Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs

1989 ◽  
Vol 256 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
G. A. Riegger ◽  
D. Elsner ◽  
E. P. Kromer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Renal Blood Flow ◽  
Plasma Levels ◽  
Filtration Rate ◽  
Sympathetic Nerve Activity ◽  
Peripheral Vascular ◽  
Nerve Activity ◽  
Low Cardiac Output

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Distribution of Renal Blood Flow in Patients with Heart Disease

1972 ◽  
Vol 42 (5) ◽  
pp. 627-634
Author(s):  
D. C. Fluck ◽  
T. R. Evans ◽  
D. C. Siggers ◽  
J. Crawley ◽  
S. A. Srivongse
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Flow Distribution ◽  
Blood Flow Distribution ◽  
Component Group ◽  
The Mean

1. The renal blood flow distribution has been studied by the Xe washout method in nineteen patients undergoing routine left-sided cardiac catheterization. 2. It was found that there were two separate groups, one in which the washout curve could be analysed by curve stripping into four exponentials, and one in which only three could be detected. 3. The mean cardiac output was found to be lower in the three-component group, whereas the mean glomerular filtration rate did not differ significantly between the two groups. 4. In the four-component group but not in the three-component group, significant linear correlations were detected between cardiac output and glomerular filtration rate, and between glomerular filtration rate and intrarenal blood flow distribution. 5. One suggestion was that the three component distribution of renal blood flow was associated with increasing renal autoregulation and the maintenance of renal function in the presence of a low cardiac output. 6. A second suggestion was that the differences between the three- and four-component group were primarily due to the more intensive diuretic therapy given to the patients in the three-component group.

Septic shock induces distinct changes in sympathetic nerve activity to the heart and kidney in conscious sheep

2009 ◽  
Vol 297 (5) ◽  
pp. R1247-R1253 ◽  
Author(s):  
Rohit Ramchandra ◽  
Li Wan ◽  
Sally G. Hood ◽  
Robert Frithiof ◽  
Rinaldo Bellomo ◽  
...  
Keyword(s):  
Septic Shock ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Large Animal Model ◽  
Large Animal ◽  
Nerve Activity ◽  
Conscious Sheep

Sepsis and septic shock are the chief cause of death in intensive care units, with mortality rates between 30 and 70%. In a large animal model of septic shock, we have demonstrated hypotension, increased cardiac output, and tachycardia, together with renal vasodilatation and renal failure. The changes in cardiac sympathetic nerve activity (CSNA) that may contribute to the tachycardia have not been investigated, and the changes in renal SNA (RSNA) that may mediate the changes in renal blood flow and function are unclear. We therefore recorded CSNA and RSNA during septic shock in conscious sheep. Septic shock was induced by administration of Escherichia coli, which caused a delayed hypotension and an immediate, biphasic increase in heart rate (HR) associated with similar changes in CSNA. After E. coli, RSNA decreased for over 3 h, followed by a sustained increase (180%), whereas renal blood flow progressively increased and remained elevated. There was an initial diuresis, followed by oliguria and decreased creatinine clearance. There were differential changes in the range of the arterial baroreflex curves; it was depressed for HR, increased for CSNA, and unchanged for RSNA. Our findings, recording CSNA for the first time in septic shock, suggest that the increase in SNA to the heart is not driven solely by unloading of baroreceptors and that the increase has an important role to increase HR and cardiac output. There was little correlation between the changes in RSNA and renal blood flow, suggesting that the renal vasodilatation was mediated mainly by other mechanisms.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Renal Blood Flow, Glomerular Filtration Rate, and Renal Oxygenation in Early Clinical Septic Shock*

2018 ◽  
Vol 46 (6) ◽  
pp. e560-e566 ◽  
Author(s):  
Jenny Skytte Larsson ◽  
Vitus Krumbholz ◽  
Anders Enskog ◽  
Gudrun Bragadottir ◽  
Bengt Redfors ◽  
...  
Keyword(s):  
Septic Shock ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate

Use of a thermal pulse decay system to assess avian renal blood flow during reduced renal arterial perfusion pressure

1992 ◽  
Vol 262 (1) ◽  
pp. R90-R98 ◽  
Author(s):  
R. F. Wideman ◽  
R. P. Glahn ◽  
W. G. Bottje ◽  
K. R. Holmes
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Regional Differences ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Portal Flow ◽  
Arterial Perfusion ◽  
Restricted Group

Using a simplified avian kidney model, renal arterial perfusion pressure (RAPP) was reduced from 120 (control) to 70 mmHg (near the glomerular filtration rate autoregulatory limit) and then to 46 mmHg (below the glomerular filtration rate autoregulatory range) in kidneys with ambient or partially restricted renal portal flow. Renal blood flow (RBF) was measured with a thermal pulse decay (TPD) system, using TPD thermistor probes inserted at three locations to evaluate regional differences in RBF. The clearance (CPAH) and extraction of p-aminohippuric acid were used to calculate renal plasma flow (RPF). CPAH, RPF, and RBF values were consistently lower for kidneys with restricted portal flow than for kidneys with ambient portal flow. Reducing RAPP to 46 mmHg did not significantly reduce CPAH, RPF, or RBF in the ambient group but did significantly reduce CPAH and RPF (regressed on RAPP) in the restricted group. RBF was not significantly affected when RAPP was reduced in the restricted group, although significant regional differences in blood flow were recorded. Renal vascular resistance decreased significantly as RAPP was reduced to 46 mmHg in the ambient group, confirming the renal autoregulatory response. In separate validation studies, significant reductions in RBF were detected by the TPD system during acute obstructions of portal and/or arterial flow. Overall, the results support previous evidence that avian RBF remains constant over a wide range of RAPPs. Observations of nonuniform intrarenal distributions of portal blood flow suggest that the portal system maintains the constancy of RBF in regions with proportionately high portal-to-arterial flow ratios.

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