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At least 631 records · Page 35Linked to original sources

PubMed1980

A photometric device for measuring blood vessel diameter in the microcirculation.

A simple photometric device has been developed for measuring changes in blood vessel diameter in the microcirculation in conjunction with a monochrome television microscope. The device consists of a photocell mounted at the end of a small conical hood, which is attached to the screen of the television monitor. The photocell responds to changes in light emitted from the screen during dilatation or constriction of a blood vessel, and a continuous record of these changes is obtained by displaying the output from the photocell on a pen recorder. By using one or more photocells, mounted in separate hoods, the diameter of a number of vessels can be recorded simultaneously. The device has been used to record changes in the diameter of precapillary arterioles and postcapillary venules in the hamster cheek pouch microcirculation. The device has the advantage over image-shearing techniques of being automatic, and it is also considerably less expensive than a number of automated electro-optical or scanning systems.

Animals↗

PubMed1995

Effects of chemical stimulation of the rostral and caudal ventrolateral medulla on cerebral and renal microcirculation in rats.

We investigated the effects of neurons in the rostral and caudal ventrolateral medulla (RVL and CVL) on cerebral and renal microcirculation in rats. Rats were anesthetized with chloralose, paralyzed with tubocurarine, and artificially ventilated. Cerebral and renal blood flows (CBF and RBF) were measured simultaneously using laser-Doppler flowmetry. Chemical stimulation of the RVL neurons by microinjection of the excitatory amino acid L-glutamate increased arterial pressure (AP), whereas that of the CVL neurons decreased AP. Stimulation of the RVL neurons also elicited a stimulus-locked increase in CBF and a decrease in RBF. The percent change in CBF and RBF was dose-dependent as stimulus intensity was increased. Cerebral and renal vascular resistance (CVR and RVR) levels were calculated from changes in CBF or RBF and changes in mean AP. The percent reduction in CVR and percent elevation in RVR were also dose-dependent. Chemical stimulation of the CVL neurons elicited a stimulus-locked decrease in CBF and an increase in RBF. The percent reduction in CBF and percent elevation in CVR were dose-dependent. The percent reduction in RVR was also dose-dependent, while the percent elevation in RBF was not significant. Blood withdrawal reduced AP by a similar degree to CVL stimulation, but did not significantly decrease CBF. The results suggest that RVL and CVL neurons integrate cerebral and systemic microcirculation.

Animals↗

PubMed1996

Time course of endothelial function in epicardial conduit coronary arteries and in the microcirculation in the long-term follow-up after cardiac transplantation.

BACKGROUND: Endothelial dysfunction has been reported in epicardial conduit coronary arteries and in the microcirculation after cardiac transplantation. It has been assumed that endothelial dysfunction may precede hemodynamically relevant transplant vasculopathy. In this study the long-term course of endothelial function was investigated in conduit coronary arteries and in the microcirculation after cardiac transplantation. METHODS: Patients were stratified according to time after transplantation (group I, up to 2 years after transplantation; group II, 2 to 4 years after transplantation; group III, more than 4 years after transplantation). Changes of the diameter of proximal, mid and distal segments of the left anterior descending coronary artery and the circumflex branch of the left coronary artery were investigated after endothelium-dependent and endothelium-independent stimulation with acetylcholine (ACh, 50 and 100 micrograms i.c.) and nitroglycerin 0.3 mg i.c. Coronary flow changes were assessed endothelium-dependently (ACh 50 and 100 micrograms i.c.) and endothelium-independently (dipyridamole 0.56 mg/kg i.v.) utilizing an 8 F Judkins-style Doppler catheter. RESULTS: Application of 50 micrograms/100 micrograms ACh resulted in a reduction of coronary artery diameter in proximal, mid and distal vascular segments of the left anterior descending coronary artery and the circumflex branch of the left coronary artery. The vasoconstrictive effect did not differ significantly between groups I,II and III. Nitroglycerin 0.3 mg i.c. increased coronary artery diameters in groups I, II and III. ACh (50 micrograms/100 micrograms) increased coronary flow index by 217 +/- 70%/236 +/- 110% (P < 0.05 vs. baseline) in group I, 113 +/- 26%/77 +/- 22% (P < 0.05 vs. baseline) in group II and 108 +/- 26%/109 +/- 21% (P < 0.05 vs. baseline) in group III. Dipyridamole increased coronary flow index by 296 +/- 78% (P < 0.05 vs. baseline) in group I, by 63 +/- 16% (P < 0.05 vs. baseline and vs. group I) in group II and by 113 +/- 30% (P < 0.05 vs. baseline and vs. group I) in group III. CONCLUSION: A constant vasosonstrictor response to ACh was observed in epicardial coronary arteries after cardiac transplantation indicating endothelial dysfunction independent of the time course. Endothelial dysfunction in these vessels may not be an early indicator of hemodynamically relevant transplant vasculopathy. Endothelium-dependent and endothelium-independent flow reserves decreased 2 years after transplantation and remained constant thereafter.

