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PubMed1999

Overshooting cytosolic Ca2+ signals evoked by capacitative Ca2+ entry result from delayed stimulation of a plasma membrane Ca2+ pump.

The effect of capacitative Ca2+ entry on cytosolic free Ca2+ concentration ([Ca2+]c) was examined in calf pulmonary artery endothelial cells treated with thapsigargin. Restoration of extracellular Ca2+ evoked an overshoot in [Ca2+]c: the initial rate of Ca2+ influx was 12.4 +/- 0.5 nM/s as [Ca2+]c rose monoexponentially (time constant, tau = 36 +/- 2 s) to a peak (322 +/- 16 nM) before declining to 109 +/- 14 nM after 2000 s. Rates of Ca2+ removal from the cytosol were measured throughout the overshoot by recording the monoexponential decrease in [Ca2+]c after rapid removal of extracellular Ca2+. The time constant for recovery (tau rec decreased from 54 +/- 4 s when Ca2+ was removed after 10 s to its limiting value of 8.8 +/- 1.0 s when it was removed after 2000 s. The time dependence of the changes in tau rec indicate that an increase in [Ca2+]c is followed by a delayed (tau = 408 s) stimulation of Ca2+ removal, which fully reverses (tau approximately 185 s) after Ca2+ entry ceases. Numerical simulation indicated that the changes in Ca2+ removal were largely responsible for the overshooting pattern of [Ca2+]c. Because prolonged (30 min) Ca2+ entry did not increase the total 45Ca2+ content of the cells, an increased rate of Ca2+ extrusion across the plasma membrane most likely mediates the Ca2+ removal, and since it persists in the absence of extracellular Na+, it probably results from stimulation of a plasma membrane Ca2+ pump. We conclude that delayed stimulation of a plasma membrane Ca2+ pump by capacitative Ca2+ entry may protect cells from excessive increases in [Ca2+]c and contribute to oscillatory changes in [Ca2+]c.

Animals↗
PubMed1983

Effect of sympathetic nerve stimulation and adrenoceptor blockade on pial arterial and venous calibre and on intracranial pressure in the cat.

Pial arterial and venous calibre were continuously recorded through a closed cranial window preparation during cervical sympathetic nerve stimulation in 10 cats before and after alpha- and beta-adrenoceptor blockade. In addition, the intracranial pressure (ICP) was simultaneously recorded in 4 of the cats. Under resting conditions 33 arteries (mean diameter 130 micron) constricted by 11.7 +/- 0.8% and 80 venous portions (mean diameter 152 micron) constricted by 13.7 +/- 0.7% during sympathetic nerve stimulation. ICP decreased simultaneously by 16.5 +/- 6.2%. Administration of the alpha-adrenoceptor antagonist phenoxybenzamine i.v. (1.5 mg X kg-1) abolished the reduction of ICP and markedly reduced, but did not completely abolish, the constrictor response of arteries and veins. The beta-adrenoceptor antagonist propranolol (1.5 mg X kg-1) did not significantly alter the reduction of ICP or the response of pial veins and small arteries, whereas the response of arteries with a diameter greater than 150 micron was attenuated. It is concluded that the constriction of pial veins and arteries during sympathetic stimulation is mediated predominantly via alpha-adrenoceptors. The sympathetic nerves of cerebral blood vessels may have stronger influence on the cerebral capacitance than on resistance vessels under normotensive and normocapnic conditions.

Adrenergic alpha-Antagonists↗
PubMed1993

Tone-dependent coronary arterial-venous pressure differences at the cessation of venous outflow during long diastoles.

