Role of transmural pressure in local regulation of blood flow through kidney

1965 ◽  
Vol 208 (5) ◽  
pp. 825-831 ◽  
Author(s):  
F. J. Haddy ◽  
J. B. Scott

In the kidney of the anesthetized dog, the pressure in an occluded hilar lymphatic vessel was used as an index of tissue pressure. While elevation of renal vein pressure produced a large rise in lymphatic pressure, reduction of renal artery pressure had little effect. Similarly, while elevation of vein pressure at constant flow produced an almost equal rise in lymphatic pressure, large changes in blood flow and hence artery pressure had little effect, despite evidence of local regulation of resistance. Intra-arterial injection of vasoactive agents at constant flow, which produced large changes in renal artery pressure, had little effect on lymphatic pressure. Sudden transient increase in renal blood flow sometimes produced changes in perfusion pressure which could have resulted from active constriction subsequent to rise in transmural pressure. These findings provide little support for the tissue pressure theory of autoregulation but suggest that tissue pressure does participate in the vascular response to elevated vein pressure. The study also provides some evidence for a vascular myogenic response to change in renal vascular transmural pressure.

1959 ◽  
Vol 197 (2) ◽  
pp. 309-312 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Stacey B. Day ◽  
Curtis H. Carlson

Experiments were performed on isolated perfused dog kidneys to determine relationships between tissue pressure, vascular volume, ‘over-all’ and ‘intraorgan’ vascular resistances. Results indicate that autoregulation of renal blood flow is brought about by disproportionately large increases in extravascular pressure. Since extravascular and intravascular pressures are opposing forces there is progressively less vascular distention with increases in arterial pressure as the increments in extravascular pressures approach the increments in intravascular pressures. The effective propellent force of blood flow through the kidney is thought to be the difference between the renal artery pressure and extravascular pressure. Vascular resistances calculated on this basis showed no significant changes throughout the range of autoregulation in four of the six experiments. It is proposed that the extravascular pressure within Bowmans capsule may exceed the renal interstitial pressure, and when the effects of renal extravascular pressures within and without Bowman's capsule are taken into account in the calculation of intrarenal vascular resistance, the pressure-flow relations of the kidney will be similar to those of other vascular beds.


1979 ◽  
Vol 236 (3) ◽  
pp. H427-H433
Author(s):  
J. A. Oliver ◽  
R. R. Sciacca ◽  
P. J. Cannon

To determine whether the prostaglandin endoperoxides PGG2 and PGH2 have direct effects in the kidney, PGG2 and PGH2 were administered into the renal artery of anesthetized dogs and their effects were compared to those of PGE2. Like PGE2, PGG2 and PGH2 induced a dose-related renal vasodilation. A 50% increase in the renal blood flow was observed with 0.05 microgram/kg body wt of PGE2 and with four- and sixfold higher doses of PGH2 and PGG2, respectively. Infusion of all three compounds at doses inducing a 50% increase in the renal blood flow resulted in 1) increases in blood flow to all cortical areas, with the greatest increase occurring in the juxtamedullary area, 2) diuresis with no change in the glomerular filtration rate, and 3) natriuresis and kaliuresis. In vitro incubation of PGH2, a maneuver known to result in its conversion to other prostaglandins, had no influence on its renal effects. The data indicate that PGH2 and PGG2 are biologically active when infused into the renal artery of the anesthetized dog and suggest that the endoperoxides exert their effects after bioconversion to other prostaglandins.


1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.


1960 ◽  
Vol 199 (5) ◽  
pp. 923-926 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert D. Flaig ◽  
Curtis H. Carlson ◽  
Nguyen K. Thuong

The objective of the present study was to evaluate the relative roles of pre- and postglomerular vascular resistance changes in the autoregulation phenomenon. Experiments were performed on isolated dog kidneys perfused during ureteral occlusion. Ureteral pressures were assumed to approximate Bowman capsule extravascular pressure. As renal artery pressure was progressively elevated through the autoregulatory range, ureteral, intrarenal venous, and tissue pressures were measured; glomerular and peritubular capillary pressures were estimated, and pre- and postglomerular resistances were calculated. Results indicate that autoregulation of renal blood flow is brought about by the combined effects of increased tissue pressure and Bowman capsule extravascular pressure. Progressive increases in postglomerular resistance are responsible for the rise in ‘over-all’ renal resistance. Data provide evidence for the absence of the ‘myogenic reflex’ as a causal factor in autoregulation. Results are in agreement with previous reports of Winton and Gómez regarding glomerular pressure estimations and renal segmental resistance calculations.


1960 ◽  
Vol 198 (4) ◽  
pp. 891-894 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert D. Flaig ◽  
Ronald L. Logemann ◽  
Curtis H. Carlson

In experiments on the isolated perfused dog kidney, intrarenal venous pressure, tissue pressure and renal blood flow were measured while renal artery pressure was progressively increased over the autoregulatory range. Results indicate that tissue pressure is closely correlated with simultaneously measured intrarenal venous pressure. As the arterial pressure is increased, the coincident rise in interstitial pressure tends to obliterate intrarenal veins, which however are maintained patent by the upstream arterial pressure head. Intrarenal venous pressures corroborate tissue pressure measurements on the basis that the venous transmural pressure is found to be small regardless of the magnitude of the venous intraluminal pressure. Increases in ‘over-all’ vascular resistance (RA/F) occur in all kidneys, while increases in ‘intrarenal’ resistance (RA-RVint./F; RA-TP/F) are small or absent. Calculated intrarenal resistance is of primary importance in renal hemodynamics since it is derived from the measured pressure drop from renal artery to large intrarenal veins including essentially all of the kidney substance.


