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At least 469 records · Page 26Linked to original sources
PubMed2003

PDGF stimulates pulmonary vascular smooth muscle cell proliferation by upregulating TRPC6 expression.

Capacitative Ca(2+) entry (CCE) through store-operated Ca(2+) (SOC) channels plays an important role in returning Ca(2+) to the sarcoplasmic reticulum (SR) and regulating cytosolic free Ca(2+) concentration ([Ca(2+)](cyt)). A rise in [Ca(2+)](cyt) and sufficient Ca(2+) in the SR are required for pulmonary artery smooth muscle cell (PASMC) proliferation. We tested the hypothesis that platelet-derived growth factor (PDGF)-mediated PASMC growth involves upregulation of c-Jun and TRPC6, a transient receptor potential cation channel. In rat PASMC, PDGF (10 ng/ml for 0.5-48 h) phosphorylated signal transducer and activator of transcription (STAT3), increased mRNA and protein levels of c-Jun, and stimulated cell proliferation. PDGF treatment also upregulated TRPC6 expression and augmented CCE, elicited by passive depletion of Ca(2+) from the SR using cyclopiazonic acid. Furthermore, overexpression of c-Jun stimulated TRPC6 expression and CCE amplitude in PASMC. Downregulation of TRPC6 using an antisense oligonucleotide specifically for human TRPC6 decreased CCE and inhibited PDGF-mediated PASMC proliferation. These results suggest that PDGF-mediated PASMC proliferation is associated with c-Jun/STAT3-induced upregulation of TRPC6 expression. The resultant increase in CCE raises [Ca(2+)](cyt), facilitates return of Ca(2+) to the SR, and enhances PASMC growth.

Animals↗
PubMed2005

Distribution and correlates of arterial compliance measures in asymptomatic young adults: the Bogalusa Heart Study.

BACKGROUND: Impaired arterial compliance is an independent predictor of early vascular damage and related adverse cardiovascular (CV) outcome. Information is scant on the distributions and correlates of measures of arterial pulsatile function in a community-based, biracial cohort of young adults. METHODS: In 800 African American and white subjects aged 18 to 44 years, pulsatile arterial function was assessed in terms of large artery (capacitive) compliance, small artery (oscillatory) compliance, systemic vascular resistance, and vascular impedance by noninvasive radial artery pressure pulse contour analysis. RESULTS: African Americans versus whites and women versus men had lower large and small artery compliances and higher systemic vascular resistance and vascular impedance (P < .001). In multiple regression analysis, mean arterial pressure, body mass index (BMI), insulin levels, and age were correlated inversely and body surface area positively with large artery compliance and accounted for 39.2% of the variance; mean arterial pressure, female gender, age, and triglyceride levels inversely and cardiac output positively with small artery compliance and explained 56.4% of the variance; mean arterial pressure and age positively and cardiac output inversely with systemic vascular resistance and accounted for 91.4% of variance; and mean arterial pressure and BMI positively and cardiac output and body surface area inversely with vascular impedance and contributed to 37.6% of the variance. CONCLUSIONS: The observed deleterious impact of traditional CV risk factors on the arterial wall dynamics in asymptomatic young adults has important implications for preventive cardiology. Noninvasive pulsatile arterial function assessment may be helpful for evaluation of early vascular damage in a high-risk young population group.

Adolescent↗
PubMed1992

Venous modulation of ventricular preload.

The objective of this discussion has been to describe a simple conceptual model of the circulation that emphasizes the role of the venous capacitance vasculature and is based on simplified vascular pressure-volume relationships. First, it is hoped that this approach will avoid some of the misunderstandings and contradictions that have resulted from an approach to the veins that is based on pressure-flow relationships. As mentioned at the outset, the confusion between venous volume and flow has led to the anomalous but logical conclusion that decreased venous pooling corresponds to increased venous return (which must equal cardiac output in the steady state). Second, it is also hoped that the model will prove to be a useful starting point from which to better understand how the veins modulate cardiac output in the normal individual and how alterations in venous capacitance affect the hemodynamic profile of congestive heart failure.

