Effects of simultaneous infusions of glucagon and cyclic AMP on glomerular filtration rate in the dog

1978 ◽  
Vol 56 (4) ◽  
pp. 596-602 ◽  
Author(s):  
Enrique Espinosa-Meléndez ◽  
Mortimer Levy
Keyword(s):  
Glomerular Filtration Rate ◽  
Cyclic Amp ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Left Renal Artery ◽  
Arterial Blood ◽  
Intracellular Release ◽  
The Right

In this study, we tested the hypothesis that the renal vasodilator properties of glucagon are mediated by the intracellular release of cyclic AMP. In eight normal dogs, we tested the effect on glomerular filtration rate (GFR) of intravenous glucagon (5 μg/min), after having administered cyclic AMP (1.6 mg/min) into the left renal artery. GFR for both the right and left kidneys increased by 38% (p < 0.05), compared with an increment of 29% when glucagon alone had previously been administered. Similar studies were carried out in five dogs with steady-state hemorrhagic hypotension (arterial blood pressure = 75 mmHg). In this group as well, the prior infusion of cyclic AMP did not blunt or abolish the tendency of glucagon to promote renal perfusion or increase GFR. When cyclic AMP was administered alone, GFR and the clearance of p-aminohippurate usually declined by about 20% (p < 0.05). In six dogs, glucagon was administered intravenously at 5 μg/min prior to the infusion of cyclic AMP (1.6 mg/min) into the left renal artery. For this kidney, the anticipated decline in renal perfusion occurred. The prior administration of theophylline into the left renal artery did not prevent an intravenous infusion of glucagon from elevating GFR. These experiments indicate that the prior flooding of the microvasculature with either cyclic AMP or glucagon does not prevent the pharmacological effects of each of these substances. The renal hemodynamic effects of glucagon in normal and hypotensive dogs does not appear to depend on the release of cyclic AMP.

The Effect of Glucagon on Glomerular Filtration Rate in Dogs During Reduction of Renal Blood Flow

1975 ◽  
Vol 53 (4) ◽  
pp. 660-668 ◽  
Author(s):  
Mortimer Levy
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Tubular Necrosis ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Beneficial Effects ◽  
Tubular Necrosis ◽  
Arterial Blood ◽  
Urine Formation

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 μg/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6–7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65–70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50–70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90–130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (ΔGFR = 120–160%) than the contralateral control (ΔGFR = 30–40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.

Role of renal dopamine D1 receptors in natriuresis induced by calcium channel blockers

1994 ◽  
Vol 267 (6) ◽  
pp. F965-F970
Author(s):  
G. M. Eisner ◽  
I. Yamaguchi ◽  
R. A. Felder ◽  
L. D. Asico ◽  
P. A. Jose
Keyword(s):  
Glomerular Filtration Rate ◽  
Renal Artery ◽  
Calcium Channel ◽  
Glomerular Filtration ◽  
Calcium Channel Blockers ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Channel Blockers ◽  
The Right

The direct tubular natriuretic effect of calcium channel blockers (CCBs) may be due to an interaction between CCBs and a renal tubular dopamine receptor. We therefore studied the effects of two chemically unrelated CCBs, diltiazem and isradipine, infused into the right renal artery of 5% saline-loaded anesthetized rats alone or in the presence of a D1 antagonist, SKF-83742. Isradipine (0.03 microgram.kg-1.min-1) or diltiazem (20 but not 10 micrograms.kg-1.min-1) alone produced an increase in urine flow and an approximate doubling of absolute and fractional sodium excretion, which was not seen in the left kidney or in the control animals (analysis of variance, Scheffe's test, P < 0.05). SKF-83742 alone given systemically or into the right renal artery did not affect these parameters but did block the actions of diltiazem or isradipine. There was no change in mean arterial pressure, renal blood flow, or glomerular filtration rate in any of the experiments. In additional studies, we found that a combined infusion of dopamine (0.1 microgram.kg-1.min-1) and diltiazem (10 micrograms.kg-1.min-1) (doses that by themselves did not alter renal function) produced a twofold or greater increase in urine flow and absolute and fractional sodium excretion; glomerular filtration rate was not significantly changed. Intrarenal arterial CCBs, without a change in renal hemodynamics, produce a natriuresis that is blocked by a D1 antagonist. Concomitant administration of diltiazem and dopamine (each in subeffective doses when used alone) produces a synergistic effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Inter-Relationship between Autoregulation of Glomerular Filtration Rate, Tubuloglomerular Feedback and Juxtaglomerular Renin Activity in Normotensive and Hypertensive Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 105s-107s
Author(s):  
J. Schnermann ◽  
D. W. Ploth ◽  
H. Dahlheim
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renin Angiotensin System ◽  
Feedback Regulation ◽  
Renal Perfusion ◽  
Tubuloglomerular Feedback ◽  
Hypertensive Rats ◽  
Arterial Blood ◽  
Proximal Tubular