Acetylcholine↗

PubMed1983

The influence of a heat pulse on the thermally induced damage to tumour microcirculation.

The effect of an initial short period of higher-temperature heat application on the stoppage of the microcirculation in the experimental rhabdomyosarcoma BA1112 in 'sandwich' chambers was investigated. The treatment consisted of an initial heat pulse of 45 degrees C for 10 min which was followed by a continuous exposure at 42.5 degrees C for 3 hr. Using the 't1/2 per degrees C' rule, the time equivalent of the heat pulse was 94 min. Taking this contribution into account, the derived 50% stoppage time of 151 min is essentially the same as the 152 min observed for 42.5 degrees C only treatments. The data therefore indicate that the effect of a heat pulse in the treatment can be accounted for by the customary correction procedure of one time exposure doubling per degrees C. However, it appeared that the microcirculation in the surrounding tumour bed was impaired more than was expected by this treatment.

Animals↗

PubMed1987

Experimental hyperthermic treatment of a human colon carcinoma xenograft. The thermal sensitivity of the tumour microcirculation.

The effect of hyperthermia on the microcirculation of a human colon tumour growing in a 'sandwich' observation chamber in immune-suppressed rats was investigated. Evaluation of the effect was based on microscopic observation, measurement of the relative flow rate of the blood in the capillaries of the tumour and photographic recording. The results indicated that moderate hyperthermia (3 h at 42.5 degrees C) has a destructive effect on the microcirculation of the tumour, followed the next day by severe necrosis. These results indicate that this human colon carcinoma xenograft has--for the endpoints that were investigated--a heat sensitivity that is comparable with rodent tumours.

Animals↗

PubMed1989

Differences in the response of the microcirculation to hyperthermia in five different tumours.

The response of the microcirculation in five different tumours, growing in 'sandwich' observation chambers in the back of the rat, to hyperthermia was investigated. The tumours investigated encompassed three human xenografted tumours, of which two were carcinomata of the colon and one of the lung, and two isologous rat tumours, the Rhabdomyosarcoma BA1112 and a rat mammary carcinoma. It was concluded (1) that the various tumours required significantly different exposure times for inducing 50% stoppage of the tumour microcirculation (ST50). This seems to indicate that differences in the characteristics of the tumour cells are more important for causing microcirculatory stoppage than is the sensitivity of the cells of the blood vessels. (2) An increase in surface (i.e. volume) was observed in all four tumours examined for this phenomenon. The rate of increase (usually 1-2% per hour at 42.5 degrees C) was, however, significantly different between the various tumours. This rate was higher exposure temperatures (43 and 43.5 degrees C), but this was only investigated for the Rhabdomyosarcoma BA1112. Extensive statistical analysis of this phenomenon of volume increase could not demonstrate a correlation with any of the circulation parameters. (3) The relative velocity of the erythrocytes in selected capillaries in the tumours decreases as a result of the hyperthermic treatment, and is probably related to the tumour-specific ST50. (4) A human colon carcinoma xenograft, one of the tumours investigated, showed strong fluctuations in the parameter 'erythrocyte velocity'. The appearance of such fluctuations did not seem to influence the heat-induced stoppage of the circulation. Probably the phenomenon of fluctuations in the velocities of the erythrocytes in the tumour capillaries is a tumour-specific phenomenon.

Adenocarcinoma↗

PubMed1984

Laser doppler flowmetry. A new non-invasive measurement of microcirculation in intensive care?