BACKGROUND: The origin and magnitude of the back pressure opposing diastolic coronary inflow remain controversial. The arterial pressure at which coronary inflow stops during a prolonged diastole, ie, "zero-flow pressure," is higher than coronary venous pressure. However, because of capacitive discharge as distending pressure falls, flow at the microcirculatory level exceeds inflow, and coronary outflow ceases later than inflow. If coronary arterial pressure continues to exceed venous pressure at the point of venous flow cessation, zero-flow pressure cannot be an artifact of capacitive discharge. METHODS AND RESULTS: Coronary inflow and outflow, arterial pressure, and right atrial pressure have been measured during long diastoles in closed-chest dogs chronically instrumented with volumetric flow probes on the great cardiac vein or coronary sinus as well as the circumflex artery. Although venous outflow continued for 1 to 4 seconds after arterial inflow ceased, coronary artery pressure at the point of venous flow cessation (Pfv = 0) always exceeded right atrial pressure (13 +/- 1.3 mm Hg [SEM] vs 6 +/- 0.7 mm Hg, P < .001). When vasomotor tone was augmented using vasopressin, the diastolic pressure-flow relation shifted to the right, with Pfv = 0 increasing to 21 +/- 2.4 mm Hg despite an unchanged right atrial pressure (6 +/- 0.5 mm Hg). CONCLUSIONS: Transcoronary pressure differences persist when venous outflow stops and are larger when vasomotor tone is augmented. Measurements of zero-flow pressure that exceed venous pressure cannot be considered an artifact of continuing capacitive discharge after the cessation of arterial inflow. Diastolic coronary back pressure exceeds right atrial pressure and is tone dependent.

Animals↗
PubMed1984

The role of alpha and beta adrenergic receptors in constriction and dilation of the systemic capacitance vessels: a study with measurements of the mean circulatory pressure in dogs.

The response of the mean circulatory pressure (MCP), an index of the tone of the systemic capacitance vessels, to the infusion of an alpha-adrenergic receptor stimulant (phenylephrine) and a beta-adrenergic receptor stimulant (isoproterenol) was studied in anesthetized, open-chest dogs. Provided that the blood volume (particularly, extra volume) remains constant, an increase in the MCP indicates an increase in the tone of the capacitance vessels ("venoconstriction") and a decrease in the MCP indicates a decrease in the tone of the capacitance vessels ("venodilation"). It was almost definitely concluded that the stimulation of the alpha-adrenergic receptor led to the increased tone of the systemic capacitance vessels and the stimulation of the beta-adrenergic receptor did not decrease the tone of the systemic capacitance vessels in anesthetized, open-chest dogs, but the stimulation of the beta-adrenergic receptor decreased the tone of the systemic capacitance vessels, when the tone had been previously elevated by angiotensin-II.

Angiotensin II↗
PubMed1985

Responses of left ventricle to changes in aortic input impedance.

In order to evaluate how pressure and flow at the outlet of a ventricle are determined by the interaction between the ventricle and an aortic input impedance, we examined the effects of independent changes in the peripheral resistance and in the aortic compliance using isolated canine left ventricle preparations. There was an inverse linear relationship of mean values between pressure and cardiac output under pure resistance changes when coronary flow was maintained constant. But, when the coronary perfusion pressure depended on mean aortic pressure, the relationship was no longer linear under a critical aortic pressure. When aortic compliance was increased, late systolic flow was enhanced and late systolic pressure decreased such that the stroke volume increased. The top part of the pressure-volume loop showed a configurational change from the right side down to the left side down. Changes in pressure and flow wave forms, and in the pressure-volume loop can be predicted by an electrical model in which time varying capacitance arranged in series with the internal resistance was used as a ventricular model.

Animals↗
PubMed1990

Effect of epidural anesthesia for cesarean delivery on maternal femoral arterial and venous, uteroplacental, and umbilical blood flow velocities and waveforms.

The effect of epidural anesthesia on the maternal femoral arterial and venous, uteroplacental, and umbilical circulations was studied by the pulsed Doppler technique in 13 women undergoing elective cesarean delivery. Resistance and pulsatility indices of umbilical arterial velocity waveforms did not change with the use of epidural anesthesia. In the uteroplacental circulation, these indices increased in 11 patients, suggesting an increase in resistance. Reduction of sympathetic tone in resistance and capacitance vessels was reflected in the femoral artery by an increase in systolic and end-diastolic velocities, a reversal of the post-systolic backward flow, and an increase in mean velocity. The latter also occurred in the femoral vein. The diameters of these large maternal vessels did not change. This study suggests an impairment in uteroplacental circulation associated with a drop in peripheral vascular resistance and an increase in leg blood flow after epidural anesthesia.