Arteries↗
PubMed1989

Effects of SIN-1 on peripheral hemodynamics and viscoelastic properties of aorta in anesthetized rabbits.

In closed-chest, non-barbiturate-anesthetized rabbits, we have used a computer-based parameter estimation method to evaluate the effects of a slow intravenous infusion of SIN-1 (15 micrograms/kg/min for 20 minutes) upon hemodynamic, geometric, viscoelastic, and energetic characteristics of the hindlimb arterial bed from the measurement of abdominal aortic diameter, blood flow, and blood pressure. To evaluate intrinsic effects of SIN-1 upon arterial wall characteristics, a moderate arterial bleeding (3 ml/kg) was performed to achieve a -10% lowering of arterial pressure, i.e., to reach an equivalent blood pressure reference threshold in the absence of the drug. The SIN-1 IV infusion induced a marked blood pressure lowering (-10.0 +/- 2.1%), resulting from a relaxing action on smooth muscle vasculature both in capacitive and resistive components of the hindlimb vascular tree, thereby eliciting a lowering in peripheral resistance (-22.8 +/- 3.1%) and an increased blood flow (+11.7 +/- 3.6%). SIN-1 enhanced vascular compliance (+28.0 +/- 2.2%) and lowered vascular input impedance (-31.2 +/- 8.9%), as confirmed by modulus and phase spectra. SIN-1 IV infusion contrasted bleeding effects by increasing blood flow and maintaining constant or increasing aortic diameter, both of them being lowered by bleeding. The relaxing effect elicited by SIN-1 was further demonstrated by changes in viscoelastic characteristics, and it was further associated with a decreasing energetic demand as well. The present results demonstrated that SIN-1, administered as a slow IV infusion, exhibits vasodilating properties by acting both on capacitive and resistive vessels of the systemic circulation.

Animals↗
PubMed1985

[Changes in the functions of the vessels of the skeletal musculature during a cardiogenic depressor reflex].

Changes of vascular resistance and capillary filtration coefficient (CFC), integral stretching ability and capacitance of venous vessels were studied during the cardiogenic depressor reflex under conditions of autoperfusion of innervated skeletal muscles of the cat hindlimb. A short-term compression of the left coronary artery induced a decrease of the perfusion pressure and an increase of the CFC in the hindlimb vessels. The integral stretching ability of the venous bed and its capacitance usually increased in response to the above action. The mechanisms underlying changes of these vascular functions, are discussed.

Animals↗
PubMedDate not supplied

Vascular smooth muscle polyploidization--from mitotic checkpoints to hypertension.

Aging and hypertension are accompanied by an increase in mass and rigidity of arterial walls. At capacitance arteries, the enlargement and stiffness of the medial smooth muscle layer promote systolic hypertension and contribute to left ventricular hypertrophy and cardiovascular morbidity. Morphological studies have demonstrated that vascular smooth muscle cell (VSMC) hypertrophy, with minimal hyperplasia, causes the enlargement of vascular smooth muscle at capacitance arteries, and that VSMC hypertrophy is strongly associated with VSMC polyploidization. Recent studies demonstrate that hypertrophic signals, such as those elicited by Angiotensin II, abrogate the mechanisms of control of M phase in VSMC and induce cell cycle re-entry and polyploidization. These polyploid VSMC have a lower replicative rate, but a higher mass, protein content and matrix production than their diploid counterparts. Both, the protein kinase Aktl and the cyclin kinase-associated protein CKsl, have been implicated in the mechanism of VSMC polyploidization during hypertension. Here, we review the function of these proteins at the mitotic spindle cell cycle checkpoint and their role in the process of VSMC polyploidization.

Adaptor Proteins, Signal Transducing↗
PubMed2000

Effects of autonomic disruption and inactivity on venous vascular function.