Laser doppler flowmetry (LDF) is a new non-invasive technique by which microcirculation changes in tissue can be studied. In recent papers, this technique has been used to measure microflow in standardized fluid models, in animals and in human clinical situations. LDF utilizes the doppler shift, i.e. the frequency (wave length) change that light as well as all waves undergo being reflected by moving objects such as, e.g. red blood cells. A beam of low power laser light (2 mW He-Ne at 632.8 nm) is led by an optical fibre to a measuring head. From here it enters the tissue to which it is applied by a hemisphere with a 1 mm radius. Blood cells traversing this volume are struck by the light and reflect it, whereby the light undergoes a doppler shift. The surrounding tissue also reflects the light, but in an unshifted manner. Thus the volume of illumination is a mixture of an unshifted and a doppler shifted component, the magnitude and frequency of the latter being related to the number of moving cells and their velocity. The measured microflow is proportional to an arbitrary scale (0 to 10). Our own experience with some applications in human clinical situations is described: Normal skin in a control group. Normal skin and burned area in burned patients. Patient in hypothermia with general anesthesia. Patient in shock. LDF seems to be an interesting new non-invasive technique, supplying a good definition of the skin microflow. In the future, this technique could be one of the non-invasive techniques used for intensive care, defining the microcirculation state of a patient.

Burns↗

PubMed1992

The acute effect of cigarette smoking on the microcirculation of a replanted digit.

Thirty-one patients who had undergone digital replantation or revascularization volunteered to participate in a study of the acute effect of smoking on the microcirculation of the skin of replanted fingers. Fourteen were smokers and 17 were nonsmokers at the time of the study. Blood flow was assessed by means of the laser Doppler flowmeter under standard conditions. Each smoker inhaled 2 cigarettes. During smoking of the first and second cigarettes a mean decrease in laser Doppler flow of 8% and 19%, respectively, was found, whereas the nonsmokers showed a slight increase of 4% and 4%, respectively. Ten minutes after the last cigarette almost no recovery could be detected. The negative effect of smoking on the microcirculation in replanted digits proved to be more pronounced in the patients operated on more recently. This experiment confirms that smoking after replantation surgery should be prohibited to guarantee optimal circulation.

Adult↗

PubMed1993

Leukocyte-depleting effect of hypothermia on muscle flap microcirculation following ischemia-reperfusion injury.

The aim of this study was to determine the effect of leukocyte-endothelial interaction and capillary perfusion on the microcirculation of muscle flaps submitted to ischemia in normothermic and hypothermic conditions. The cremaster muscle flap model was employed. Sixty rats were studied in six groups: normothermic and hypothermic control groups and groups that underwent reperfusion after 4 and 6 hours of ischemia in both normothermic and hypothermic conditions. In each group the following measurements were made: main vessel diameters, red blood cell velocities, the number of perfused capillaries, and the number of leukocytes rolling and sticking in the postcapillary venules. Hypothermia decreased the flow rate significantly and eliminated leukocytes from the microcirculation. Six hours of ischemia under normothermic conditions proved to be lethal for these muscle flaps, whereas hypothermia preserved flap viability.

Animals↗

PubMed1991

Changes in cutaneous microcirculation, hemorrheology and platelet aggregation function in dermatomyositis.

Marked disturbance of microcirculation was observed in 85 cases of dermatomyositis: decrease in number and irregular pattern of the capillaries, many being tortuous and dilated and having a slow and granular blood stream, as well as an increase of vascular permeability. The changes were more marked in cases with visceral disorders, or in active disease; however, there was no correlation between these changes and the duration of illness. Blood hyperviscosity was found in an hemorrheological study. The cause is considered to be due to high plasma viscosity, high fibrinogen levels, and increase of aggregation of erythrocytes and platelets. Modulation of microcirculation is advisable in the treatment of dermatomyositis.

Adolescent↗

PubMed1992

Real-time measurement of microcirculation of skin by reflectance spectrophotometry.

A reflectance spectrophotometric measurement was developed to analyze the microcirculation of the skin in real time. The relative absorption (RA) spectra were obtained from skin tissue 10 times per second using a spectro-multi-channel-photodetector system. In this system, white light was projected onto the skin of the back of the anesthetized rat and the spectrum of the reflected light between 450 and 643 nm was analyzed. Two absorption peaks at wavelengths of about 540 and 577 nm were observed, corresponding to the absorption peaks in the oxyhemoglobin (HbO2) spectrum. Either phlebotomy or the i.v. injection of norepinephrine (NE) reduced the RA spectrum. Peaks of the reduction in spectrum [(RA spectrum before the treatment) - (RA spectrum after the treatment)] were observed at about 540 and 577 nm. Injection of NE (0.75-48 ng/100 g B.W., i.v.) reduced the RA value at 577 nm dose-dependently, suggesting a decrease in the skin blood flow due to vasoconstriction. In addition, the content of HbO2 and capillary permeation were measured at the same time after the i.v. injection of Evans blue (EB) dye. As indices of HbO2 content and capillary permeation, RA changes at 540 and 610 nm (the latter is an absorption peak in the EB spectrum) were measured in real time, respectively. Both RA values increased dose-dependently after the intradermal injection of histamine (0.3-100 micrograms/site), suggesting the presence of vasodilation and an increase in permeability. The time at which the RA value for HbO2 reached a maximum was shorter than that for EB. These observations suggest that the method described here can detect changes in the HbO2 content and permeation of skin microcirculation at the same time, and in real time.

