Intrarenal venous and tissue pressure and autoregulation of blood flow in the perfused kidney

1960 ◽  
Vol 198 (4) ◽  
pp. 891-894 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Robert D. Flaig ◽  
Ronald L. Logemann ◽  
Curtis H. Carlson
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Venous Pressure ◽  
Pressure Head ◽  
Intraluminal Pressure ◽  
Tissue Pressure ◽  
Dog Kidney ◽  
Intrarenal Veins ◽  
Measured Pressure

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.

Tissue pressure as a causal factor in the autoregulation of blood flow in the isolated perfused kidney

1959 ◽  
Vol 197 (2) ◽  
pp. 309-312 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Stacey B. Day ◽  
Curtis H. Carlson
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Interstitial Pressure ◽  
Tissue Pressure ◽  
Vascular Volume ◽  
Flow Through ◽  
Vascular Beds ◽  
The Difference ◽  
Bowman's Capsule

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.

scholarly journals Effect of increased venous pressure on renal hemodynamics

1963 ◽  
Vol 204 (1) ◽  
pp. 119-123 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Charles M. Brake ◽  
P. F. Iampietro ◽  
Thomas E. Emerson
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Pressure Range ◽  
Venous Pressure ◽  
Renal Hemodynamics ◽  
Total Resistance ◽  
Tissue Pressure ◽  
Wide Range ◽  
The Face ◽  
Venous Segment

Evidence is conflicting regarding the effects of increased venous pressure on renal hemodynamics. Experiments to clarify its role were carried out on 28 intact, innervated or isolated, perfused dog kidneys. Findings indicate the absence of a "venous-arteriolar" reflex. Decreases in total resistance occur as venous pressure is increased through a wide range in both innervated and isolated perfused kidneys. Intrarenal venous and tissue pressures and blood flow are unaffected by large increases in venous pressure (21–75 mm Hg) although venous segment resistance declines markedly. Decreases in blood flow are seen when renal vein pressure approaches or exceeds intrarenal venous and tissue pressures. Results confirm previous investigations regarding the importance of tissue pressure and intrarenal venous pressure in renal hemodynamics, which appear to "buffer" the kidney against effects of elevated venous pressure through a variable but unusually large venous pressure range. The phenomenon of autoregulation may be extended to include a tendency for renal blood flow constancy in the face of wide swings in both renal artery and venous pressures.

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

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
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Transmural Pressure ◽  
Constant Flow ◽  
Tissue Pressure ◽  
Local Regulation ◽  
Artery Pressure ◽  
Flow Through ◽  
Response To Change ◽  
Renal Vascular

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.

Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Content ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Mesenteric Blood Flow ◽  
Initial Tendency ◽  
Elevated Heart Rate

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

Vascular resistance and arterial pressure in autoperfused dog hind limb

1962 ◽  
Vol 203 (4) ◽  
pp. 615-620 ◽  
Author(s):  
Kenneth M. Hanson ◽  
Paul C. Johnson
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Hind Limb ◽  
Venous Blood ◽  
Significant Rise ◽  
Tissue Pressure ◽  
Hind Limbs ◽  
Polyethylene Tubing

Arterial and venous vascular resistance was studied in 30 isolated dog hind limbs. The preparations were autoperfused from the contralateral femoral artery through a short piece of polyethylene tubing. By application of the isogravimetric technique of Pappenheimer and Soto-Rivera the capillary pressure was determined and the arterial and venous resistances were separately calculated. As arterial pressure in the limbs was progressively reduced from approximately 100 mm Hg down to 20 mm Hg the arterial resistance decreased in 25 of the 30 experiments. The reduction in resistance was particularly evident at arterial pressures below 50 mm Hg. The venous resistance remained relatively constant as the arterial pressure was reduced; a significant rise was seen in only three experiments. Arterial and venous blood oxygen and carbon dioxide contents were determined at various levels of blood flow in ten of the experiments. In general, as the blood flow was decreased, venous oxygen content decreased and carbon dioxide content increased, while oxygen consumption fell. It is concluded that autoregulation of blood flow in the hind limb may, in part, be due to tissue hypoxia. It cannot be explained by the tissue pressure hypothesis.