Anesthesia, Epidural↗
PubMed1998

Origin and function of epoxyeicosatrienoic acids in vascular endothelial cells: more than just endothelium-derived hyperpolarizing factor?

1. In addition to their contribution to endothelium-derived hyperpolarization, our understanding of the physiological function of epoxyeicosatrienoic acids (EET) within the vascular wall and the actual enzymes involved in the formation of the EET in endothelial cells is very limited. In the present study, the expression of potential cytochrome P450 (CYP) mono/epoxygenases was assessed in endothelial cells isolated from porcine and bovine aortas as well as in the human umbilical vein-derived cell lines EA.hy926 and ECV304. 2. Expression of CYP2B1, CYP2E1 and CYP3A could be found. The latter were inducible by dexamethasone/clofibrate for 72 h, a procedure that also enhanced CYP epoxygenase activity in endothelial cells. 3. Enzyme induction yielded increases in capacitative Ca2+ entry and membrane hyperpolarization in response to autacoids, such as bradykinin and thapsigargin. Thiopentone sodium, an inhibitor of endothelial CYP mono/epoxygenase(s), diminished autacoid-induced capacitative Ca2+ entry and membrane hyperpolarization, while the effect of EET remained unchanged. 4. Epoxyeicosatrienoic acids activated endothelial tyrosine kinase activity in a concentration-dependent manner. Arachidonic acid, at 20-fold higher concentrations, also increased tyrosine kinase activity. Because only the effect of arachidonic acid was inhibited by thiopentone sodium, an inhibitor of CYP mono/epoxygenases, these data suggest that arachidonic acid needs to be converted to the EET in order to stimulate tyrosine kinase. 5. All these data provide clear evidence that the CYP epoxygenase-derived arachidonic acid metabolites (EET) not only serve as potential endothelium-derived hyperpolarizing factors but also constitute highly active intracellular messengers with a physiological role including the control of Ca2+ signalling, membrane potential and tyrosine kinase activity.

8,11,14-Eicosatrienoic Acid↗
PubMed1998

The annexin II-p11 complex is involved in regulated exocytosis in bovine pulmonary artery endothelial cells.

Annexin II is a member of a multigene family of Ca2+-regulated, membrane-binding proteins implicated through biochemical and perforated cell experiments in Ca2+-triggered secretion. Within most cells annexin II resides in a tight heterotetrameric complex with a cellular protein ligand, p11, and complex formation is mediated via the N-terminal 14 residues of annexin II including the N-terminal acetyl group. To analyze at the single cell level whether the annexin II-p11 complex is involved in regulated secretion, we used membrane capacitance measurements to follow exocytotic fusion events in bovine aortic endothelial cells manipulated with respect to their annexin II-p11 complex formation. Upon guanosine 5'-O-(thiotriphosphate) (GTPgammaS) stimulation, the endothelial cells show a significant increase in membrane capacitance which is generally preceded by a transient rise in intracellular Ca2+ and thus indicative of the occurrence of Ca2+-regulated secretion. The GTPgammaS-induced capacitance increase is markedly reduced in cells loaded with a synthetic peptide, Ac1-14, which corresponds in sequence to the N-terminal 14 residues of annexin II in their correctly acetylated form and which is capable of disrupting preformed annexin II-p11 complexes. The effect of the peptide is highly specific as the nonacetylated variant, N1-14, which is incapable of disrupting annexin II-p11, does not interfere with the GTPgammaS-induced increase in membrane capacitance. These data show that intact annexin II-p11 complexes are indispensable for regulated exocytosis to occur in an efficient manner in endothelial cells.

Animals↗
PubMed1981

Structurally reduced distensibility of cardiovascular low-pressure' compartments in primary hypertension, as studied in spontaneously hypertensive rats (SHR).