Animals↗

PubMed2004

Microvascular endothelial cell activation is present in the umbilical placental microcirculation in fetal placental vascular disease.

OBJECTIVE: Fetal growth restriction is associated with an abnormal umbilical artery Doppler study. A vascular disease is present in the fetal umbilical placental microcirculation. We hypothesized that the local production of factors that are injurious to microvessel endothelium is responsible for this vascular disease and that endothelial cell activation is a feature of this. Because the expression of the cell adhesion molecules is associated with endothelial cell activation, we isolated endothelial cells from the microvessels of the umbilical placenta and examined them for evidence of gene expression of cell adhesion molecules. STUDY DESIGN: Endothelial cells from the microcirculation of human placenta were isolated and purified with collagenase digestion and extraction with superparamagnetic beads that were coated with monoclonal antibody against CD31. Microvessel endothelial cells were isolated from the placentae of 13 women with a normal pregnancy and delivery at term and 10 placentas with umbilical placental vascular disease that was defined by abnormal umbilical artery Doppler study. Total RNA was extracted from isolated endothelial cells. The messenger RNA expressions of cell adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and platelet endothelial cell adhesion molecule-1) were assessed by semiquantitative reverse transcription-polymerase chain reaction. RESULTS: Microvessel endothelial cells from the fetal placentae of pregnancies that were complicated by umbilical placental vascular disease showed an enhanced expression of intercellular adhesion molecule-1 messenger RNA (2.12+/-0.45 vs 0.92+/-0.25) and platelet endothelial cell adhesion molecule-1 messenger RNA (4.29+/-0.87 vs 2.41+/-0.42) in comparison to normal pregnancies. There was no significant difference in expression of vascular cell adhesion molecule-1 messenger RNA (1.55+/-0.37 vs 1.68+/-0.38). CONCLUSION: We have shown that vascular disease in the fetal umbilical placental circulation is associated with an increase in the expression of intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 by microvessel endothelial cells. We postulate that locally released factors cause injury and activation to microvessel endothelial cells. In this regard, the process in the fetus is similar to that of atherothrombotic vascular disease of later life.

Adult↗

PubMed2005

The effect of hypertonic saline resuscitation on responses to severe hemorrhagic shock by the skeletal muscle, intestinal, and renal microcirculation systems: seeing is believing.

BACKGROUND: Decompensated hemorrhagic shock is often refractory to resuscitation, and we show here that it is associated with loss of vascular tone in skeletal muscle precapillary arterioles. We tested the hypothesis that microvascular derangements in the skeletal muscle, intestinal, and renal microcirculation systems would be reversed by initial hypertonic saline-dextran infusion. METHODS: Male Sprague-Dawley rats underwent precollicular brain stem transection without anesthesia for study. Parameters measured by in vivo videomicroscopy included cardiac output, mean arterial pressure, and microvascular responses in the skeletal muscle, ileum, and renal (i.e., the hydronephrotic kidney) microcirculation systems. Hemorrhaged was induced to a mean arterial pressure of 50 mmHg until decompensation occurred. The rats were then initially resuscitated with (1) 4 mL/kg 7.5% NaCl in 6% dextran 70, (2) 33 mL/kg .9% NaCl in 6% dextran 70, or (3) 33 mL/kg .9% NaCl. Twenty minutes later they received shed blood plus 33 mL/kg .9% NaCl to maintain mean arterial pressure at baseline levels. RESULTS: Decompensated hemorrhagic shock decreased cardiac output to between 24% and 35% of baseline values and profoundly decreased microvascular blood flow to between 10% and 19% of baseline. At the completion of resuscitation cardiac output increased to greater than baseline in all groups. Microvascular blood flow increased toward baseline transiently but then progressively deteriorated to between 36% and 69% of baseline in the 3 tissues. There was no significant difference between the three resuscitative fluids. CONCLUSIONS: Despite return of cardiac output to greater than baseline levels, muscle, intestinal, and renal microvascular blood flows remained significantly depressed. Hypertonic saline and/or dextran did not improve these deficits.

