Hypercapnia potentiates renal vasoconstriction during hemorrhagic hypotension in awake rabbits

1984 ◽  
Vol 246 (5) ◽  
pp. H671-H674
Author(s):  
D. W. Busija
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Vasoconstriction ◽  
Hemorrhagic Hypotension ◽  
Severe Hypotension ◽  
Unanesthetized Animals ◽  
Renal Vascular

Although both hemorrhagic hypotension and hypercapnia increase renal vascular resistance (RVR) modestly, effects of interaction between these stimuli on RVR have not been examined systematically in unanesthetized animals. The purpose of this study was to test the hypothesis that renal vasoconstriction during hemorrhagic hypotension is affected by arterial CO2 tension (PCO2). Unanesthetized rabbits were placed into an environmental chamber, and six were exposed to normocapnia (PCO2 approximately 29 mmHg) and six to hypercapnia (PCO2 approximately 62 mmHg). Renal blood flow (RBF) was measured with 15-micrograms microspheres during 1) normotension [mean arterial pressure (MAP) 84-88 mmHg]; 2) moderate hemorrhagic hypotension (MAP 61-64 mmHg); and 3) severe hemorrhagic hypotension (MAP 44-50 mmHg). When MAP was normal, RBF was 437 +/- 59 and 345 +/- 59 ml X min-1 X 100 g-1 in the normocapnic and hypercapnic groups, respectively (NS; P greater than 0.05). In addition, RVR (MAP/RBF) was 0.22 +/- 0.04 in the normocapnic group and 0.32 +/- 0.08 mmHg X ml-1 X min X 100 g in the hypercapnic group (NS; P greater than 0.05). During moderate hypotension, RVR was 0.48 +/- 0.18 in the normocapnic group and 1.74 +/- 0.36 mmHg X ml-1 X min X 100 g in the hypercapnic group (P less than 0.05, comparison between groups). During severe hypotension, RVR was 0.46 +/- 0.14 and 3.13 +/- 1.13 mmHg X ml-1 X min X 100 g during normocapnia and hypercapnia, respectively (P less than 0.05, comparison between groups). Thus, in unanesthetized rabbits, although hypercapnia does not increase RVR compared with normocapnia when arterial pressure is normal, hypercapnia greatly potentiates renal vasoconstriction during hemorrhagic hypotension.

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.

scholarly journals Renal function and histology after acute hemorrhage in rats under dexmedetomidine action

2007 ◽  
Vol 22 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Marco Aurelio Marangoni ◽  
Alex Hausch ◽  
Pedro Thadeu Galvão Vianna ◽  
José Reinaldo Cerqueira Braz ◽  
Rosa Marlene Viero ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Filtration Fraction ◽  
Acute Hemorrhage ◽  
Renal Vascular

PURPOSE: About 50 % of indications for dialysis in acute renal failure are related to problems originated during the perioperative period. Intraoperative hemodynamic changes lead to renal vasoconstriction and hypoperfusion. Previous studies have not defined the dexmedetomidine renal role in hemorrhage situations. This study evaluated the effect of dexmedetomidine on renal function and histology after acute hemorrhage in rats. METHODS: Covered study with 20 Wistars rats, anesthetized with sodium pentobarbital, 50 mg. kg-1, intraperitoneal, randomized into 2 groups submitted to 30% volemia bleeding: DG - iv dexmedetomidine, 3 µg. kg-1 (10 min) and continuous infusion - 3 µg. kg-1. h-1; CG - pentobarbital. For renal clearance estimative, sodium p-aminohippurate and iothalamate were administered. Studied attributes: heart rate, mean arterial pressure, rectal temperature, hematocrit, iothalamate and p-aminohippurate clearance, filtration fraction, renal blood flow, renal vascular resistance, and histological evaluations of the kidneys. RESULTS: DG showed smaller values of heart rate, mean arterial pressure, and renal vascular resistance, but iothalamate clearance and filtration fraction values were higher. There was similarity in p-aminohippurate clearance and renal blood flow. Both groups had histological changes ischemia-like, but dexmedetomidine determined higher tubular dilatation scores. CONCLUSION: In rats, after acute hemorrhage, dexmedetomidine determined better renal function, but higher tubular dilation scores.

Prostaglandin control of renal circulation in the unanesthetized dog and baboon

1975 ◽  
Vol 229 (3) ◽  
pp. 826-830 ◽  
Author(s):  
JA Swain ◽  
GR Heyndrickx ◽  
DH Boettcher ◽  
SF Vatner
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Reactive Hyperemia ◽  
Renal Vascular Resistance ◽  
Conscious Dogs ◽  
Minor Role ◽  
Renal Circulation ◽  
Renal Vasoconstriction ◽  
Renal Vascular