The effects of autonomic disruption and inactivity were studied on the venous vascular system. Forty-eight subjects, 24 with spinal cord injury (SCI) and 12 sedentary and 12 active able-bodied controls, participated in this study. Peripheral autonomic data were obtained to estimate sympathetic vasomotor control [low-frequency component of systolic blood pressure (LF(SBP))]. Vascular parameters were determined using strain-gauge venous occlusion plethysmography: venous capacitance (VC), venous emptying rate (VER), and total venous outflow (VO(t)). An additional vascular parameter was calculated: venous compliance [(VC/occlusion pressure) x 100]. VC and VO(t) were significantly different (SCI < sedentary < active). VER adjusted for VC was not different for any group comparison, whereas venous compliance was significantly lower in the SCI group than in the able-bodied groups and in the sedentary group compared with the active group. Regression analysis for the total group revealed a significant relationship between LF(SBP) and venous compliance (r = 0.64, P < 0.0001). After controlling for LF(SBP) through analysis of covariance, we found that mean differences for all venous vascular parameters did not change from unadjusted mean values. Our findings suggest that in subjects with SCI, the loss of sympathetic vasomotor tone contributes more than inactivity to reductions in venous vascular function. Heightened VC, VO(t), vasomotor tone, and venous compliance in the active group compared with the sedentary group imply that regular endurance training contributes to optimal venous vascular function and peripheral autonomic integrity.

Adult↗
PubMed1993

Assessment of the human splanchnic venous volume-pressure relation using radionuclide plethysmography. Effect of nitroglycerin.

BACKGROUND: No method exists to assess human splanchnic venous function, the most important region in terms of vascular capacity. METHODS AND RESULTS: We studied 25 stable patients without heart failure or hypertension to develop a method to assess the splanchnic venous volume-pressure (V-P) relation and to determine the effect of nitroglycerin (GTN). We used blood pool scintigraphy to assess changes in regional splanchnic vascular volume (SVV) and low levels of continuous positive airway pressure (CPAP) to passively alter venous pressure and thus, SVV. We postulated that the relation between SVV and the CPAP used would reflect the capacitance of the splanchnic venous bed and that changes in the position of this relation would provide a relative measurement of any change in capacitance. In 12 patients (group 1), the splanchnic vascular V-P curves were recorded before and 2, 9, and 20 minutes after 0.6 mg sublingual GTN; in eight patients (group 2), recordings were made at similar times before and after sublingual administration of placebo; in five patients (group 3), the hemodynamic effects of CPAP were assessed by means of right and left cardiac catheterization. Right atrial and femoral venous pressures increased (p < 0.001) and cardiac output fell (p < 0.05) during CPAP. There was an apparently linear relation between CPAP and SVV (r = 0.74-0.98); SVV increased an average of 7.4 +/- 2.2% (p < 0.001) by 12 cm H2O CPAP: The splanchnic vascular V-P curves were reproducible with minimal variability in SVV (+/- 2%, p > 0.2) in group 2. After administration of GTN, the splanchnic vascular V-P curve shifted away from the pressure axis in a parallel fashion by an average of 9.4 +/- 5.4% (p < 0.001). CONCLUSIONS: We have developed a reproducible noninvasive technique that may be used to assess human splanchnic venous V-P relations. We have demonstrated for the first time in humans that GTN exerts its dilatory effect by increasing the unstressed splanchnic venous volume.

Erythrocytes↗
PubMedDate not supplied

[Characteristics of microcirculatory changes in various forms of rheumatoid arthritis in children].

Using the method of biomicroscopy of bulbar conjunctiva with application of vessel gaging the authors made observation of 125 patients: 110--with RA and 15--with reactive arthritis. Marked vascular and intravascular changes in combination with dilatation of the capacitive vessels and narrowing of the resistive ones in vasculo-visceral form of RA correlated with the increase of immunological indices of the blood. In patients with vascular form of RA less marked changes of the vessels in dilatation of the capacitive part correlated with immunological indices of the synovial fluid.

Adolescent↗
PubMed2002

Inhibition of endogenous TRP1 decreases capacitative Ca2+ entry and attenuates pulmonary artery smooth muscle cell proliferation.

