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PubMed1991

[Effects of lidocaine on arterial and venous circulation of limbs in man].

The effects of intravenous lidocaine on limb arteries and veins were investigated in a placebo-controlled study. Seven young healthy volunteers, 23 to 28-years-old, were included. Electrocardiogram, arterial pressure and arm and leg blood flows were recorded continuously. Systolic and diastolic blood pressures were measured in the left arm by finger photoplethysmography. Limb blood flow and the limb venous system were studied by venous occlusive plethysmography. The venous parameters studied were venous tone, lowest closing pressure, venous volume at 30 mmHg, and venous distensibility. After an initial bolus of 1.5 mg.kg-1 lidocaine had been given, 30, and then 60, micrograms.kg-1.min-1 were given for one hour each. Plasma noradrenaline and serum lidocaine titres were measured before giving the lidocaine, and at the end of each one hour period. Placebo consisted in a two hour infusion of 0.25 ml.min-1 normal saline. Lidocaine titres were 1.64 +/- 0.40 microgram.ml-1 after one hour, and 2.55 +/- 0.69 microgram.ml-1 after two hours. Lidocaine increased vascular resistances in both the forearm (+81% to +93%) and the calf (+38% to +57%). There was a concomitant increase in mean arterial blood pressure (+21% to +28%) without any change in heart rate. There was a significant dose-dependent increase in plasma noradrenaline levels during the second period of the lidocaine infusion with respect to the preinfusion period and the same period during the placebo infusion. Venous capacitance measured before any infusion had been started was greater in the leg than in the arm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1999

Calcium influx factor, further evidence it is 5, 6-epoxyeicosatrienoic acid.

We present evidence in astrocytes that 5,6-epoxyeicosatrienoic acid, a cytochrome P450 epoxygenase metabolite of arachidonic acid, may be a component of calcium influx factor, the elusive link between release of Ca2+ from intracellular stores and capacitative Ca2+ influx. Capacitative influx of extracellular Ca2+ was inhibited by blockade of the two critical steps in epoxyeicosatrienoic acid synthesis: release of arachidonic acid from phospholipid stores by cytosolic phospholipase A2 and cytochrome P450 metabolism of arachidonic acid. AAOCF3, which inhibits cytosolic phospholipase A2, blocked thapsigargin-stimulated release of arachidonic acid as well as thapsigargin-stimulated elevation of intracellular free calcium. Inhibition of P450 arachidonic acid metabolism with SKF525A, econazole, or N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide, a substrate inhibitor of P450 arachidonic acid metabolism, also blocked thapsigargin-stimulated Ca2+ influx. Nano- to picomolar 5, 6-epoxyeicosatrienoic acid induced [Ca2+]i elevation consistent with capacitative Ca2+ influx. We have previously shown that 5, 6-epoxyeicosatrienoic acid is synthesized and released by astrocytes. When 5,6-epoxyeicosatrienoic acid was applied to the rat brain surface, it induced vasodilation, suggesting that calcium influx factor may also serve a paracrine function. In summary, our results suggest that 5,6-epoxyeicosatrienoic acid may be a component of calcium influx factor and may participate in regulation of cerebral vascular tone.

8,11,14-Eicosatrienoic Acid↗
PubMed2000

K(+) channel inhibition, calcium signaling, and vasomotor tone in canine pulmonary artery smooth muscle.

We investigated the role of K(+) channels in the regulation of baseline intracellular free Ca(2+) concentration ([Ca(2+)](i)), alpha-adrenoreceptor-mediated Ca(2+) signaling, and capacitative Ca(2+) entry in pulmonary artery smooth muscle cells (PASMCs). Inhibition of voltage-gated K(+) channels with 4-aminopyridine (4-AP) increased the membrane potential and the resting [Ca(2+)](i) but attenuated the amplitude and frequency of the [Ca(2+)](i) oscillations induced by the alpha-agonist phenylephrine (PE). Inhibition of Ca(2+)-activated K(+) channels (with charybdotoxin) and inhibition (with glibenclamide) or activation of ATP-sensitive K(+) channels (with lemakalim) had no effect on resting [Ca(2+)](i) or PE-induced [Ca(2+)](i) oscillations. Thapsigargin was used to deplete sarcoplasmic reticulum Ca(2+) stores in the absence of extracellular Ca(2+). Under these conditions, 4-AP attenuated the peak and sustained components of capacitative Ca(2+) entry, which was observed when extracellular Ca(2+) was restored. Capacitative Ca(2+) entry was unaffected by charybdotoxin, glibenclamide, or lemakalim. In isolated pulmonary arterial rings, 4-AP increased resting tension and caused a leftward shift in the KCl dose-response curve. In contrast, 4-AP decreased PE-induced contraction, causing a rightward shift in the PE dose-response curve. These results indicate that voltage-gated K(+) channel inhibition increases resting [Ca(2+)](i) and tone in PASMCs but attenuates the response to PE, likely via inhibition of capacitative Ca(2+) entry.