Analysis of Variance↗

PubMed2005

Palmar microcirculation after harvesting of the radial artery in coronary revascularization.

PURPOSE: To evaluate real-time parameters of palmar microcirculation before and after harvesting of the radial artery in coronary revascularization using a laser Doppler flowmetry and remission spectroscopy system (O2C). DESCRIPTION: Fifteen patients (11 males, 54 +/- 4 years, mean New York Heart Association [NYHA] class of 2.3 +/- 0.3) were prospectively scheduled with control measurements of the fingertips of D1, D3, and D5 at base line, after suprasystolic, and after selective radial or ulnar compression for tissue oxygen saturation (SO2), postcapillary venous recombinant hemoglobin (rHb) concentration, superficial (2 mm) blood flow, and deep (8 mm) blood flow. EVALUATION: Preoperatively during suprasystolic compression SO2 decreased significantly for the fingertips of D1, D3, and D5 by -58%, -74%, and -63%, respectively (p < 0.05). Radial compression reduced SO2 for all fingertips (-12%, -14%, and -16%), as did ulnar compression (-24%, -18%, and -10%). rHb did not change significantly for either compression type. Superficial and deep blood flow decreased significantly after suprasystolic and only slightly after radial and ulnar compression at either side. No side differences were noted. After radial artery harvesting, microcirculatory parameters did not change considerably versus preoperatively. CONCLUSIONS: Radial artery harvesting does not remarkably change microcirculatory parameters of the hand. The O2C system is a safe and quantitative method to assess both preoperatively and postoperatively the palmar microcirculation and therefore adds further functional clinical information.

Coronary Artery Bypass↗

PubMed2004

Deleterious effects of oxygen during extracorporeal circulation for the microcirculation in vivo.

OBJECTIVE: Clinical complications arising from extracorporeal circulation (ECC) have been linked to disturbances in the microcirculation. Hyperoxia, a mainstay of supportive treatment, is clinically used for a variety of pathological states. In previous in vivo animal experiments we found increased leukocyte/endothelial (L/E) cell interaction following ECC due to oxygen derived free radicals. This study was carried out to investigate the link between arterial pO2 during ECC and the potential damage to the microcirculation, supposedly caused by oxygen derived radicals. METHODS: Intravital fluorescence microscopy was used on the dorsal skinfold chamber preparation in syrian golden hamsters. ECC was introduced via a micro-rollerpump (0.7 ml/min) and a 60 cm silicon tube (1 mm inner diameter) shunted between the carotid artery and the jugular vein after application of 300 IE Heparin/kg/bw. Experiments were performed in chronically instrumented, awake animals (age: 10-14 weeks, weight: 65-75 g). Control inspired room air, experimental group 1 inspired 100% oxygen, group 2 received 100% oxygen and 2000 IE of Heparin i.v. (n=7/group), that releases endothelial bound superoxide dismutase, a natural scavenger of oxygen derived free radicals in the hamster. RESULTS: Normobaric inhalation of 100% oxygen increased arterial pO2 from 64+/-8.1 mmHg to 512+/-124 mmHg (P<0.05 vs. baseline). ECC under 100% oxygen reduced functional capillary density (FCD) to 70% of baseline values 8 h after ECC (P<0.05). Adherent leukocytes in postcapillary venules and arterioles increased significantly (P<0.05). 2000 IE Heparin prevented the reduction in FCD and decreased the number of adherent leukocytes. CONCLUSIONS: Reduction in FCD, increased leukocyte adherence to the microvascular endothelium of postcapillary venules and arterioles under hyperoxia compared to ECC under room air conditions, demonstrates harmful effects of oxygen during ECC in vivo. A high dose of Heparin enhances functional capillary density, thus attenuating the microvascular dysfunction/damage in the period after ECC.

Animals↗

PubMed2005

Protective effect of polyethylene glycol-superoxide dismutase on leukocyte dynamics in rat retinal microcirculation under lipid hydroperoxide-induced oxidative stress.