Pulmonary vascular medial hypertrophy due to proliferation of pulmonary artery smooth muscle cells (PASMC) greatly contributes to the increased pulmonary vascular resistance in pulmonary hypertension patients. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) is an important stimulus for cell growth in PASMC. Resting [Ca2+]cyt, intracellularly stored [Ca2+], capacitative Ca2+ entry (CCE), and store-operated Ca2+ currents (I(SOC)) are greater in proliferating human PASMC than in growth-arrested cells. Expression of TRP1, a transient receptor potential gene proposed to encode the channels responsible for CCE and I(SOC), was also upregulated in proliferating PASMC. Our aim was to determine if inhibition of endogenous TRP1 gene expression affects I(SOC) and CCE and regulates cell proliferation in human PASMC. Cells were treated with an antisense oligonucleotide (AS, for 24 h) specifically designed to cleave TRP1 mRNA and then returned to normal growth medium for 40 h before the experiments. Then, mRNA and protein expression of TRP1 was downregulated, and amplitudes of I(SOC) and CCE elicited by passive depletion of Ca2+ from the sarcoplasmic reticulum using cyclopiazonic acid were significantly reduced in the AS-treated PASMC compared with control. Furthermore, the rate of cell growth was decreased by 50% in AS-treated PASMC. These results indicate that TRP1 may encode a store-operated Ca2+ channel that plays a critical role in PASMC proliferation by regulating CCE and intracellular [Ca2+](cyt).

Blood Proteins↗
PubMed1993

Neuropeptide Y and differential sympathetic control of splenic blood flow and capacitance function in the pig and dog.

The roles of different mediators in the sympathetic regulation of the pig and dog spleens were investigated using a preparation with intact vascular perfusion in vivo. Sympathetic nerve stimulation caused overflow of neuropeptide Y-like immunoreactivity (NPY-LI) and noradrenaline (NA), arterial vasoconstriction, increase in venous blood flow and haematocrit. The dog spleen responded to single impulse stimulation, whereas more prolonged stimulation was required to elicit vascular responses in the pig spleen. Furthermore, the maximal splenic capacitance response was about 10 times larger in the dog than in the pig. After depletion of neuronal NA content by reserpine combined with preganglionic denervation, about 70% of the splenic arterial vasoconstrictor responses in the dog and pig still remained at 5 Hz stimulation. Fifty per cent of the capacitance response evoked by nerve stimulation still remained in the pig while in the dog spleen the capacitance response was virtually abolished after reserpine. The stimulation-evoked overflow of NPY-LI in pig spleen was increased several fold after reserpine treatment as compared to controls reaching levels in the venous effluent where exogenous NPY evokes vasoconstriction. In the dog spleen, overflow of NPY-LI was only observed after reserpine. Administration of NA caused arterial vasoconstriction with an initial increase in venous blood flow while NPY mainly reduced arterial blood flow. It is concluded that NA is involved in both the splenic arterial vasoconstriction and the capacitance responses while a non-adrenergic splenic vasoconstriction at least in the pig may be mediated by NPY.

Animals↗
PubMed1985

A mechanical model of the dynamics of the coronary circulation in dog.

A mechanical model of the coronary circulation, including a capacitive extramyocardial compartment and a collapsible intramyocardial vascular bed has been described. The phasic coronary blood flow (CBF) in the circumflex artery of 11 anesthetized open chest dogs was studied in control conditions and during thoracic aortic constriction and arteriovenous fistula (AVF). We measured pressures in aortic and left ventricle, phasic CBF by pulsed Doppler flowmetry and in three dogs, pressure in the left anterior descending coronary artery. After aortic and AVF unclamping, we observed a major reverse flow in the circumflex artery. This reverse flow may be explained by the displacement of the collapse point of the intramyocardial compartment, due to the relative distribution of the intramyocardial tissue pressure and the intravascular coronary pressure. The specific role of the epicardial capacitive coronary compartment and of the intramyocardial pump action has been illustrated during coronary artery clamping, ectopic beats and changes in myocardial contractility. Under all the experimental conditions, the reported results demonstrated the ability of the model to describe the patterns of the dynamic of the coronary circulation.

