Decreased nephron population resulting from increased ureteral pressure

1964 ◽  
Vol 207 (4) ◽  
pp. 835-839 ◽  
Author(s):  
Richard L. Malvin ◽  
Howard Kutchai ◽  
Fred Ostermann

The glucose Tm and GFR were determined for each kidney in anesthetized dogs. After three control periods a hydrostatic pressure was applied to one ureter. This resulted in a decrease in GFR over all ranges of ureteral pressures. Tm glucose remained essentially unchanged until the ureteral pressure was elevated to more than 30% of mean blood pressure. At ureteral pressures greater than this, Tm glucose was significantly depressed. The data were used in an attempt to calculate the range and the mean glomerular capillary pressure.

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Scott C Thomson

It is generally accepted that renal blood flow (RBF) autoregulation is mediated by myogenic and tubuloglomerular feedback responses acting on the pre-glomerular resistance. If this is so, then autoregulation of RBF and glomerular capillary pressure (PGC) should change in the same direction throughout an autoregulatory step response. We computed autoregulatory step responses from time series recordings of arterial blood pressure (BP) and RBF (Transonics) blood flow or tubular stop-flow pressure (micropuncture), which is a surrogate for PGC in Wistar-Froemter rats fed for one week on low or high salt diets (n=6-10 ). Autoregulatory step responses were generated from time series by an algorithm that treats BP as a leading indicator of RBF or PGC and uses the projection theorem to solve for the impulse response which is integrated to obtain the step response. Step responses shown in the figure represent the uncompensated changes in RBF and PGC (mean + SEM) following a 1 mmHg BP step. The data clearly reveal that the time courses of RBF and PGC differ such that changes in RBF cannot predict changes in PGC. This implies that the renal hemodynamic response to a blood pressure disturbance is not confined to the pre-glomerular resistance. Furthermore, the participation of post-glomerular resistance in the autoregulatory response is sensitive to dietary salt such that PGC is more sensitive to BP on low salt diet.


1996 ◽  
Vol 7 (12) ◽  
pp. 2590-2599 ◽  
Author(s):  
F B Gabbai ◽  
L De Nicola ◽  
O W Peterson ◽  
S Obagi ◽  
S C Thomson ◽  
...  

Concurrent renal disease appears to augment greatly the adverse effects of systemic hypertension on renal function and the development of glomerulosclerosis. This study examined the effects of systemic hypertension and treatment of hypertension in groups of normal non-nephritic rats and rats submitted to 16 wk of glomerulonephritis induced by the administration of anti-glomerular basement membrane antibody. Hypertension was produced by application of a clip to the right renal artery and blood pressure was treated with an angiotensin-converting enzyme (ACE) inhibitor, quinapril. Glomerulosclerosis of two types developed: a diffuse type that is characteristic of anti-glomerular basement membrane glomerulonephritis, and a focal segmental glomerulosclerosis that is characteristic of systemic hypertension. Glomerulonephritis significantly reduced the capacity of ACE inhibitors to decrease systolic blood pressure in awake animals. In addition, glomerulonephritis produced significant effects on plasma angiotensin II concentrations, whereby ACE inhibition no longer lowered plasma angiotensin II levels and in fact produced an increase. Glomerular capillary hydrostatic pressure and hydrostatic pressure gradient correlated with systolic blood pressure and with the incidence of focal glomerulosclerosis in non-nephritic rats. However, in glomerulonephritis, systolic blood pressure no longer correlated with glomerular capillary pressure, and glomerular capillary pressure no longer correlated with the development of glomerulosclerosis, although systolic blood pressure did correlate with the degree of focal segmental glomerulosclerosis. Concurrent glomerulonephritis strongly conditions the effects of superimposed hypertension by altering the relationship between systemic blood pressure and glomerular capillary hydrostatic pressure and by decreasing the response of hypertension to therapy.


1998 ◽  
Vol 275 (4) ◽  
pp. F576-F584 ◽  
Author(s):  
Fred Ivan Kvam ◽  
Jarle Ofstad ◽  
Bjarne M. Iversen

The relationship between systemic blood pressure and glomerular capillary pressure (Pgc) in spontaneously hypertensive rats (SHR) during treatment with antihypertensive drugs is still unclear. The effects of an angiotensin-converting enzyme inhibitor (enalapril), two calcium channel antagonists (nifedipine and verapamil), and an α1-receptor blocker (doxazosin) on renal blood flow (RBF) autoregulation, Pgc, and renal segmental resistances were therefore studied in SHR. Recordings of RBF autoregulation were done before and 30 min after intravenous infusion of the different drugs, and Pgcwas thereafter measured with the stop-flow technique. When the mean arterial pressure (MAP) was reduced to ∼120 mmHg by infusions of doxazosin or enalapril, the lower pressure limit of RBF autoregulation was reduced significantly. Nifedipine or verapamil abolished RBF autoregulation. Doxazosin did not change Pgc (43.6 ± 1.4 vs. 46.7 ± 1.5 mmHg in controls, P > 0.5), enalapril lowered (41.3 ± 0.8 mmHg, P < 0.01), and the calcium channel antagonists increased Pgc[53.7 ± 1.4 mmHg (nifedipine) and 54.8 ± 1.2 mmHg (verapamil), P < 0.01]. When MAP was reduced to ∼85 mmHg by drugs, Pgc was reduced to 43.3 ± 1.7 mmHg after nifedipine ( P > 0.2 vs. control), whereas Pgc after enalapril was 38.5 ± 0.5 mmHg ( P < 0.05 vs. control). Enalapril reduced Pgc mainly by reducing efferent resistance. During treatment with calcium channel antagonists, Pgc became strictly dependent on MAP. Monotherapy with nifedipine may increase Pgc and by this mechanism accelerate glomerulosclerosis if a strict blood pressure control is not obtained.