Adult male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared to explore to what extent venous "unstressed" volume, compliance and wall distensibility are structurally altered in primary hypertension. The perfused, maximally vasodilated hindquarters and the entire, completely relaxed cardiovascular system during cardiac arrest were used for comparisons of "initial" volumes and pressure volume characteristics of the respective low-pressure compartments. In both preparations SHR and WKY showed identical "unstressed" venous volumes, computed by extrapolation to zero pressure from initial volumes and the nearly linear pressure-volume relationships, while venous compliance (delta V/delta P) was in each case about 20% reduced iun SHR. Consequently, the structurally determined wall distensibility of the low-pressure compartment, calculated as the square root of volume compliance/unstressed (or initial) volume, was significantly reduced in SHR; about 10%. Such venous "structural resetting" has important hemodynamic consequences, not least because it reinforces increase of venous return and cardiac filling pressure in SHR, caused by given sympathetic activations. Evidently, not only resistance, cardiac and barostat functions but also the venous capacitance function are structurally reset early in primary hypertension, implying a redesign of the entire cardiovascular system to operate at a higher pressure equilibrium.

Animals↗
PubMed1986

Functional characteristics of intramyocardial capacitance vessels during diastole in the dog.

In order to evaluate the functional characteristics of the intramyocardial capacitance vessels during prolonged diastole, we analyzed the response of coronary vein flow after stepwise changes of coronary artery pressure in anesthetized open-chest dogs by using our newly developed laser Doppler velocimeter with an optical fiber. The peripheral portion of the great cardiac vein was isolated and the optical fiber tip was inserted into the vessel. The left anterior descending coronary artery was cannulated and connected to a reservoir to regulate coronary perfusion pressure. Intracoronary adenosine administration was carried out to avoid any change in coronary vasomotor tone. After 15 seconds of occlusion of the perfusion route, the heart was arrested by pacing-off. Two seconds later, coronary perfusion pressure was increased stepwise to a preset target pressure. This procedure was repeated by changing target pressure at 4 (or 5) different pressure levels (31-105 mm Hg). The great cardiac vein flow became zero due to the cardiac arrest and remained at zero for a moment (dead time) after the initiation of reperfusion. Then the flow reappeared and increased with first order time delay. The presence of dead time indicates the existence of unstressed volume, and the first order time delay represents the product of resistance and capacitance. The unstressed volume with a minimal vasomotor tone for perfusion pressure of 60-90 mm Hg was 5.2 +/- 2.2 ml per 100 g left ventricle, which is comparable to coronary blood flow for several beats. The capacitance at perfusion pressure of 60-90 mm Hg was 0.08 +/- 0.04 ml/mm Hg per 100 g left ventricle, while that at low perfusion pressure (30-50 mm Hg) was 0.14 +/- 0.09 ml/mm Hg per 100 g left ventricle. These results indicate that the intramyocardial capacitance vessels have two functional components, and that the phasic nature of coronary vein flow is solely the result of the myocardial squeezing of the blood in the capacitance vessels.

Animals↗
PubMed1991

Pharmacology of endothelin-1 in vivo in humans.

Endothelin-1 (ET-1) is a potent vasoconstrictor and pressor agent with a prolonged action in animal preparations. We have investigated the vascular pharmacology of ET-1 in healthy human volunteers. In arterial studies, blood flow was measured in both forearms and the left brachial artery cannulated for infusion of drugs and vehicle. Local blood flow was reduced in a dose-dependent manner by ET-1. At 5 pmol/min, the response was maximal by 60 min, and flow returned to baseline only after a further 120 min. ET-1 and angiotensin II, both at 5 pmol/min, reduced flow by 40% at 60 min. These responses were reversed to a similar degree by the dihydropyridine calcium antagonist nicardipine (0.3-10 micrograms/min). At 1 pmol/min, ET-1 did not affect sympathetic vasoconstriction to arterial norepinephrine or lower body negative pressure. In venous studies, the internal diameter of a dorsal hand vein was measured during local infusion of drugs and vehicle. ET-1 (5 pmol/min) produced local venoconstriction, with a maximal reduction in vein size of 83 +/- 12% at 60 min. Reversal of responses was slow, and unaffected by nicardipine (1.5 micrograms/min). We have shown that ET-1 is a potent vasconstrictor producing prolonged effects in resistance and capacitance vessels in humans. Low-dose ET-1 does not appear to affect sympathetically mediated vasoconstriction. Studies with nicardipine do not provide support for the hypothesis that ET-1 is an endogenous ligand of the dihydropyridine-sensitive calcium channel.