Animals↗
PubMed1977

Haemodynamic effects of pindolol in hypertensive patients.

Five men and five women, mean age 48 years, with hypertension in stages I or II of the WHO classification, were given preoral treatment with pindolol. The pindolol treatment lead a significant decrease in the systolic and diastolic blood pressure, at rest and during work both after 2 months and after 16 months treatment. Three mechanisms seem to be involved in the antihypertensive effect of pindolol: 1) a negative chronotropic effect on the heart, 2) a decrease in peripheral vascular resistance and 3) an increase in venous capacitance affecting the venous return. Comparison of the results after 2 and after 16 months of treatment suggests that a decrease in cardiac output is an early mechanism in the lowering of the blood pressure, while a decrease in vascular resistance seems to be more important after long-term treatment with pindolol.

Cardiac Output↗
PubMed1996

Pharmacology of a capacitative Ca2+ entry in Xenopus oocytes.

We have characterized pharmacological properties of inositol trisphosphate (InsP3)-mediated calcium entry pathway in Xenopus oocytes via activation of Ca(2+)-dependent Cl- channels (ICl, Ca) as a sensitive indicator for increase in cytosolic [Ca2+]. This type of Ca2+ entry mechanism is known as a capacitative Ca2+ entry (CCE). Voltage-clamped oocytes were maintained in Ca(2+)-free medium and injected with InsP3 which depleted the InsP3-sensitive Ca2+ stores. 10-20 min later, the oocytes were exposed, at 2-3 min intervals, to 5 mM Ca(2+)-containing medium for 5-10 s which evoked repeated inward Cl- current. No effect of external Ca2+ was apparent before InsP3 injection. To determine the pharmacological characteristics of CCE, oocytes were incubated with various chemical agents in Ca(2+)-free solution and exposed to Ca2+ again in presence of the chemical. It was found that organic Ca2+ channel blockers were relatively ineffective in blocking CCE while the inorganic Ca2+ channel blocker La3+ was most efficient in blocking the current. Attempts to measure conductance increase when the Cl- channels were blocked during activation of Ca2+ influx were unsuccessful. Therefore we tested the hypothesis that the Ca2+ influx is mediated via a Ca-H transporter. Lowering the external pH (to pH 6.5) or application of the protonophore carbonylcyanide p-trifluoromethoxyphenyl hydrazone (EC50 = 2 x 10(-8) M) effectively blocked CCE. Since Ca-H countertransport in the plasma membrane is coupled to Ca2+ extrusion by Ca-ATPase in vascular smooth muscle we suggest that the capacitative Ca2+ entry in Xenopus oocytes may possibly arise from slippage of plasma membrane Ca-ATPase coupled to proton countertransport, a mechanism reported in a variety of cells. Ca2+ slippage may arise from the large Ca2+ gradient produced by the Ca2+ depletion protocol.

Animals↗
PubMed2003

Cardiac homeostasis is independent of calf venous compliance in subjects with paraplegia.

The purpose of this study was to examine cardiac hemodynamics during acute head-up tilt (HUT) and calf venous function during acute head-down tilt (HDT) in subjects with paraplegia compared with sedentary nondisabled controls. Nineteen paraplegic males (below T6) and nine age-, height-, and weight-matched control subjects participated. Heart rate, stroke volume, and cardiac output were assessed using the noninvasive acetylene uptake method. Venous vascular function of the calf was assessed using venous occlusion plethysmography. After supine measurements were collected, the table was moved to 10 degrees HDT followed by the three levels of HUT (10, 35, and 75 degrees ) in random order. Cardiac hemodynamics were similar between the groups at all positions. Calf circumference was significantly reduced in the paraplegic group compared with the control group (P < 0.001). Venous capacitance and compliance were significantly reduced in the paraplegic compared with control group at supine and HDT. Neither venous capacitance (P = 0.37) nor compliance (P = 0.19) increased from supine with 10 degrees HDT in the paraplegic group. A significant linear relationship was established between supine venous compliance and supine cardiac output in the control group (r = 0.80, P < 0.02) but not in the paraplegic group. The findings of reduced calf circumference and similar venous capacitance at supine rest and 10 degrees HDT in the paraplegic group imply that structural changes may have limited venous dispensability in individuals with chronic paraplegia. Furthermore, the lack of a relationship between supine venous compliance and supine cardiac output suggests that cardiac homeostasis does not rely on venous compliance in subjects with paraplegia.