PEDIATRICS ◽  
1990 ◽  
Vol 86 (6) ◽  
pp. 1006-1007
Author(s):  
EDWARD H. PERRY ◽  
HENRIETTA S. BADA ◽  
JOHN D. DAY ◽  
SHELDON B. KORONES ◽  
KRISTOPHER L. ARHEART ◽  
...  

In Reply.— We appreciate the interest and comments of Drs Puccio and Soliani regarding our article "Blood Pressure Increase, Birth Weight Dependent Stability Boundary and Intraventricular Hemorrhage."1 In response, we address the following points: 1. Although mean blood pressure (BP) values greater than 100 mm Hg were observed in some of our patients, these were quite rare. The mean BP was found to be less than 60 mm Hg 99% of the time. Thus, unless one is recording BPs through long periods and sampling quite often, the brief spikes likely would not be observed.


1996 ◽  
Vol 19 (8) ◽  
pp. 487-492 ◽  
Author(s):  
F.G.R. Prior ◽  
V. Morecroft ◽  
T. Gourlay ◽  
K.M. Taylor

Pulse reverse osmosis (1) is a new theory of fluid balance and exchange which suggests that the mean blood pressure and osmotic gradient control fluid balance and that the pulse controls fluid exchange. In vitro testing has confirmed some of the physico chemical principles underlying the theory (2). The hypothesis suggests a relationship between mean capillary blood pressure and osmotic gradient. Imbalance in this relationship can be related to the development of hypertension, hypotension, oedema and shock. In an attempt to test this concept mean blood pressures and colloid osmotic pressures were measured and compared in a group of 50 healthy human volunteers. The results suggest a curvilinear correlation between the mean blood pressure and the COP.


1970 ◽  
Vol 5 (1) ◽  
pp. 25-28 ◽  
Author(s):  
M Begum ◽  
P Akter ◽  
MM Hossain ◽  
SMA Alim ◽  
UHS Khatun ◽  
...  

Haemodynamic stability is an integral and essential goal of any anaesthetic management plan. Laryngoscopy and intubation can cause striking changes in haemodynamics. Increase in blood pressure and heart rate occurs most commonly from reflex sympathetic and vagal discharge in response to laryngotracheal stimulation, which in turn leads to increased plasma norepinephrine concentration. This study was designed to compare efficacy of esmolol and lignocaine for attenuating haemodynamics response due to laryngoscopy and endotracheal intubation. The aim of this study was to compare the effects of Esmolol with that of Lignocaine to attenuate the detrimental rise in heart rate and blood pressure during laryngoscopy and tracheal intubation. One hundred and twenty adult patients randomized into group-L and group-E, were received lignocaine 1.5 mg/kg and Esmolol 1.5 mg/kg I.V. respectively. Heart rate and blood pressure in each minutes for the 10 minutes after intubation was recorded. Time span around intubation up to 4 minutes has been looked specifically to isolate the effect of the study drugs at the time of intubation. For statistical analysis Student's 't' test was used for comparing means of quantitative data and chi-square test was used for qualitative data. Difference was considered statistically significant if p<0.05. The mean heart rate, systolic, diastolic, and mean blood pressure, and rate-pressure product before starting anesthesia were similar in group-L (Lignocaine group) and in group-E (Esmolol group) (p>0.05). The mean values of heart rate, systolic, diastolic, and mean blood pressure, and rate-pressure product at 2, 3 and 4 minutes after intubation were significantly lower in group-E than group-L (p<0.05). In conclusion, esmolol 1.5 mg/kg is superior to lignocaine (1.5 mg/kg) for attenuation of haemodynamic response to laryngoscopy and endotracheal intubation. Key words: Haemodynamics; heart rate; intubation; esmolol; lignocaine DOI: 10.3329/fmcj.v5i1.6810Faridpur Med. Coll. J. 2010;5(1):25-28


1957 ◽  
Vol 189 (3) ◽  
pp. 605-608 ◽  
Author(s):  
W. F. Rosse ◽  
A. L. Bennett ◽  
A. R. McIntyre

Shock was induced in dogs by the release of tourniquets which had been applied to the hind legs for 5 hours. The serum potassium level was followed by spaced sampling. It was seen to rise slightly (from an average of 4.02 mEq/l. to an average of 4.66 mEq/l.) during the prerelease period. Five minutes after the release of the tourniquets, the level had risen to an average of 7.50 mEq/l. and thirty minutes after the release, it had risen to an average of 8.56 mEq/l. At the critical point in the progress of the syndrome (when the mean blood pressure was approximately 50 mm Hg) the average value was 8.46 mEq/l. Ouabain was administered and the level of serum potassium was seen to rise, attaining values as high as 14.67 mEq/l. in one case. The results and significance of these increased levels are briefly discussed as well as an animadversion upon the effects of ouabain on the mean blood pressure.


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