1. Reduction of renal perfusion pressure from 133 mmHg to 117 mmHg in control rats did not induce a significant change of kidney glomerular filtration rate (GFR) or nephron GFR determined in distal tubules. In contrast, nephron GFR measured in proximal tubular segments (NGFR-P) fell significantly. 2. Qualitatively the same response of filtration rate to changes of arterial blood pressure was found in the chronically clipped kidneys of Goldblatt hypertensive rats after acute removal of the clip. 3. In contrast, autoregulation of kidney GFR, NGFR-D and NGFR-P was abolished in the contralateral kidneys of Goldblatt hypertensive rats. 4. Microperfusion studies showed that tubuloglomerular feedback regulation of NGFR was present in the renin-rich ischaemic kidneys of Goldblatt rats after removal of the constricting clip, but greatly attenuated in the renin-depleted contralateral kidneys. 5. These data indicate that tubuloglomerular feedback participates in establishing renal autoregulation, possibly by mediation of the renin-angiotensin system.

Age-related changes in the pressure diuresis and natriuresis response

1997 ◽  
Vol 273 (2) ◽  
pp. R578-R582 ◽  
Author(s):  
F. Vargas ◽  
M. C. Ortiz ◽  
L. A. Fortepiani ◽  
N. M. Atucha ◽  
J. Garcia-Estan
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Adult Rats ◽  
Water Excretion ◽  
Age Related ◽  
Old Adult ◽  
The Right

The renal-excretory responses to changes in renal perfusion pressure (RPP) were studied in anesthetized young (3 mo old), adult (12 mo old), and senescent (24 mo old) rats to evaluate whether the pressure diuresis and natriuresis mechanism is altered as a function of age. Experiments were performed in anesthetized animals in which nervous and systemic hormonal influences to the kidney were fixed. Mean arterial pressure was similar in all three groups: 97.6 +/- 2.6, 102.1 +/- 3.7, and 95.2 +/- 5.2 mmHg in young, adult, and senescent rats, respectively. The relationships between RPP and diuresis/natriuresis or fractional excretions of water and sodium were similar in young and adult rats. However, in senescent rats the pressure-diuretic and pressure-natriuretic responses were slightly shifted to the right, so that diuresis and natriuresis were significantly lower at higher levels of RPP. Glomerular filtration rate was well autoregulated, and there were no differences between young and adult rats at each level of RPP. However, a significantly lower glomerular filtration rate was observed in senescent rats. These results indicate an age-related decline in the pressure-dependent sodium and water excretion that appears to be due to a decrease in glomerular filtration and an increase in tubular sodium reabsorption.

STUDY OF RADIATION CHARACTERISTICS THE RENAL FUNCTION IN PATIENTS WITH TYPE 2 DIABETES

2014 ◽  
pp. 73-77
Author(s):  
Van Chuong Nguyen ◽  
Thi Kim Anh Nguyen
Keyword(s):  
Type 2 Diabetes ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Disease Duration ◽  
Left Kidney ◽  
Cross Sectional ◽  
The Right