1996 ◽  
Vol 16 (6) ◽  
pp. 1255-1262 ◽  
Author(s):  
James M. Clark ◽  
Brett E. Skolnick ◽  
Robert Gelfand ◽  
Roger E. Farber ◽  
Maria Stierheim ◽  
...  

Cerebral blood flow (CBF) was measured by 133Xe clearance simultaneously with the velocity of blood flow through the left middle cerebral artery (MCA) over a wide range of arterial PCO2 in eight normal men. Average arterial PCO2, which was varied by giving 4% and 6% CO2 in O2 and by controlled hyperventilation on O2, ranged from 25.3 to 49.9 mm Hg. Corresponding average values of global CBF15 were 27.2 and 65.0 ml 100 g min−1, respectively, whereas MCA blood-flow velocity ranged from 42.8 to 94.2 cm/s. The relationship of CBF to MCA blood-flow velocity over the imposed range of arterial PCO2 was described analytically by a parabola with the equation: [Formula: see text] The observed data indicate that MCA blood-flow velocity is a useful index of CBF response to change in arterial PCO2 during O2 breathing at rest. With respect to baseline values measured while breathing 100% O2 spontaneously, percent changes in velocity were significantly smaller than corresponding percent changes in CBF at increased levels of arterial PCO2 and larger than CBF changes at the lower arterial PCO2. These observed relative changes are consistent with MCA vasodilation at the site of measurement during exposure to progressive hypercapnia and also during extreme hyperventilation hypocapnia.


1978 ◽  
Vol 234 (2) ◽  
pp. H219-H222 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody

A method is described for continuous measurement of renal blood flow in the anesthetized rat without dissection of the renal artery. Blood flow and arterial pressure were measured in an extracorporeal flow circuit between the carotid artery and an aortic pouch from which the left renal artery was the only outlet. Injection into the flow circuit allowed delivery of drugs directly into the arterial blood supply of the kidney. Electrical stimulation of undamaged periarterial renal kidney. Electrical stimulation of undamaged periarterial renal nerves was possible since the renal artery remained undisturbed. Extracorporeal autoperfusion of the rat kidney produced renal flow and resistance measurements that did not differ from those obtained with a flow probe placed directly on the renal artery. Renal nerve stimulation was found to cause renal vasoconstriction due to activation of alpha-adrenergic receptors by norepinephrine released from postganglionic sympathetic neurons. Renal vascular responses to a variety of intra-arterial vasoactive agents were also determined. The method described here allows the evaluation of renal vascular control in the variety of disease states for which suitable rat models have been developed.


1993 ◽  
Vol 16 (7) ◽  
pp. 505-509 ◽  
Author(s):  
H.D. Polaschegg ◽  
R. Wojke

Single-needle (SN) dialysis employs tidal blood flow at the point of vascular access. The simplest SN systems convert this tidal flow to a pulsatile flow in the dialyser. It has been assumed that constant flow through the dialyser is necessary for optimal efficiency. Therefore SN blood circuits are designed to smooth the pulsatile flow in the dialyser to a relatively constant flow. This increases the complexity and cost of the SN system. In order to test the hypothesis that pulsatile flow results in lower clearances than constant flow, we performed measurements of clearance in vitro using pulsatile blood flow at time-averaged rates of 50-250 ml/min and tidal volumes 200-100 ml/min. These were compared with clearances using constant blood flow at the same rates. At all flow rates and at tidal volumes up to 50 ml, the clearance measurements obtained during pulsatile flow were identical to those obtained during constant flow.


2020 ◽  
Vol 48 (4) ◽  
pp. 313-316
Author(s):  
Marwan Ma’ayeh ◽  
Vidhya Krishnan ◽  
Stephen E. Gee ◽  
Jessica Russo ◽  
Cynthia Shellhaas ◽  
...  

AbstractBackgroundPreeclampsia (PE) is a pregnancy-specific vascular endothelial disorder characterized by multi-organ system involvement. This includes the maternal kidneys, with changes such as continuous vasospasm of renal arteries and reduced renal blood flow. However, it is unclear whether similar renal vascular changes are seen in the fetus. This study sought to compare renal artery impedance in fetuses of women with and without PE.MethodsThis was a prospective Doppler assessment study of the fetal renal artery impedance in 48 singleton fetuses. The group with PE consisted of 24 appropriately grown fetuses in pregnancy complicated by both mild and severe PE and a control group of 24 uncomplicated pregnancies. Doppler studies included renal artery systolic/diastolic (S/D) ratio, pulsatility index (PI), resistance index (RI), and identification of end-diastolic blood flow.ResultsFetuses of mothers with PE were more likely to have a lower renal artery Doppler S/D ratio (7.85 [6.4–10.2] vs. 10.8 [7.75–22.5], P = 0.03) and lower RI (0.875 [0.842–0.898] vs. 0.905 [0.872–0.957], P = 0.03). However, there was no statistically significant difference in PI. There was also no difference in the incidence of absent end-diastolic flow.ConclusionThis study suggests that PE results in changes in blood flow to the renal arteries of the fetus. This may be associated with long-term adverse health effects later in adulthood.


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