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.

Late Evaluation of Glomerular Filtration Rate, Proteinuria, and Urinary Acidification After Acute Tubular Necrosis

Renal Failure ◽  
1992 ◽  
Vol 14 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Regina Abdulkader ◽  
Patricio Malheiro ◽  
Elizabeth Daher ◽  
Helga Cruz ◽  
Luiz Yu ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Tubular Necrosis ◽  
Filtration Rate ◽  
Tubular Necrosis ◽  
Urinary Acidification

Peripheral Haemodynamics and Renal Function in Relation to the Menstrual Cycle

1996 ◽  
Vol 91 (2) ◽  
pp. 163-168 ◽  
Author(s):  
E. Van Beek ◽  
A. J. H. M. Houben ◽  
P. N. Van Es ◽  
C. Willekes ◽  
E. C. C. M. Korten ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Menstrual Cycle ◽  
Glomerular Filtration ◽  
Luteal Phase ◽  
Filtration Rate ◽  
Vascular Tone ◽  
Vascular Relaxation ◽  
Arterial Blood

1. The objective of this study was to investigate whether the luteal phase of the menstrual cycle differs from the follicular phase by the development of a state of general vascular relaxation. 2. Once in the follicular and once in the luteal phase of the menstrual cycle, we measured by non-invasive techniques: arterial blood pressure (by finger blood pressure measurements), vascular tone (by pulse-wave velocity and plethysmography), blood flow to skin (by laser-Doppler), blood flow to forearm (by plethysmography) and blood flow to kidneys (by para-aminohippurate clearance), and the glomerular filtration rate (by inulin clearance). The data points obtained in the luteal phase were compared with those in the follicular phase by non-parametric tests. 3. Arterial blood pressure, vascular tone and the blood flows to the forearm and kidneys were comparable in the two phases of the menstrual cycle. In contrast, the blood flow to the skin was consistently lower, and the glomerular filtration rate higher in the luteal phase of the menstrual cycle. 4. The results of the present study do not support our hypothesis of a general vascular relaxation in the luteal phase of the menstrual cycle. The lower skin flow in the luteal phase may be an adaptation needed to ensure the higher core temperature of 0.3–0.5°C in the luteal phase. The higher glomerular filtration rate was in most cases paralleled by a higher renal blood flow in the luteal phase. This suggests that the higher glomerular filtration rate is secondary to a selective vasorelaxation of the afferent renal arterioles.

The Effects of Vandellia Cordifolia on Renal Functions and Arterial Blood Pressure

1989 ◽  
Vol 17 (03n04) ◽  
pp. 203-210
Author(s):  
Huei-Yann Tsai ◽  
Ruey-Tean Chiang ◽  
Tzu-Wei Tan ◽  
Ho-Chan Chen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Renal Tubules ◽  
Diuretic Effect ◽  
Renal Functions ◽  
Arterial Blood

Vandellia cordifolia (COLSM) G, DON of Scrophulariaceae (V. cordifolia) is an annual wild herb indigenous to Taiwan. It can be found in plains, low altitudes, swampy places, and paddy fields. Taiwanese folk physicians use it in "nephritis, uremia, furnucle, carbuncle." The LD50 (95% confidence limit) of the crude exract of V. codifolia given by the oral route was more than 10 g/kg in rats. By the intraperitoneal route, it was 4.6 g/kg (4.35–4.93), The extraction rate was 16.6%. We studied its effects on renal functions and blood pressure and found that (1) it had diuretic effect on normal rats, (2) it decreased glomerular filtration rate and renal blood flow on normal kidneys in rabbits, (3) it had no effects on glomerular filtration rate and renal blood flow on glycerin-induced insufficient kidneys in rabbits, (4) it had diuretic effects on both normal and glycerin-induced insufficient kidneys in rabbits, (5) it could inhibit Na+ and K+ reabsorptionn on normal and glycerin-induced insufficient kidneys in rabbits, (6) it had hypertensive effect and this effect could be blocked by phenoxybenzamine. From the above facts, we conclude that V, cordifolia had diuretic effect and it may act on renal tubules to inhibit Na+ and K+ reabsorption.