The levels of lipid hydroperoxide (LHPs) in vitreous are elevated in a variety of retinal disorders. Recently, we have shown that increased levels of LHPs in the vitreous enhanced leukocyte-endothelium interaction in the retina, which should contribute to the initial disturbance of the retinal microcirculation. Based upon the previous work, the purpose of the present study was to investigate the effect of polyethylene glycol-superoxide dismutase (PEG-SOD), one of the important enzyme antioxidants, on leukocyte-endothelial interaction in the retinal microcirculation under LHP-induced oxidative stress. Male Brown-Norway rats weighing approximately 250 g were used. LHP(18:2) was made from linoleic acid (LA) with lipoxygenase and 10 microg of LHP dissolved in 5 microl of sodium borate buffer (SBB, 0.02 m) was slowly injected into the vitreous using a 33-gauge needle. PEG-SOD (5000 units/kg) was given intravenously 5 min before LHP injection. At 2, 4, 6, 12, 24 and 48 hr after the vitreous injections, we evaluated the number of rolling leukocytes along the major retinal veins and the number of leukocytes that accumulated in the retinal microvasculature with acridine orange digital fluorography. In LHP-treated rats, leukocyte rolling along the major retinal veins was maximal at 6 hr after LHP injection. The number of rolling leukocytes in the PEG-SOD-treated rats was decreased to 5.5% of those in the LHP-treated rats at 6 hr after LHP injection (P<0.01). No rolling leukocytes were observed in either control or vehicle-treated eyes. The number of accumulated leukocytes in LHP-treated eyes started to increase at 12 hr, and peaked at 24 hr which was significantly higher than in both control and vehicle-treated eyes (P<0.01). The number of accumulated leukocytes in the PEG-SOD-treated rats was reduced by 88.0% at 24 hr (P<0.01). Intravenous injection of PEG-SOD significantly inhibited the leukocyte rolling and its accumulation under LHP-induced oxidative stress. These results suggest that PEG-SOD might attenuate various retinal microcirculatory disorders associated with LHP.

Animals↗

PubMed2004

Acute impairment of hepatic microcirculation and recruitment of nonparenchymal cells by intrasplenic hepatocyte transplantation.

BACKGROUND/PURPOSE: Over the last 20 years, hepatocyte transplantation (HcTx) has advanced from the experimental to the clinical stage. To date, HcTx has been performed in 30 patients in the United States. Regardless whether hepatocytes are transplanted into the spleen and migrate to the liver or are injected directly into the portal vein, transplanted liver cells will, to some extent, congest the recipient liver microcirculation. The potential negative consequences of intrasplenic HcTx were the subject of this study. METHODS: By using intravital microscopy, the authors investigated whether intrasplenic HcTx of 20 x 10(6) allogenic hepatocytes would influence liver perfusion, excretory liver function, and nonparenchymal cells (Kupffer and Ito cells) in vivo. RESULTS: The sinusoidal perfusion rate declined significantly from 94% (control) to 84% on day 1 and 76% on day 7. Bile acid excretion decreased in a similar fashion from 0.924 mg/h (control) to 0.669 mg/h on day 7. The authors observed a significant increase of Ito cells from 81.1 cells per microscopic field (control) to 97.1 (day 1) and an increase of Kupffer cells (KC; 6.1 cells per microscopic field on day 1 v 3.8 on control). CONCLUSIONS: This study shows an acute impairment of hepatic microcirculation and hepatucellular function along with an recruitment and activation of nonparenchymal cells in the early posttransplantation period after intrasplenic HcTx. Kupffer cell recruitment indicates an activation of local host defense, and Ito cell activation implies the initiation of liver repair mechanisms owing to ischemia-related cell damage.

Animals↗

PubMed2006

Rapid non-genomic vasoconstrictor actions of aldosterone in the renal microcirculation.

There is increasing evidence for the pathophysiological importance of aldosterone in renal diseases. Studies have so far demonstrated that aldosterone exerts deleterious renal effects by inducing oxidative stress, endothelial dysfunction, inflammation and fibrosis through a mineralocorticoid receptor (MR)-dependent genomic mechanisms. On the other hand, a number of recent studies provided evidence that aldosterone can act through a rapid non-genomic mechanism in cardiovascular tissues including the kidney, though the relative importance of such actions in renal diseases remains to be determined. We have recently found that physiological concentrations of aldosterone cause rapid vasoconstriction in the renal microcirculation. The vasoconstrictor actions were compatible with non-genomic; the major characteristics was its relatively early onset (apparent within 5min), which was not affected by either actinomycin D or cycloheximide (inhibitors of transcription or protein synthesis). Thus, in addition to genomic actions, such non-genomic vasoconstrictor actions in the renal microcirculation may contribute to the deleterious renal effects of aldosterone in renal diseases.

Aldosterone↗