scholarly journals Association of Noise Annoyance with Measured Renal Hemodynamic Changes

2021 ◽  
pp. 1-8
Author(s):  
Dennis Kannenkeril ◽  
Susanne Jung ◽  
Christian Ott ◽  
Kristina Striepe ◽  
Julie Kolwelter ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Filtration Fraction ◽  
Noise Annoyance ◽  
Renal Hemodynamic ◽  
Renal Vascular

<b><i>Background:</i></b> Chronic mental stress is recognized as a modifiable risk factor for cardiovascular disease. The aim of this study was to demonstrate that noise annoyance-induced stress is associated with changes in renal hemodynamics. <b><i>Methods:</i></b> Renal hemodynamic parameters were measured using steady-state input clearance with infusion of para-aminohippuric acid and inulin in individuals with normal, high normal, and elevated blood pressure. All individuals ranked subjective annoyance due to noise in everyday life on a 7-grade Likert scale. The median of all rankings was used as a cutoff point to divide the group into noise-annoyed and non-noise-annoyed individuals. Different renal hemodynamic parameters were calculated based on the Gomez equation. <b><i>Results:</i></b> Noise-annoyed individuals (<i>n</i> = 58) showed lower renal plasma flow (599 ± 106 vs. 663 ± 124 mL/min, <i>p</i> = 0.009), lower renal blood flow (1,068 ± 203 vs. 1,172 ± 225 mL/min, <i>p</i> = 0.047), higher filtration fraction (22.7 ± 3.3 vs. 21.3 ± 3.0, <i>p</i> = 0.012), higher renal vascular resistance (88.9 ± 25.6 vs. 75.8 ± 22.9 mm Hg/[mL/min], <i>p</i> = 0.002), and higher resistance of afferent arteriole (2,439.5 ± 1,253.4 vs. 1,849.9 ± 1,242.0 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.001) compared to non-noise-annoyed individuals (<i>n</i> = 55). There was no difference in measured glomerular filtration rate (133 ± 11.8 vs. 138 ± 15 mL/min, <i>p</i> = 0.181), resistance of efferent arteriole (2,419.4 ± 472.2 vs. 2,245.8 ± 370.3 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.060), and intraglomerular pressure (64.0 ± 3.1 vs. 64.6 ± 3.5 mm Hg, <i>p</i> = 0.298) between the groups. After adjusting for age, renal plasma flow, renal blood flow, and renal vascular resistance remained significantly different between the groups, with a trend in increased afferent arteriolar resistance and filtration fraction. <b><i>Conclusion:</i></b> In this study, noise annoyance was associated with reduced renal perfusion attributed to increased renal vascular resistance predominantly at the afferent site. Long-term consequences of this renal hemodynamic pattern due to noise annoyance need to be investigated.

scholarly journals Enhanced Responses of Blood Pressure, Renal Function, and Aldosterone to Angiotensin I in the DD Genotype Are Blunted by Low Sodium Intake

2002 ◽  
Vol 13 (4) ◽  
pp. 1025-1033
Author(s):  
Frank G. H. van der Kleij ◽  
Paul E. de Jong ◽  
Rob H. Henning ◽  
Dick de Zeeuw ◽  
Gerjan Navis
Keyword(s):  
Renal Function ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Angiotensin I ◽  
Low Sodium ◽  
Renal Hemodynamic ◽  
Intake Level ◽  
Renal Vascular

ABSTRACT. Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, renal hemodynamic parameters, and renin-angiotensin system parameters were similar for all genotypes with either sodium intake level. With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes ± 95% confidence intervals), with mean MAP increases of 22 ± 2% (DD genotype), 13 ± 5% (ID genotype), and 12 ± 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 ± 19.7% (DD genotype), 73.0 ± 16.3% (ID genotype), and 63.2 ± 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 ± 189% (DD genotype), 343 ± 71% (ID genotype), and 254 ± 99% (II genotype) (P < 0.05). Also, the decrease in GFR was more pronounced for the DD genotype, with mean decreases of 17.9 ± 4.7% (DD genotype), 8.8 ± 3.4% (ID genotype), and 6.4 ± 5.9% (II genotype) (P < 0.05). The effective renal plasma flow, plasma AngII concentration, and plasma renin activity values were similar for the genotypes. In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. The responses to AngII were also similar for all genotypes, with either sodium intake level. In conclusion, the responses of MAP, renal hemodynamic parameters, and aldosterone concentrations to AngI are enhanced for the DD genotype with liberal but not low sodium intake. These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake.