4-Aminopyridine↗
PubMed1987

Characterization of capacitance-free pressure-flow relations during single diastoles in dogs using an RC model with pressure-dependent parameters.

Although previous studies have proposed a variety of models to characterize diastolic pressure-flow relations, the models' ability to predict capacitance-free pressure-flow relations from dynamic information in individual studies has not been determined. This study tested the ability of a lumped RC model with pressure-dependent parameters to predict diastolic capacitance-free flow during maximum vasodilation in anesthetized dogs. Model parameters were characterized by perturbing the circumflex coronary artery with a ramp pressure waveform that caused coronary artery pressure to decline at rates varying from 30-150 mm Hg/sec. Capacitance-free relations constructed from declining and rising ramp pressure-flow data corresponded with capacitance-free pressure-flow points constructed during constant-pressure coronary artery perfusion (which are model-independent). The model parameters derived from analysis of the ramp data indicate that conductance of the coronary bed varies directly with coronary pressure and is independent of the rate of coronary pressure decay. Values of coronary capacitance vary inversely with coronary artery pressure and with the magnitude of dPLC/dt. Thus, a simple, lumped diastolic model with pressure-dependent parameters can predict capacitance-free pressure-flow behavior from dynamic pressure-flow data and characterize model parameters over a wide range of coronary pressure.

Adenosine↗
PubMed1977

Hemodynamic effect of long--term treatment with pindolol in essential hypertension with special reference to the resistance and capacitance vessels of the forearm.

Ten patients with essential hypertension have been studied at rest, during and after exercise following oral treatment for on an average 16 months with a beta-adrenoreceptor blocking agent, pindolol. The study was a direct continuation of an earlier, performed after 2 months' treatment. The hypotensive effect of pindolol was highly significant after 2 as well as 16 months of treatment. Heart rate was similarly lowered at 2 and 16 months, while carciac output, which was significantly lower during exercise after 2 months, had increased to the pretreatment level after 16 months. Peripheral vascular resistance, which was not affected after 2 months, had decreased significantly during and after exercise in the long-term study. A comparison between the hemodynamic situations after 2 and 16 months thus suggests that while a decrease in cardiac output is an early mechanism in the lowering of BP, changes in systemic vascular resistance seem to be more important after long-term treatment with pindolol.

Administration, Oral↗
PubMed1989

Sympathetic vascular control of the pig nasal mucosa: adrenoceptor mechanisms in blood flow and volume control.

1. The adrenoceptor mechanisms influencing the total blood flow, volume and superficial blood flow in the nasal mucosa of pigs anaesthetized with pentobarbitone have been characterized by use of various agonists and antagonists. 2. Local intra-arterial bolus injection of the selective alpha 1-agonist phenylephrine, the selective alpha 2-agonist UK 14.304, the mixed alpha 1/alpha 2-agonist oxymetazoline and the mixed alpha/beta-agonists noradrenaline (NA) and adrenaline induced dosed-related reduction of nasal arterial blood flow (BF), nasal mucosal volume (V, reflecting capacitance vessel function) and the laser Doppler flowmetry signal (LDF, reflecting superficial movement of blood cells). The rank order of alpha-agonist potency regarding BF reduction was UK 14.304 greater than oxymetazoline greater than phenylephrine = adrenaline. For the volume response the potency order was UK 14.304 greater than oxymetazoline = NA = adrenaline greater than phenylephrine while for the reduction of the LDF signal the potency was UK 14.304 = NA = adrenaline greater than oxymetazoline greater than phenylephrine. The selective beta 2-agonist terbutaline caused dose-dependent increase of BF whereas only a small augmentation of the V was obtained upon the highest dose (40 nmol) while no modification of the LDF signal was observed. 3. After pretreatment with the selective alpha 1-antagonist prazosin, the response to phenylephrine was abolished while the selective alpha 2-antagonist idazoxan attenuated the effect of UK 14.304. After pretreatment with alpha-antagonists, both NA and adrenaline caused biphasic effects with constriction followed by vasodilatation for BF, but not for V or LDF. This vasodilatation was blocked by the beta-antagonist propranolol. 4. The reduction in nasal BF and V upon sympathetic nerve stimulation was attenuated both by prazosin and idazoxan. Propranolol enhanced the remaining reduction of BF but not of V in the presence of alpha-antagonists. 5. It is concluded that alpha 2-adrenoceptor mechanisms in the pig nasal mucosa are dominating for the BF, V and LDF responses to exogenous agonists. alpha 1-Adrenoceptors also seem to be involved in the sympathetic control of BF, V and LDF. Activation of beta 2-receptors increases mainly BF and does not influence the LDF signal.

Animals↗
PubMed1989

Application of electrocapacitography to investigation of cephalic and cerebral circulation in the rabbit.