Background: A Research glomerular filtration rate (GFR) of 61 patients with type 2 diabetes mellitus with renal scanning 99mTc-DTPA glomerular filtration rate at the hospital 175. Objective: (1) To study characteristics of imaging of renal function. (2) Understanding the relationship between GFR with blood sugar, HbA1c, blood pressure and albuminuria in patients with type 2 diabetes. Methods: Descriptive, prospective, cross-sectional study. Clinical examination, Clinical tests and 99mTc-DTPA GFR gamma - camera renography for patients. Result: GFR of the study group was 75,4 ± 22,3 ml/phut/1,73m2, the left kidney was 35,0 ± 13,0 is lower than the right kidney and 39,8 ± 11,9; p <0,01. There is no correlation between GFR with blood glucose and HbA1c, the risk of reduced GFR in hypertensive group associated is OR = 6,5 with p<0,01; albuminuria (+) is OR = 4,2 with p <0,01; and disease duration > 10 years is OR = 3,5 with p <0.01. Conclusion: GFR of the left kidneys is lower than the right kidney; correlation decreased GFR associated with hypertension, albuminuria and disease duration. Keywords: GFR, diabetes, albuminuria

Meclofenamate and urine concentration with and without exposure of the renal papilla

1981 ◽  
Vol 240 (5) ◽  
pp. F423-F429 ◽  
Author(s):  
R. J. Roman ◽  
C. Lechene
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Renal Papilla ◽  
Arterial Blood ◽  
Pelvic Urine

The recent finding that inhibitors of prostaglandin synthesis prevent the fall in urine concentration produced by papillary exposure challenges the hypothesis that contact between the pelvic urine and papilla is essential to the renal concentrating process. The present study examines the change in urine osmolality produced by exposure of the renal papilla in rats given meclofenamate. In control animals urine osmolality(Uosmol) decreased 57% after 2 h of exposure of the renal papilla. In rats given meclofenamate 4 mg/kg urine osmolality increased 16%, urine flow decreased 30%, and glomerular filtration rate was unchanged in the nonexposed kidney. Meclofenamate, however, did not alter the decrease in Uosmol seen in the kidney with the exposed papilla. Meclofenamate 10 mg/kg was also ineffective in preventing the fall in urine osmolality produced by papillary exposure, although this higher dose decreased glomerular filtration rate and arterial blood pressure. These results are consistent with the finding that pelvic urine urea is important to the urinary concentrating process and with the hypothesis that urine osmolality falls after papillary exposure because contact between pelvic urine and papilla is interrupted.

Increased tubuloglomerular feedback activity in Milan hypertensive rats

1986 ◽  
Vol 250 (6) ◽  
pp. F967-F974 ◽  
Author(s):  
U. Boberg ◽  
A. E. Persson
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Tubuloglomerular Feedback ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Single Nephron ◽  
Flow Pressure ◽  
Normotensive Strain

Studies of whole-kidney function and micropuncture measurements in superficial nephrons were performed to investigate the role of the tubuloglomerular feedback (TGF) in the excretion of salt and water in hydropenic and volume-expanded rats of the spontaneously hypertensive Milan strain (MHS). The rats were 3.5-5 and 5-7 wk old, and age-matched animals from the Milan normotensive strain (MNS) served as controls. There was no difference in mean arterial blood pressure (Pa) between the 3.5- to 5-wk-old prehypertensive MHS (MHSp) and MNS rats, but the glomerular filtration rate (GFR) was higher in MHSp than in MNS [1.35 vs. 0.80 ml X min-1 X g kidney wt (KW)-1, P less than 0.01]. The distal single-nephron glomerular filtration rate (SNGFR) was also higher in MHSp than in MNS (28.6 vs. 20.2 nl X min-1 X g KW-1, P less than 0.05). TGF was determined from both stop-flow pressure response and proximal and distal SNGFR. It was found that MHSp exhibited essentially no TGF response. During development of hypertension 5- to 7-wk-old MHS (MHSd) had a higher Pa than MNS (120 vs. 98 mmHg, P less than 0.01). Normally GFR and SNGFR increase with age, and such was the case with MNS (0.8 to 1.02 ml X min-1 X g KW-1 and 20.2 to 23.4 nl X min-1 X g KW-1), but in MHSd there was a decrease in both GFR and SNGFR with age (1.35 to 1.10 ml X min-1 X g KW-1 and 28.3 to 18.3 nl X min-1 X g KW-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal and hemodynamic effects of losartan in conscious dogs during controlled mechanical ventilation