Comparative responses to endothelin 2 and sarafotoxin 6b in systemic vascular bed of cats

1990 ◽  
Vol 258 (5) ◽  
pp. H1550-H1558
Author(s):  
R. K. Minkes ◽  
P. J. Kadowitz
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Aortic Blood Flow ◽  
Vasodilator Activity ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
Dose Dependent ◽  
Higher Doses

Cardiovascular responses to endothelin 2 (ET-2) and sarafotoxin 6b (S6b) were investigated in the cat. ET-2 (0.1-1 nmol/kg iv) decreased or elicited biphasic changes in arterial pressure (AP), whereas S6b (0.1-1 nmol/kg iv) only decreased AP. Central venous pressure (CVP), cardiac output (CO), and pulmonary arterial pressure (PAP) were increased. ET-2 produced biphasic changes in systemic vascular resistance (SVR), whereas S6b decreased SVR at the two lower doses and caused a biphasic change at the 1 nmol/kg dose. The effects of ET-1 and ET-2 were similar, whereas the effects of S6b were similar to ET-3. ET-2 and S6b had small effects on right ventricular contractile force and caused transient increases in heart rate. Distal aortic blood flow was increased in response to all doses of both peptides, whereas increases in carotid blood flow were observed only in response to the higher doses of ET-2 and S6b. ET-2 produced dose-dependent decreases in superior mesenteric artery (SMA) blood flow, whereas decreases in SMA flow in response to S6b were observed only at the 1 nmol/kg dose. Renal blood flow was decreased significantly only at the higher doses of ET-2 and S6b. The present data show that ET-2 and S6b can produce both vasodilation and vasoconstriction in the systemic and regional vascular beds of the cat and demonstrate previously unrecognized vasodilator activity in response to S6b. It is concluded that ET-2 and S6b produce complex cardiovascular responses in the anesthetized cat.

Effect of an angiotensin II antagonist on autoregulation in the isolated dog kidney

1976 ◽  
Vol 230 (4) ◽  
pp. 1078-1083 ◽  
Author(s):  
GJ Kaloyanides ◽  
GF DiBona
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Flow Distribution ◽  
Renin Angiotensin System ◽  
Vascular Effects ◽  
Isolated Kidney ◽  
Angiotensin Ii Antagonist ◽  
Dog Kidney ◽  
Isolated Dog Kidney

The effect of the specific angiotensin II antagonist (AIIA), [1-sarcosine-8-alanine]angiotensin II, on autoregulation of glomerular filtration rate (GFR) and renal blood flow (RBF) in an isolated dog kidney was examined. Infusing the AIIA into the renal artery at 1.9 mug/min inhibited the renal vasoconstrictor action of angiotension II infused simultaneously at 1.15 mug/min. Under conditions of constant renal arterial pressure the AIIA had no significant effect on sodium excretion, GFR, RBF, cortical blood flow distribution (microsphere method), or renin secretion in non-renin-depleted kidneys. Similarly, no agonist properties were observed when the AIIA was infused into renin-depleted kidneys. This dose of the AIIA did not impair the capacity of the isolated kidney to regulate GFR or RBF when renal arterial pressure was increased from 100 to 150 mmHg. Efficiency of autoregulation of GFR and RBF was 77 and 82% of that predicted for perfect autoregulation. These values are not significantly different from those of the isolated kidney not infused with the antagonist. It is concluded that the angiotensin II antagonist, [1-sarcosine-8-alanine]angiotensin II, has no significant agonist properties, that it antagonizes the renal vascular effects of exogenously administered angiotensin II, but does not impair renal autoregulation. These data provide no support for the hypothesis that the renin-angiotensin system mediates the autoregulation of GFR and RBF.

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.

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