloride ◽  
Chloride Transport ◽  
Plasma Renin ◽  
Saline Infusion ◽  
Renin Release ◽  
Loop Of Henle ◽  
Water Drinking ◽  
Before And After ◽  
Adrenalectomized Rats ◽  
Stimulation Of

Renin release is increased in the adrenalectomized rat and is not inhibited by sodium chloride administration. The purpose of this study was to determine whether increased renin release is related to impaired absorptive chloride transport in the loop of Henle. Chloride transport in the loop was measured before and after acute saline infusion in three groups of rats: 1) saline-drinking adrenalectomized rats (Adx); 2) saline-drinking dexamethasone-treated adrenalectomized rats (Dex); and 3) water-drinking sham-operated controls. Unrelated to differences of arterial pressure, glomerular filtration rate, or net sodium chloride balance, chloride reabsorption in the loop of Henle of Adx [836 +/- 172 peq/min (SE)] was less (P less than 0.01) than in controls (1,646 +/- 353) and Dex (1,377 +/- 318) before saline infusion. After saline infusion, chloride delivery to the loop increased (P less than 0.05) in all three groups. However, loop chloride reabsorption increased (P less than 0.01) only in controls and Dex but not in Adx. Before saline infusion, plasma renin concentration (PRC) of Adx (350 +/- 108 U/ml) was greater (P less than 0.01) than that in controls (56 +/- 6) or Dex (108 +/- 36); sodium chloride infusion failed to inhibit PRC in Adx, whereas PRC was suppressed (P less than 0.01) by saline in Dex and controls. Thus stimulation of renin release in adrenalectomized animals was associated with decreased absorptive chloride transport in the loop of Henle. Dexamethasone normalized loop function and renin responsiveness to sodium chloride.

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