Analysis of renal denervation in the hydropenic rat: interactions with angiotensin II

1984 ◽  
Vol 246 (1) ◽  
pp. F87-F95 ◽  
Author(s):  
J. C. Pelayo ◽  
R. C. Blantz
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Wistar Rats ◽  
Renal Denervation ◽  
Tubular Reabsorption ◽  
Arteriolar Resistance ◽  
Proximal Tubular ◽  
Glomerular Ultrafiltration ◽  
Renal Vascular ◽  
Proximal Tubular Reabsorption

Nephron filtration rate (SNGFR), its determinants, and proximal tubular reabsorption were measured in hydropenic Munich-Wistar rats with sham-operated (sham) or denervated (DNx) kidneys before and during the administration of [Sar1, Ala8]angiotensin II or SQ 14225. The glomerular ultrafiltration coefficient (LpA) was significantly lower in DNx than in sham rats (P less than 0.025). However, SNGFR was not altered due to an offsetting increment in transcapillary glomerular hydrostatic pressure (delta P) in DNx (P less than 0.005). The marked increment of delta P in DNx was due to an increase in the glomerular capillary hydrostatic pressure, secondary to decreased afferent arteriolar resistance. The infusion of angiotensin II inhibitors to denervated kidneys completely normalized LpA but did not alter sham values. SQ 14225 but not [Sar1, Ala8]angiotensin II infusion provided a nephron plasma flow-dependent increase in SNGFR, secondary to a striking reduction in both glomerular vascular resistances. Endogenous angiotensin II activity may be enhanced by renal denervation, and angiotensin II acts to reduce LpA in this condition and may modulate the final level of renal vascular resistances after acute renal denervation.

Effects of beta-adrenergic stimulation with isoproterenol on glomerular hemodynamics

1989 ◽  
Vol 257 (5) ◽  
pp. F866-F873 ◽  
Author(s):  
J. C. Pelayo ◽  
B. J. Tucker ◽  
R. C. Blantz
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Arteriolar Resistance ◽  
Single Nephron ◽  
Vasodilatory Action ◽  
Glomerular Ultrafiltration ◽  
Glomerular Hemodynamics ◽  
Isoproterenol Infusion

To evaluate the contribution of beta 1-2-adrenergic receptor stimulation to the regulation of single-nephron glomerular filtration rate (SNGFR), we examined by micropuncture techniques the effects of systemic and intrarenal infusion of isoproterenol on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Isoproterenol infused systemically was consistently associated with an elevation in glomerular capillary hydrostatic pressure difference (delta P) from 44.2 +/- 1.2 to 50.1 +/- 1.3 mmHg, P less than 0.01, the consequence of a 5.9-mmHg fall in Bowman's space hydrostatic pressure, P less than 0.005. The potentially beneficial effect of increased delta P on SNGFR was overcome by a 40% reduction in the glomerular ultrafiltration coefficient (LpA) from 0.043 +/- 0.003 to 0.026 +/- 0.003 nl.s-1.mmHg-1.g kidney wt-1, P less than 0.005, with a net effect of a modest 13% decline in SNGFR, P less than 0.01. In contrast, the intrarenal infusion of isoproterenol did not modify glomerular hemodynamics. Suppression of angiotensin II activity eliminated the influences of systemic isoproterenol infusion on LpA and delta P, the latter was the consequence of lower efferent arteriolar resistance. The findings suggest that systemic infusion of a beta 1-2-adrenergic agonist results in a decrease in LpA via angiotensin II effects and exerts a vasodilatory action on postglomerular vessels during angiotensin II inhibition.