Renal autoregulation of blood flow and filtration rate in the rabbit

1979 ◽  
Vol 237 (6) ◽  
pp. F479-F482 ◽  
Author(s):  
C. E. Ott ◽  
R. C. Vari
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Rabbit Kidney ◽  
Renal Perfusion Pressure

Electromagnetic flow techniques and inulin clearance were used to determine the autoregulatory capabilities of the rabbit kidney in vivo. Renal blood flow was measured in 13 animals over a renal perfusion pressure range of 40–110 mmHg. Normal renal blood flow averaged 3.2 +/- 0.3 ml.min-1.g kidney-1 and was efficiently autoregulated above a renal artery pressure of 75 mmHg. For every 10 mmHg renal pressure change above 75 mmHg renal blood flow changed only 0.96%. Renal perfusion pressure was reduced from 102 +/- 3 to 74 +/- 2 mmHg in six animals. Over this pressure range glomerular filtration rate was not significantly decreased and averaged 4.2 +/- 0.5 ml/min at high pressure compared to 4.0 +/- 0.5 ml/min at low perfusion pressure. Results show that the rabbit kidney autoregulates renal blood flow and glomerular filtration rate efficiently above 75 mmHg. This range of autoregulation compares well with the autoregulatory range of the dog. The results also show that in the autoregulatory range the rabbit and the rat appear to autoregulate with equal efficiency but that the rabbit kidney begins to autoregulate at a low perfusion pressure than the average of approximately 100 mmHg usually found in the rat.

Acute effect of changes in renal arterial pressure and sympathetic blockade on kidney function

1959 ◽  
Vol 197 (3) ◽  
pp. 595-600 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
William J. Gillespie
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Spinal Anesthesia ◽  
Renal Blood Flow ◽  
Kidney Function ◽  
Filtration Rate ◽  
Sympathetic Blockade ◽  
Urine Formation

The effect of varying the renal arterial pressure on kidney function has been studied before and after complete spinal anesthesia. It is concluded that an increase in renal arterial pressure between 60 and 300 mm Hg always results in an increase in renal blood flow, glomerular filtration rate and urine formation, and that filtration rate and urinary output are related to renal arterial pressure in a linear fashion at pressures above 120 mm Hg. Sympathetic blockade, accomplished by complete spinal anesthesia, resulted in a higher rate of urine formation and renal blood flow but not of glomerular filtration rate at each level of arterial pressure than before the spinal anesthesia was administered. Since the sympathetic blockade was not followed by an increase in glomerular filtration rate, it is concluded that the diuresis which followed this blockade resulted from a decrease in reabsorption of glomerular filtrate.

Autoregulation of renal blood flow and glomerular filtration rate in the pregnant rabbit

1987 ◽  
Vol 252 (1) ◽  
pp. R69-R72 ◽  
Author(s):  
L. L. Woods ◽  
H. L. Mizelle ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Pregnant Rabbit ◽  
In Pregnancy

Our purpose was to determine whether renal autoregulatory capability is retained in pregnancy despite the marked renal vasodilation that occurs at this time. Renal blood flow and glomerular filtration rate (GFR) were measured in anesthetized pregnant (22–27 days gestation) and nonpregnant rabbits during step reductions in renal perfusion pressure from control (100 +/- 3 mmHg) to 50 mmHg. Control renal blood flow and GFR were significantly higher in pregnant animals, averaging 65 +/- 5 and 13.1 +/- 1.1 ml/min, respectively, compared with 50 +/- 5 and 9.4 +/- 1.2 ml/min in nonpregnant rabbits. Filtration fraction was also significantly elevated in pregnant animals (0.33 +/- 0.02 vs. 0.27 +/- 0.01 in nonpregnant rabbits). During step reductions in renal perfusion pressure, renal blood flow was well autoregulated down to approximately 70 mmHg in both nonpregnant and pregnant animals, falling by only 9 +/- 4 and 12 +/- 5%, respectively. Likewise, GFR was also well autoregulated, falling by 10 +/- 2 and 8 +/- 3% in nonpregnant and pregnant animals, respectively, when perfusion pressure was reduced from 90 to 70 mmHg. These results suggest that renal autoregulation is preserved in pregnancy despite the fact that the renal circulation is already markedly vasodilated.