Abstract 12882: Renal Hemodynamics in Chronic Heart Failure With Preserved and Reduced Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Susanne Jung ◽  
Agnes Bosch ◽  
Julie Kolwelter ◽  
Kristina Striepe ◽  
Dennis Kannenkeril ◽  
...  
Keyword(s):  
Heart Failure ◽  
Renal Function ◽  
Chronic Heart Failure ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Inverse Association ◽  
Hemodynamic Parameters ◽  
Renal Hemodynamic ◽  
Renal Vascular

Introduction: Chronic heart failure (CHF) and impaired renal function are two co-existing medical conditions and known to be associated with adverse outcome. The cardiorenal interaction has not yet been analyzed thoroughly. The aim of this study was to assess renal and intraglomerular hemodynamics by constant infusion input clearance technique in subjects with CHF compared to healthy controls. Methods: This was a cross-sectional observational study including 85 subjects. The group of subjects with CHF consisted of 27 individuals with HFpEF and 27 individuals with HFrEF, who were compared to 31 controls. All subjects underwent renal clearance examination to determine measured -not estimated- glomerular filtration rate (GFR), renal blood and plasma flow (RBF, RPF) and to calculate renal hemodynamic parameters such as filtration fraction (FF), renal vascular resistance (RVR), intraglomerular pressure (P glom ) and resistances of the afferent (R A ) and efferent arterioles (R E ). Results: GFR was lower in subjects with CHF (88.6±13.1ml/min/1.73m 2 ) compared to controls (108.6±17. ml/min/1.73m 2 ) after adjustment for age and BP (p adj =0.037). There were no significant differences regarding RPF, RBF, FF, RVR, P glom , R A as well as R E after adjustment for age and BP. Similarly, there were no significant differences regarding renal hemodynamic parameters between HFpEF and HFrEF subjects. Bivariate correlation analysis in the group of subjects with CHF revealed an inverse association between NT-proBNP and RPF (R=-0.421, p=0.002), RBF (R=-0.414, p=0.002) and a positive association with FF (R=0.324, p=0.019), RVR (R=0.346, p=0.012) and R E (R=0.318, p=0.022). Conclusions: The findings of this study indicate that in CHF renal function is slightly reduced even though renal perfusion is preserved. With progressive severity of CHF as indicated by increasing NT-proBNP, renal vascular resistance in particular at the postglomerular side increases. Our data are in accordance with neuroendocrine activation in CHF since vasoconstriction at the postglomerular site points towards angiotensin II as mediator. The association between NT-proBNP and renal hemodynamics documents a close cardiorenal interaction in CHF.

Abnormal Renal Haemodynamics and Renin Suppression in Hypertensive Patients

1970 ◽  
Vol 38 (1) ◽  
pp. 101-110 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
M. P. A. Schalekamp-Kuyken ◽  
W. H. Birkenhäger
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Hypertensive Disease ◽  
Filtration Fraction ◽  
Plasma Renin Concentration ◽  
Renal Vascular ◽  
Intravascular Pressure

1. Intra-arterial pressure, renal plasma flow and glomerular filtration rate were estimated in thirty-two patients with benign essential hypertension. In twenty cases plasma renin concentrations were also determined. Variability of blood pressure was estimated by automatic indirect pressure recording. 2. There was an even distribution between high and low values of renal vascular resistance and filtration fraction. Variability of blood pressure was inversely related to renal vascular resistance. 3. In five patients plasma renin concentration was found to be abnormally low both in the recumbent and in the 45° tilt position. 4. Plasma renin concentration was related to renal blood flow, renal vascular resistance, filtration fraction and variability of blood pressure. 5. The results suggest that in hypertension renin release is suppressed by an increase in intravascular pressure at the level of the juxtaglomerularcells. The extent of renin suppression seems to be related to the stage of hypertensive disease.

