Glucagon increases medullary interstitial electrolyte concentration in rat kidney

1995 ◽  
Vol 73 (9) ◽  
pp. 1289-1291 ◽  
Author(s):  
E. Kompanowska-Jezierska ◽  
J. Sadowski ◽  
A. Walkowska

In anesthetized rats, tissue electrical admittance of the inner medulla (a measure of total ion concentration in the interstitium), medullary blood flow (laser Doppler technique), and renal clearances were measured simultaneously before and during i.v. infusion of glucagon at 110 and 330 ng∙min−1∙kg−1 body weight. Admittance increased modestly, 5.4% after a large glucagon dose (p < 0.01), whereas medullary blood flow was stable. Glomerular filtration rate increased transiently and then fell during high-dose glucagon infusion. The increase in tissue electrolyte (mostly NaCl) concentration in the medulla observed with stable medullary blood flow and decreasing glomerular filtration rate indicates that stimulation of NaCl reabsorption in the medullary ascending limb of Henle's loop by glucagon was the mechanism underlying augmentation of medullary ionic hypertonicity. This suggests that glucagon can contribute to the urine concentration process.Key words: glucagon, loop of Henle, tubular NaCl transport, medullary blood flow.

1994 ◽  
Vol 267 (2) ◽  
pp. F296-F302 ◽  
Author(s):  
K. Ujiie ◽  
J. Yuen ◽  
L. Hogarth ◽  
R. Danziger ◽  
R. A. Star

Nitric oxide (NO) has effects on renal blood flow, glomerular filtration rate, renin secretion, and renal sodium excretion. Four isoforms of nitric oxide synthase (NOS) have been cloned to date. However, the molecular identity of NOS present in the renal vasculature is unknown. Endothelial NOS (NOS-III) is regulated both acutely by cell calcium and chronically by shear stress. To determine if renal blood vessels and the glomerulus express NOS-III mRNA, we used degenerate polymerase chain reaction (PCR) to clone a portion of rat NOS-III. We then assayed NOS-III mRNA in microdissected renal structures by reverse transcriptase-PCR. NOS-III mRNA was expressed at high levels in glomeruli, arcuate vessels, and interlobular artery/afferent arterioles. NOS-III mRNA was detected inconsistently in proximal tubules, thick ascending limbs, and cortical and inner medullary collecting ducts. Previous studies have shown that chronic oral treatment with the NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) decreases NO synthesis and causes hypertension. To determine if the systemic blockade occurs only by competitive inhibition, we determined the effect of L-NAME on glomerular NOS-III mRNA. L-NAME administration (5 days) decreased NOS-III mRNA in the glomerulus to 25 +/- 12% of control levels. We conclude that endothelial NOS-III mRNA is preferentially expressed in the glomerulus and renal vasculature, where it can modulate renal blood flow and glomerular filtration rate. Furthermore, glomerular NOS-III may be modulated at the level of mRNA abundance in vivo by systemic L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)


1982 ◽  
Vol 63 (s8) ◽  
pp. 215s-217s ◽  
Author(s):  
R. Golin ◽  
A. Stella ◽  
A. Zanchetti

1. In anaesthetized cats, reversible nenal nerve denervation (cooling of the renal nerves on one side at 4°C for 16 min) was performed and its effects on haemodynamic and excretory functions of the ipsilateral and the contralateral kidneys were studied. 2. Renal nerve cooling did not cause any change in arterial pressure. Slight increase in blood flow, no change in glomerular filtration rate and a large increase in water and sodium excretion occurred in the ipsilateral kidney; simultaneously, no change in blood flow, a slight and transient decrease in glomerular filtration rate, and a significant decrease in diuresis and natriuresis were observed in the contralateral kidney. 3. Ipsilateral and contralateral renal changes were equally evident in the early (minutes 0 to 8) and late phases (minutes 8 to 16) of the cooling period. 4. When renal nerve cooling was repeated after surgical denervation of the contralateral kidney all contralateral effects were abolished.


1983 ◽  
Vol 245 (5) ◽  
pp. R743-R748 ◽  
Author(s):  
R. W. Davis ◽  
M. A. Castellini ◽  
G. L. Kooyman ◽  
R. Maue

Renal and hepatic function were studied during voluntary dives in Weddell seals by measuring the clearance rate of inulin and indocyanine green (ICG). Inulin is cleared exclusively by the kidneys and measures renal glomerular filtration rate (GFR). ICG is cleared by the liver and is blood flow dependent at concentrations used. Studies were conducted from a portable hut with a trapdoor placed over an isolated hole in the sea ice near McMurdo Station, Antarctica. An intravertebral extradural catheter was inserted percutaneously under light anesthesia in subadult seals weighing 130-200 kg. When released into the ice hole, the seals made voluntary dives, but always had to return to breathe. Serial blood samples were taken after single injections of inulin and ICG and analyzed within 24 h. The mean half time (t 1/2) for inulin clearance while resting at the surface was 27.3 +/- 13.0 min (n = 43) and the mean t 1/2 for ICG clearance was 18.3 +/- 7.3 min (n = 23). The mean resting GFR was 3.6 ml X min-1 X kg-1 (range 3.2-3.9, n = 3). Inulin and ICG clearance rates did not change from resting levels during dives shorter than the seal's aerobic dive limit (ADL). Inulin clearance decreased over 90% during dives longer than the ADL, but there was no significant reduction in ICG clearance during dives lasting up to 23 min. It appears that normal renal GFR and hepatic blood flow continue during natural aerobic dives. During dives that exceed the ADL, GFR is reduced but hepatic blood flow may be maintained.


2005 ◽  
Vol 360 (1-2) ◽  
pp. 205-207 ◽  
Author(s):  
Lorenz Risch ◽  
Christoph Saely ◽  
Ursula Reist ◽  
Kurt Reist ◽  
Martin Hefti ◽  
...  

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.


2018 ◽  
Vol 46 (6) ◽  
pp. e560-e566 ◽  
Author(s):  
Jenny Skytte Larsson ◽  
Vitus Krumbholz ◽  
Anders Enskog ◽  
Gudrun Bragadottir ◽  
Bengt Redfors ◽  
...  

PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 95-99
Author(s):  
Ekkehard W. Reimold ◽  
Walter J. Reynolds ◽  
David E. Fixler ◽  
LaVerne McElroy

Hemodialysis was used in addition to forced diuresis in the treatment of quinidine poisoning of a 3-year-old girl. The estimated retained dose of quinidine was 1,600 mg. During a 36-hour treatment period the patient excreted through the kidneys 768.1 mg quinidine (21.3 mg/hr). Hemodialysis almost doubled the quinidine elimination by removing 145 mg in eight hours (18.1 mg/hr): renal excretion, 55%; hemodialysis, 45%. The quinidine elimination with dialysis is high when high blood flow rates through the artificial kidney can be maintained. Adequate glomerular filtration rate and urine acidification are necessary for high renal excretion of quinidine.


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