Chronic Sodium-Potassium-ATPase Inhibition with Ouabain Impairs Renal Haemodynamics and Pressure Natriuresis in the Rat

1996 ◽  
Vol 91 (4) ◽  
pp. 497-502 ◽  
Author(s):  
Toshiaki Kurashina ◽  
Kent A. Kirchner ◽  
Joey P. Granger ◽  
Ami R. Patel
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Control Group ◽  
Renal Perfusion Pressure

1. Chronic Na+,K+-ATPase inhibition with ouabain induces hypertension in the rat. To examine the role of the kidney in this process, the effect of changes in renal perfusion pressure on glomerular filtration rate, renal blood flow and urinary sodium excretion were determined in rats treated intraperitoneally with ouabain (27.8 μg day−1 kg−1 body weight) or vehicle for 6 weeks. 2. After ouabain administration, baseline mean arterial pressure was significantly higher (P < 0.05) in ouabain-treated rats (151 ± 2 mmHg; n = 9) than in control rats (116 ± 4 mmHg; n = 8). 3. At equivalent renal perfusion pressures, glomerular filtration rate was significantly lower (P < 0.05) in ouabain-treated rats compared with control rats. Glomerular filtration rate was 721 ± 73μl/min at 150 mmHg, and fell significantly to 322 ± 64 μl/min at 100 mmHg. In the control group, glomerular filtration rate was well autoregulated. The glomerular filtration rate autoregulatory index was calculated to determine the ability to maintain glomerular filtration rate during changes in renal perfusion pressure (0 reflects perfect autoregulation; >1 reflects the absence of autoregulation). This index was greater in the ouabain group than in the control group (1.54 ± 0.2 compared with 0.29 ± 0.2; P < 0.05). Renal blood flow showed a similar pattern. 4. Absolute urinary sodium excretion rate was less in ouabain-treated rats than in control rats at equivalent renal perfusion pressures. The slope of the relationship between absolute urinary sodium excretion rate and renal perfusion pressure was greater (P < 0.05) in the control group than in the ouabain group (309.1 ± 57.1 compared with 82.1 ± 14.8 μmol min−1 mmHg−1). 5. Thus, chronic inhibition of Na+,K+-ATPase induces less efficient autoregulation of glomerular filtration rate and renal blood flow as well as a rightward shift in the pressure natriuresis relationship, such that a 25–30 mmHg higher renal perfusion pressure is necessary to excrete any given sodium load. These abnormalities may contribute to the development and maintenance of hypertension in this model.

Effect of Hypoxia and Hypercapnic Acidosis on Renal Autoregulation in the Dog: Role of Renal Nerves

1983 ◽  
Vol 65 (5) ◽  
pp. 533-538 ◽  
Author(s):  
Robert J. Anderson ◽  
Richard G. Pluss ◽  
William T. Pluss ◽  
Jon Bell ◽  
Gary G. Zerbe
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Hypercapnic Acidosis ◽  
Renal Perfusion Pressure

1. Previous studies suggest that hypoxia and hypercapnic acidosis exert a renal nerve mediated adverse effect on renal haemodynamic function. We therefore examined the effect of hypoxia and hypercapnic acidosis on renal blood flow and glomerular filtration rate responses to lowering renal perfusion pressure from 125 to 75 mmHg in the anaesthetized dog. To study the role of renal nerves in these responses, paired innervated and denervated kidneys were studied in each animal. 2. Hypoxia (Po2 43 ± 3 mmHg) affected neither renal blood flow nor glomerular filtration rate responses to decreasing renal perfusion pressure. 3. Hypercapnic acidosis (Pco2 71 ±2 mmHg; pH 7.03 ± 0.01) significantly decreased both renal blood flow and glomerular filtration rate as renal perfusion pressure was lowered. This effect of hypercapnic acidosis could be abolished by renal denervation. 4. These findings suggest that hypercapnic acidosis results in renal nerve stimulation, which prevents the usual decrease in renal afferent arteriolar tone that occurs in response to lowering of renal perfusion pressure.

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.

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.

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