Adult↗
PubMed2002

Relationship between the sarcoplasmic reticulum and the plasma membrane.

Ionic interactions between the plasma membrane (PM) and the sarcoplasmic reticulum (SR) play a crucial role in smooth muscle activation and homeostasis. The most common form of Ca2+ signalling seen in vascular smooth musde of conduit arteries and capacitance veins consists of repetitive asynchronous Ca2+ waves. In the inferior vena cava of the rabbit these waves are initiated by Ca2+ release via InsP3 receptors (InsP3R) and propagated by regenerative Ca2+ release. Maintenance of the [Ca2+] oscillations is dependent on Ca2+ entry through the Na+/Ca2+-exchanger (NCX) which is driven in the reverse mode by Na+ entry through non-specific cation channels. The latter are also responsible for depolarization and activation of voltage-gated Ca2+ channels. The sarcoplasmic-endoplasmic reticulum Ca2+-ATPase (SERCA) in the sheet-like junctional SR is responsible for refilling and completing the cycle. Under resting conditions the interaction between the superficial SR and the NCX is reversed with Ca2+ release channels supplying Ca2+ to the NCX in the PM to be extruded in exchange of extracellular Na+. It is proposed that the above Ca2+ transport between the SR lumen and the extracellular space takes place at PM-SR junctions across a narrow junctional space.

Animals↗
PubMed1989

The effects of dihydroergotamine in patients with head injury and raised intracranial pressure.

In the first study 6 patients with raised intracranial pressure due to brain oedema following head injury were given dihydroergotamine because of low perfusion pressure. The intracranial pressure fell simultaneously with the increase in arterial pressure. The intracranial pressure fell from 24 +/- 2 mmHg by a maximum of 12 +/- 1 mmHg after a single intravenous injection of 0.25 mg of dihydroergotamine and remained at a low level for 35-70 min before stabilizing at a new level 5 +/- 1 mmHg below the baseline. The initial rapid and marked decrease in intracranial pressure may be the result of a reduced intracranial blood volume, due predominantly to constriction of the more voluminous venous capacitance vessels (by analogy with the corresponding vascular effect of dihydroergotamine on skeletal muscle and skin.) In the second study, experiments using sympathectomized cat skeletal muscle, showed that dihydroergotamine also reduced the hydrostatic capillary pressure, inducing absorption of fluid from the interstitial tissue to blood. It is suggested that a similar transcapillary absorption effect in the damaged brain may be an explanation for the observation that the intracranial pressure stabilized at a level below the initial one following dihydroergotamine.

Adolescent↗
PubMed1976

Hemodynamic effects of nitroglycerin ointment in congestive heart failure.

The hemodynamic effects of nitroglycerin absorbed transcutaneously from an ointment base were determined in 10 patients with chronic congestive heart failure (9 with ischemic heart disease and 1 with cardiomyopathy). The response was characterized by a decrease in pulmonary capillary wedge pressure from an average of 30 to 19 mm Hg, and an increase in cardiac index from 1.7 to 2.2 liter/min per m2, with concomitant decreases in systemic and pulmonary vascular resistance and an increase in venous capacitance. Mean arterial pressure decreased from 85 to 80 mm Hg, and heart rate remained unchanged. The hemodynamic effects persisted for 3 to 6 hours. These results indicate that nitroglycerin ointment is a hemodynamically potent vasodilating agent with potential value in the therapy of congestive heart failure.

Aged↗