Evidence for endothelin-induced renal vasoconstriction independent of ETA receptor activation

1993 ◽  
Vol 264 (1) ◽  
pp. R222-R226 ◽  
Author(s):  
D. M. Pollock ◽  
T. J. Opgenorth
Keyword(s):  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Vascular Resistance ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Experiments were designed to examine the role of endothelin (ET) receptors, specifically ETA receptors, in mediating the renal vasoconstrictor effects of ET-1 in anesthetized Sprague-Dawley rats. Intravenous infusion of ET-1 at 25 pmol.kg-1 x min-1 for 60 min produced a significant increase in mean arterial pressure (20 +/- 7%) and decreases in renal plasma flow (-60 +/- 6%) and glomerular filtration rate (-47 +/- 6%). Renal vascular resistance was significantly increased from 17 +/- 1 mmHg.ml-1 x min.g kidney wt during control period to 54 +/- 11 mmHg.ml-1 x min.g kidney wt during the experimental period. A second group of rats was infused with both ET-1 and the specific ETA receptor antagonist BQ-123 (0.1 mg.kg-1 x min-1). ET-1-induced increases in mean arterial pressure were completely blocked by BQ-123 (the average change was -7 +/- 4%). However, the renal vasoconstrictor effects of ET-1 were not affected by the antagonist, since renal plasma flow and glomerular filtration rate were again significantly reduced (-54 +/- 4 and -56 +/- 6%, respectively). Once again, renal vascular resistance was significantly increased from 16 +/- 2 mmHg.ml-1 x min.g kidney wt during the control period to 33 +/- 5 mmHg.ml-1 x min.g kidney wt during the experimental period. In a third group, infusion of BQ-123 alone produced a significant decline in mean arterial pressure (-13 +/- 2%), with no significant changes in renal plasma flow or glomerular filtration rate, thus producing a significant decrease in renal vascular resistance (15 +/- 1 vs. 11 +/- 2 mmHg.ml-1 x min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of volume expansion on renal nerve activity, renal blood flow, and sodium and water excretion in conscious dogs

1985 ◽  
Vol 249 (5) ◽  
pp. F680-F687 ◽  
Author(s):  
H. Morita ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Renal Vascular Resistance ◽  
Conscious Dogs ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Renal Vascular

Effects of acute volume expansion with isotonic isoncotic 3% dextran in saline were examined on renal nerve activity (RNA), renal blood flow, vascular resistance, and sodium and water excretion in conscious dogs. In intact dogs, acute volume expansion increased mean arterial pressure 15 +/- 3 mmHg, left atrial pressure 5.5 +/- 0.6 mmHg, and decreased RNA 88 +/- 2%, whereas renal blood flow did not change and renal vascular resistance increased slightly. When renal perfusion pressure was maintained at control levels, volume expansion decreased RNA 87 +/- 2% and renal vascular resistance 15 +/- 4%. During the 80-min period after volume expansion, urine flow rate increased 0.66 +/- 0.13 ml/min and sodium excretion rose 3.89 +/- 0.54 mueq X min-1 X kg-1, whereas RNA remained depressed. Arterial baroreceptor denervation (ABD) did not diminish responses of RNA, renal blood flow, renal vascular resistance, or sodium and water excretion to volume expansion. After ABD plus bilateral cervical vagotomy, volume expansion did not decrease RNA, and diuretic and natriuretic responses were significantly attenuated (P less than 0.025). However, responses of renal blood flow to volume expansion were not altered significantly. In conscious dogs with renal denervation, responses of renal blood flow to volume expansion were not impaired, whereas diuretic and natriuretic responses were attenuated (P less than 0.025). Thus, in intact conscious dogs, vagally mediated reflex decreases in RNA induced by acute volume expansion exerted a significant effect on sodium and water excretion but little control of renal blood flow and renal vascular resistance.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Alterations in Cardiovascular and Renal Hemodynamic Function Following Hypophysectomy in the Dog