Effects of indomethacin and meclofenamate, inhibitors of prostaglandin synthesis, were evaluated in the regulation of renal blood flow in conscious and anesthetized dogs and in tranquilized baboons, instrumented with arterial pressure catheters and renal blood flow probes. Indomethacin, 10 mg/kg, did not alter renal blood flow or resistance significantly in the conscious dog. In the anesthetized dog, however, indomethacin caused a reduction in renal blood flow (25 +/- 3% of control) and an elevation of renal vascular resistance (45 +/- 8% of control). Meclofenamate, 4 mg/kg, reduced renal flow (12 +/- 2%) and increased renal vascular resistance 15 +/- 4% in conscious dogs. In conscious dogs and tranquilized primates, indomethacin and meclofenamate reduced the reactive hyperemia in the renal bed after 15 s occlusion from a control of 36 +/- 5 ml to 6 +/- 2 ml, and after 45 s occlusion from a control of 98 +/- 9 ml to 17 +/- 5 ml. Methoxamine (10-50 mug/kg per min) and angiotensin II (0.03-0.12 mug/kg per min), infused in graded doses, induced significantly greater renal vasoconstriction in conscious dogs in the presence of indomethacin. Thus, in the conscious animal, prostaglandins appear to play only a minor role in the control of the renal circulation at rest, but are of greater importance in mediating the renal responses to reactive hyperemia and to vasoconstriction.

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

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.

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.

scholarly journals Effects of serelaxin on renal microcirculation in rats under control and high-angiotensin environments

2018 ◽  
Vol 314 (1) ◽  
pp. F70-F80 ◽  
Author(s):  
Weijian Shao ◽  
Carla B. Rosales ◽  
Camila Gonzalez ◽  
Minolfa C. Prieto ◽  
L. Gabriel Navar
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
No Synthase ◽  
Urine Flow ◽  
Ang Ii ◽  
Afferent Arterioles

Serelaxin is a novel recombinant human relaxin-2 that has been investigated for the treatment of acute heart failure. However, its effects on renal function, especially on the renal microcirculation, remain incompletely characterized. Our immunoexpression studies localized RXFP1 receptors on vascular smooth muscle cells and endothelial cells of afferent arterioles and on principal cells of collecting ducts. Clearance experiments were performed in male and female normotensive rats and Ang II-infused male rats. Serelaxin increased mean arterial pressure slightly and significantly increased renal blood flow, urine flow, and sodium excretion rate. Group analysis of all serelaxin infusion experiments showed significant increases in GFR. During infusion with subthreshold levels of Ang II, serelaxin did not alter mean arterial pressure, renal blood flow, GFR, urine flow, or sodium excretion rate. Heart rates were elevated during serelaxin infusion alone (37 ± 5%) and in Ang II-infused rats (14 ± 2%). In studies using the in vitro isolated juxtamedullary nephron preparation, superfusion with serelaxin alone (40 ng/ml) significantly dilated afferent arterioles (10.8 ± 1.2 vs. 13.5 ± 1.1 µm) and efferent arterioles (9.9 ± 0.9 vs. 11.9 ± 1.0 µm). During Ang II superfusion, serelaxin did not alter afferent or efferent arteriolar diameters. During NO synthase inhibition (l-NNA), afferent arterioles also did not show any vasodilation during serelaxin infusion. In conclusion, serelaxin increased overall renal blood flow, urine flow, GFR, and sodium excretion and dilated the afferent and efferent arterioles in control conditions, but these effects were attenuated or prevented in the presence of exogenous Ang II and NO synthase inhibitors.

scholarly journals ACUTE AND CHRONIC EFFECTS OF THE INSECTICIDE ENDRIN ON RENAL FUNCTION AND RENAL HEMODYNAMICS

1964 ◽  
Vol 42 (5) ◽  
pp. 599-608 ◽  
Author(s):  
D. A. Reins ◽  
D. D. Holmes ◽  
L. B. Hinshaw
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Renal Blood Flow ◽  
Systemic Hypertension ◽  
Adrenergic Agents ◽  
Renal Vasoconstriction ◽  
Chronic Effects ◽  
Renal Vascular ◽  
Acute And Chronic Effects ◽  
Marked Drop

Variable effects of chlorinated hydrocarbon insecticides on the kidney have been reported. The purpose of the present study was to determine the acute and chronic effects of the insecticide endrin on renal function and hemodynamics in dogs. Dogs were exposed to endrin acutely by intravenous infusion, and chronically by intramuscular injection. In acute experiments, dogs developed systemic hypertension and increased renal vascular resistance attributable to a sympatho-adrenal action. Acute effects of endrin were predominantly afferent arteriolar vasoconstriction as evidenced by decreases in renal blood flow, glomerular filtration rate, and urine flow. Phentolamine and phenoxybenzamine increased renal blood flow after endrin, providing evidence for humorally induced renal vasoconstriction due to adrenergic agents. Adrenalectomy partially offset the marked drop in renal blood flow after endrin although systemic hypertension and bradycardia were unaffected. Results from renal denervation experiments were variable. Changes in renal function in chronic studies were minimal and appeared to be due to secondary alterations in systemic hemodynamics. Results from this investigation provide no evidence for renal failure attributable to the direct effects of endrin.

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