Adult↗
PubMed2004

ATP-induced mitogenesis is mediated by cyclic AMP response element-binding protein-enhanced TRPC4 expression and activity in human pulmonary artery smooth muscle cells.

Extracellular ATP and intracellular cyclic AMP response element-binding protein (CREB, a transcription factor) promote cell proliferation in many cell types. The canonical transient receptor potential (TRPC) channels, which putatively participate in forming store- and receptor-operated Ca2+ channels, have been implicated in the pulmonary vascular remodeling processes. A link between extracellular ATP, CREB activation, and TRPC4 channel expression and activity has not been shown in human pulmonary artery smooth muscle cells (PASMC). Long-term (24-48 h) treatment of human PASMC with a low dose (100 microM) of ATP, which did not trigger a transient rise in free cytosolic Ca2+ concentration ([Ca2+]i) when applied acutely to the cells, caused marked increases in CREB phosphorylation and TRPC4 protein expression. The time course indicated that the ATP-mediated CREB phosphorylation preceded TRPC4 upregulation, whereas transfection of a nonphosphorylatable CREB mutant abolished ATP-mediated TRPC4 expression. Furthermore, treatment of human PASMC with ATP also enhanced the amplitude of capacitative Ca2+ entry (CCE) induced by passive store depletion, whereas the small interfering RNA specifically targeting TRPC4 attenuated ATP-mediated increases in TRPC4 expression and CCE amplitude and inhibited ATP-induced PASMC proliferation. These data suggest that low-dose ATP exerts part of its mitogenic effect in human PASMC via CREB-mediated upregulation of TRPC4 channel expression and activity and the subsequent increase in CCE and [Ca2+]i.

Adenosine Triphosphate↗
PubMed2002

Expression and functional role of bTRPC1 channels in native endothelial cells.

We have analyzed the expression and localization of bovine transient receptor potential-C1 (bTRPC1) in bovine aortic endothelial cells, and its possible involvement in the store-independent calcium influx induced by basic fibroblast growth factor (bFGF). RT-PCR experiments confirmed the existence of two btrpc1 mRNA isoforms; conversely, the btrpc3 gene was not transcribed. Anti-TRPC1 antibody revealed the presence of the protein in the membrane-rich compartment only. Application of anti-TRPC1 during the response to bFGF caused a partial but significant reduction of calcium entry. This is the first evidence of TRP channel involvement in a non-capacitative calcium influx induced by a biologically relevant agonist such as the angiogenic factor bFGF in native endothelial cells.

Alternative Splicing↗
PubMed1980

Effects of nifedipine on resistance vessels, arteries and veins in man.

1 The effect of nifedipine on peripheral blood vessels has been studied in man. 2 Nifedipine induced dilatation of the forearm resistance vessels when given either by local intra-arterial infusion or sublingually (10 mg). 3 Local infusion of the drug did not relax hand veins preconstricted by infusion of noradrenaline and neither local infusion nor sublingual administration prevented constriction mediated by the sympathetic nervous system. Nifedipine was, however, a potent inhibitor of hand vein contractions induced by high concentrations of potassium provided that the noradrenergic component of the response was suppressed by simultaneous infusion of phentolamine. 4 Sublingual nifedipine (10 mg) did not dilate the elbow collateral arteries. 5 The effects of nifedipine on peripheral blood vessels are similar, but not identical, to those of verapamil. The pattern of action, with dilatation of resistance vessels but not capacitance, resembles that of hydralazine rather than glyceryl trinitrate and this suggest that nifedipine may prove useful in the treatment of hypertension.