1957 ◽  
Vol 188 (3) ◽  
pp. 529-534 ◽  
Author(s):  
M. Jay Goodkind ◽  
James O. Davis ◽  
Wilmot C. Ball ◽  
Robert C. Bahn
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Renal Plasma Flow ◽  
Functional Change ◽  
Peripheral Vascular ◽  
Appreciable Change ◽  
Renal Hemodynamic ◽  
Hemodynamic Function ◽  
Renal Vascular ◽  
Oxygen Difference

In studies of unanesthetized dogs, hypophysectomy resulted in a decrease in cardiac output, oxygen consumption, and stroke volume. No appreciable change in arteriovenous oxygen difference, mean femoral arterial pressure, or heart rate was observed. Glomerular filtration rate, renal plasma flow and renal fraction of cardiac output were markedly reduced in the hypophysectomized animals. Renal vascular resistance increased two- to threefold in contrast to a 24% increase in total peripheral vascular resistance. Although a marked reduction in cardiovascular and renal hemodynamic function resulted following hypophysectomy, there was no correlation between the degree of functional change and either the amount of anterior pituitary tissue remaining or the degree of atrophy of the adrenal cortex.

Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F490-F496 ◽  
Author(s):  
J. A. Winston ◽  
R. Safirstein
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Single Nephron ◽  
Renal Vascular

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 +/- 0.06 vs. 1.17 +/- 0.06 ml X min-1 X g kidney wt-1 and 5.30 +/- 0.62 vs. 8.25 +/- 0.43 ml X min-1 X g kidney wt-1, respectively; P less than 0.001), as were superficial nephron GFR and stop-flow pressure (20.2 +/- 2.1 vs. 34.5 +/- 2.0 nl X min-1 X g kidney wt-1 and 29.0 +/- 1.9 vs. 39.8 +/- 1.3 mmHg, respectively; P less than 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 +/- 0.07 ml X min-1 X g kidney wt-1, single nephron filtration rate increased to 29.9 +/- 3.5 nl X min-1 X g kidney wt-1 (P less than 0.005), and renal plasma flow increased to 5.62 +/- 0.60 ml X min-1 X g kidney wt-1 (P less than 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.

scholarly journals Losartan does not decrease renal oxygenation and norepinephrine effects in rats after resuscitated hemorrhage

2018 ◽  
Vol 315 (2) ◽  
pp. F241-F246
Author(s):  
Sofia Jönsson ◽  
Jacqueline M. Melville ◽  
Mediha Becirovic-Agic ◽  
Michael Hultström
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Oxygen Tension ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Oxygen Consumption ◽  
Significant Difference ◽  
Renal Vascular

Renin-angiotensin-system blockers are thought to increase the risk of acute kidney injury after surgery and hemorrhage. We found that losartan does not cause renal cortical hypoxia after hemorrhage in rats because of decreased renal vascular resistance, but we did not evaluate resuscitation. We aimed to study losartan’s effect on renal cortical and medullary oxygenation, as well as norepinephrine’s vasopressor effect in a model of resuscitated hemorrhage. After 7 days of losartan (60 mg·kg−1·day−1) or control treatment, male Wistar rats were hemorrhaged 20% of their blood volume and resuscitated with Ringerʼs acetate. Mean arterial pressure, renal blood flow, and kidney tissue oxygenation were measured at baseline and after resuscitation. Finally, the effect of norepinephrine on mean arterial pressure and renal blood flow was investigated. As expected, losartan lowered mean arterial pressure but not renal blood flow. Losartan did not affect renal oxygen consumption and oxygen tension. Mean arterial pressure and renal blood flow were lower after resuscitated hemorrhage. A smaller increase of renal vascular resistance in the losartan group translated to a smaller decrease in cortical oxygen tension, but no significant difference was seen in medullary oxygen tension, either between groups or after hemorrhage. The effect of norepinephrine on mean arterial pressure and renal blood flow was similar in control- and losartan-treated rats. Losartan does not decrease renal oxygenation after resuscitated hemorrhage because of a smaller increase in renal vascular resistance. Further, losartan does not decrease the efficiency of norepinephrine as a vasopressor, indicating that blood pressure may be managed effectively during losartan treatment.

Sign in / Sign up

Export Citation Format

Share Document