Effect of Angiotensin II on Proximal Tubular Reabsorption in Normal Humans

1991 ◽  
Vol 11 (4) ◽  
pp. 271-275 ◽  
Author(s):  
Mario Usberti ◽  
Mario Rondina ◽  
Salvatore Campisi ◽  
Mario Brognoli ◽  
Claudio Poiesi ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Tubular Reabsorption ◽  
Proximal Tubular ◽  
Normal Humans ◽  
Proximal Tubular Reabsorption

Intrarenal Control of Proximal Tubular Reabsorption of Sodium and Water

Nephron ◽  
1969 ◽  
Vol 6 (3) ◽  
pp. 247-259 ◽  
Author(s):  
E.E. Windhager ◽  
J.E. Lewy ◽  
A. Spitzer
Keyword(s):  
Tubular Reabsorption ◽  
Proximal Tubular ◽  
Proximal Tubular Reabsorption

Posttranscriptional regulation of the proximal tubule NaPi-II transporter in response to PTH and dietary Pi

1999 ◽  
Vol 277 (5) ◽  
pp. F676-F684 ◽  
Author(s):  
Heini Murer ◽  
Ian Forster ◽  
Nati Hernando ◽  
Georg Lambert ◽  
Martin Traebert ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Proximal Tubule ◽  
Posttranscriptional Regulation ◽  
Apical Membrane ◽  
Tubular Reabsorption ◽  
Transport Capacity ◽  
Phosphate Intake ◽  
Proximal Tubular ◽  
Dietary Phosphate ◽  
Proximal Tubular Reabsorption

The rate of proximal tubular reabsorption of phosphate (Pi) is a major determinant of Pi homeostasis. Deviations of the extracellular concentration of Piare corrected by many factors that control the activity of Na-Pi cotransport across the apical membrane. In this review, we describe the regulation of proximal tubule Pi reabsorption via one particular Na-Pi cotransporter (the type IIa cotransporter) by parathyroid hormone (PTH) and dietary phosphate intake. Available data indicate that both factors determine the net amount of type IIa protein residing in the apical membrane. The resulting change in transport capacity is a function of both the rate of cotransporter insertion and internalization. The latter process is most likely regulated by PTH and dietary Pi and is considered irreversible since internalized type IIa Na-Picotransporters are subsequently routed to the lysosomes for degradation.

Flash photolysis of caged nitric oxide inhibits proximal tubular fluid reabsorption in free-flow nephron

2005 ◽  
Vol 289 (2) ◽  
pp. R620-R626 ◽  
Author(s):  
Kay-Pong Yip
Keyword(s):  
Nitric Oxide ◽  
Proximal Tubule ◽  
Flash Photolysis ◽  
Tubular Reabsorption ◽  
Fluid Reabsorption ◽  
Proximal Tubular ◽  
Tubular Flow ◽  
Tubular Fluid Reabsorption ◽  
Reabsorption Rate ◽  
Proximal Tubular Reabsorption

A nonobstructing optical method was developed to measure proximal tubular fluid reabsorption in rat nephron at 0.25 Hz. The effects of uncaging luminal nitric oxide (NO) on proximal tubular reabsorption were investigated with this method. Proximal fluid reabsorption rate was calculated as the difference of tubular flow measured simultaneously at two locations (0.8–1.8 mm apart) along a convoluted proximal tubule. Tubular flow was estimated on the basis of the propagating velocity of fluorescent dextran pulses in the lumen. Changes in local tubular flow induced by intratubular perfusion were detected simultaneously along the proximal tubule, indicating that local tubular flow can be monitored in multiple sites along a tubule. The estimated tubular reabsorption rate was 5.52 ± 0.38 nl·min−1·mm−1 ( n = 20). Flash photolysis of luminal caged NO (potassium nitrosylpentachlororuthenate) was induced with a 30-Hz UV nitrogen-pulsed laser. Release of NO from caged NO into the proximal tubule was confirmed by monitoring intracellular NO concentration using a cell-permeant NO-sensitive fluorescent dye (DAF-FM). Emission of DAF-FM was proportional to the number of laser pulses used for uncaging. Photolysis of luminal caged NO induced a dose-dependent inhibition of proximal tubular reabsorption without activating tubuloglomerular feedback, whereas uncaging of intracellular cGMP in the proximal tubule decreased tubular flow. Coupling of this novel method to measure reabsorption with photolysis of caged signaling molecules provides a new paradigm to study tubular reabsorption with ambient tubular flow.

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