Adult↗
PubMed1996

A mathematical model of cytosolic calcium dynamics in human umbilical vein endothelial cells.

Important among the responses of endothelial cells are cytosolic free calcium transients. These transients are mediated by several factors, including blood-borne agonists, extracellular calcium, and fluid-imposed shear forces. The transients are characterized by a rapid rise followed by a plateau phase. A base mathematical model is presented that reasonably reproduces the measured calcium transient in cultured human umbilical vein endothelial cells responding to thrombin. Kinetic equations for receptor activation and calcium mobilization comprise the model. A graded response of intracellular free calcium to increasing concentrations of agonist is predicted. Also predicted is the elevation of the peak value and the plateau level by steady nonspecific leak of calcium across the plasma membrane. The influences of capacitative calcium entry, calcium-induced calcium release, and buffering by cytosolic proteins are investigated parametrically. The model predicts significant depletion of cellular calcium in response to agonist stimulation.

Buffers↗
PubMed1982

[Acute hemodynamic effects of prostacyclin in severe or malignant hypertension].

The antihypertensive effect of Prostacyclin (PGI2) was investigated in 7 patients with severe or malignant hypertension. Cardiac output (dilution method), arterial blood pressure and total blood volume (TBV, radio-albumin dilution method) were measured before and during a PGI2 infusion, the effective dose ranging from 10 to 20 ng/kg/min. Cardiac index(CI) rose from 2.8 to 3.9 1/min/m2 and heart rate (HR) from 75 to 94 beats/min (p less than 0.01) Mean blood pressure decreased from 154 to 120 mmHg (p less than 0.001) and total peripheral resistances from 4650 to 2540 dynes.s.cm-5 (p less than 0.001). The ratio: central blood volume/total blood volume increased from 0.21 to 0.26 (p less than 0.001). The results confirm that PGI2 produces a potent vasodilatation of the systemic compartment with a marked decrease in blood pressure; however the antihypertensive effect is blunted by the increase in CI mainly related to the increase in HR; significant central translocation of blood suggests that PGI2 does not produce dilatation of the capacitance vessels. Sympathetic nervous system is highly stimulated by PGI2 very likely through the baroreceptor system.

Antihypertensive Agents↗
PubMed1983

Factors modifying the early nondiuretic vascular effects of furosemide in man. The possible role of renal prostaglandins.

Animal experiments have suggested that salt-balance, prostaglandin synthesis, and renal function are important determinants of the nondiuretic vascular effects of furosemide. To investigate the influence of these factors in humans, we studied 10 normal volunteers and five anephric patients. The volunteers were studied on three occasions: when on a 10 mEq/day sodium diet, on a 250 mEq/day sodium diet, and on a 10 mEq/day sodium diet with indomethacin, 200 mg/day. The anephric patients were studied immediately after dialysis. Plethysmographic methods were used to measure venous capacitance and blood flow in the calf before, and at 5, 10, and 15 minutes after furosemide, 80 mg, iv. Blood was obtained before and 15 minutes after furosemide for determination of plasma renin activity by radioimmunoassay and of plasma 6-keto-prostaglandin F1 alpha by chromatography-mass spectrometry. We found that furosemide significantly increased venous capacitance in the calf of the normal volunteers on a low salt diet. Indomethacin, high salt intake, or lack of renal function was sufficient to inhibit this effect. Plasma renin activity increased only in the group that had the increase in venous capacitance. Limb blood flow decreased gradually in the 15 minutes following administration of furosemide in the normal volunteers, regardless of salt balance or indomethacin, but remained unchanged in the anephric patients. Plasma 6-keto-prostaglandin F1 alpha was less than 30 pg/ml in all samples. Indomethacin concentration averaged 1.3 micrograms/ml in volunteers on the drug. To determine whether indomethacin, salt intake or renal function affected another venodilator, we studied an additional group of normal and uremic volunteers who received 0.6 mg nitroglycerin sublingually.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