1999 ◽  
Vol 276 (3) ◽  
pp. F425-F432 ◽  
Author(s):  
Martin O. Krebs ◽  
Thorsten Kröhn ◽  
Willehad Boemke ◽  
Rainer Mohnhaupt ◽  
Gabriele Kaczmarczyk
Keyword(s):  
Mechanical Ventilation ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Volume ◽  
Conscious Dogs ◽  
Positive End Expiratory Pressure ◽  
Arterial Blood ◽  
Controlled Mechanical Ventilation

In 12 conscious dogs, we investigated whether the angiotensin II-receptor antagonist losartan increases renal sodium excretion and urine volume during controlled mechanical ventilation (CMV) with positive end-expiratory pressure. In four experimental protocols, the dogs were extracellular volume (ECV) expanded (electrolyte solution, 0.5 ml ⋅ kg−1 ⋅ min−1iv) or not and received losartan (100 μg ⋅ kg−1 ⋅ min−1iv) or not. They breathed spontaneously during the 1st and 4th hour and received CMV with positive end-expiratory pressure (mean airway pressure 20 cmH2O) during the 2nd and 3rd hours. In the expansion group, dogs with losartan excreted ∼18% more sodium (69 ± 7 vs. 38 ± 5 μmol ⋅ min−1 ⋅ kg−1) and 15% more urine during the 2 h of CMV because of a higher glomerular filtration rate (5.3 ± 0.3 vs. 4.5 ± 0.2 ml ⋅ min−1 ⋅ kg−1) and the tubular effects of losartan. In the group without expansion, sodium excretion (2.0 ± 0.6 vs. 2.6 ± 1.0 μmol ⋅ min−1 ⋅ kg−1) and glomerular filtration rate (3.8 ± 0.3 vs. 3.8 ± 0.4 ml ⋅ min−1 ⋅ kg−1) did not change, and urine volume decreased similarly in both groups during CMV. Plasma vasopressin and aldosterone increased in both groups, and plasma renin activity increased from 4.9 ± 0.7 to 7.8 ± 1.3 ng ANG I ⋅ ml−1 ⋅ h−1during CMV in nonexpanded dogs without losartan. Mean arterial pressure decreased by 10 mmHg in nonexpanded dogs with losartan. In conclusion, losartan increases sodium excretion and urine volume during CMV if the ECV is expanded. If the ECV is not expanded, a decrease in mean arterial blood pressure and/or an increase in aldosterone and vasopressin during CMV attenuates the renal effects of losartan.

Renal actions of atrial natriuretic peptide on the postischemic kidney

1988 ◽  
Vol 66 (5) ◽  
pp. 601-607 ◽  
Author(s):  
Satoshi Akabane ◽  
Masahito Imanishi ◽  
Yohkazu Matsushima ◽  
Minoru Kawamura ◽  
Morio Kuramochi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Filtration Rate ◽  
Systemic Arterial Pressure

The objective of this study was to evaluate the renal actions of atrial natriuretic peptide (ANP) in the unilateral postischemic kidney of anesthetized dogs with a severe reduction in glomerular filtration rate. The dose of atrial natriuretic peptide (50 ng∙kg−1∙min−1) we gave did not alter the mean systemic arterial pressure, renal blood flow, and glomerular filtration rate in the normal kidney, as determined in foregoing studies. ANP was infused into the intrarenal artery continuously for 60 min after the release from 45 min of complete renal artery occlusion. In the vehicle-infused group, the glomerular filtration rate fell dramatically (6% of control), the renal blood flow decreased (60% of control), and the mean systemic arterial pressure tended to increase (136% of control). The urine flow rate and urinary excretion of sodium decreased significantly (25 and 25%, respectively) at 30 min after reflow in the postischemic period. Continuous renal artery infusion of ANP resulted in a marked increase in urine flow rate (246% of control) and the urinary excretion of sodium (286% of control). The administration of ANP led to an improvement in renal blood flow (99% of control) and glomerular filtration rate (40% of control), and attenuated the rise in mean systemic arterial pressure (109% of control), compared with findings in the vehicle-infused group. Plasma renin activity and prostaglandin E2 concentration in the renal venous blood were elevated after the release from complete renal artery occlusion in both groups. These results indicate that the vascular effects of ANP on the postischemic kidney were enhanced and that the peptide maintained the natriuretic effect.

Sign in / Sign up

Export Citation Format

Share Document