Electrocapacitography devised for medical purposes by Hatakeyama was applied as a noninvasive volumetric method to investigate circulation in the rabbit head and brain. The effective electric capacitance was measured by means of a highly sensitive device. An electrocapacitogram (ECPG) of the head, considered to reflect the volume of intracranial as well as extracranial blood vessels, varied rhythmically with cardiac beat and respiratory movement. In general, the pulsatile variations of ECPG in synchronization with cardiac beat (ECPG pulse) bore a resemblance to arterial pulse. Occlusion of the common carotid artery caused the ECPG level corresponding to mean vascular volume to fall markedly and in most cases the amplitude of ECPG pulse was diminished. By rapid infusion of 5 ml of the blood into intracranial blood vessels via the internal carotid artery or into extracranial blood vessels via the external carotid artery, ECPG level was raised transitorily, the effect of extracranial infusion being larger than that of intracranial infusion. Stimulation of the central cut end of the cervical sympathetic nerve reduced ECPG level considerably. This response was greatly diminished by carotid occlusion and sometimes a temporary rise of ECPG was observed at the beginning of the stimulation. In several cases the effect was reversed completely by carotid occlusion and an increase of ECPG during the stimulation was observed. These findings suggest the existence of a sympathetic vasoconstrictor in the head as well as a sympathetic vasodilator of the brain, although in confirmation of this review further investigation is required. ECPG of the head is demonstrated to be a useful method for investigating circulation in the head including brain.

Animals↗
PubMed1994

Alterations of neutrophil responses to tumor necrosis factor alpha and interleukin-8 following human endotoxemia.

Interleukin-8 (IL-8), a neutrophil chemoattractant and activating cytokine, has been implicated as a proinflammatory mediator in gram-negative sepsis. In vitro data support the notion of IL-8 as an endothelial adherence inhibitor. To evaluate this issue, we infused six volunteers with reference endotoxin and measured plasma levels of IL-8, neutrophil tumor necrosis factor alpha (TNF-alpha) receptors, TNF-alpha-induced adherence to fibronectin, and neutrophil chemotaxis to IL-8 and other attractants. We found that, at 3 h postinfusion, IL-8 but not TNF-alpha plasma levels were elevated. Neutrophils had shed L-selectin (mean channel fluorescence decrease, 79 +/- 9 to 49 +/- 7; P = 0.0625) and TNF-alpha receptors (decrease in number of receptors per cell, 1,596 +/- 340 to 574 +/- 93; P = 0.004). Cells were chemotactically desensitized to IL-8. TNF-alpha-induced adherence to fibronectin was suppressed from 69% +/- 5% of the phorbol myristate acetate response to 38% +/- 7% (P = 0.0154). These findings support the notion that release of IL-8 into the vascular space may be an in vivo mechanism for suppression of neutrophil accumulation at extravascular sites. L-Selectin loss would reduce the ability of neutrophils to adhere to activated endothelial cells. The specific loss of migratory response to IL-8 would impair neutrophil delivery to areas where IL-8 was the predominant chemoattractant. Loss of TNF-alpha-induced adherence to fibronectin would blunt those responses, including production of oxidants, capacitated by adherence.

Endotoxins↗
PubMed1998

[The role of nitric oxide in reproduction].

Nitrix oxide (NO) is a highly reactive and short-lived radical (half-life time: 10-12 s), which is derived from L-arginine by the NO synthases (NOS) in several organ systems. The release of NO by endothelial cells leads to rapid relaxation of vascular smooth muscle cells, whereas release by several neuronal cells causes neurotransmission. When NOS is actively induced in immune cells or certain epithelia it causes cytotoxicity and/or apoptosis of these cells. In the reproductive organs NO is now considered to be an important trigger molecule for several physiological mechanisms. Follicular synthesized NO is involved in rupture of the follicle during ovulation. Moreover, NO participates in the acrosome reaction of spermatozoa during capacitation. Apoptosis and collagenolysis of the functional endometrium may be involved in endometrial shedding during menstruation. Since NO induces both apoptosis and collagenolysis, the newly discovered production of NO in late secretory endometrium could act as a key mechanism in the process of menstrual disintegration of the endometrium. Additionally, NO is necessary to support and maintain the decidualization process and plays a pivotal role in implantation.

Female↗
PubMed1989

Vascular pressure-volume relationships in pregnant and estrogen-treated guinea pigs.

We investigated the relationship between mean circulatory filling pressure (MCFP) and blood volume in nonpregnant (NP), estrogen-treated (E), and pregnant (P) guinea pigs. Reversible circulatory arrest was produced by rapid ventricular pacing or acetylcholine in unanesthetized animals remote from surgery. MCFP (mmHg) was higher for E (7.1 +/- 0.3) than for NP (5.8 +/- 0.5) or P (5.3 +/- 0.4). The gradient for venous return, the difference between MCFP and right atrial pressure (mmHg), did not differ in NP- (6.0 +/- 0.5), P- (5.8 +/- 0.5), or E- (5.8 +/- 0.4) treated animals. Capacitance, the blood volume (ml/kg) at an MCFP of 6 mmHg, was increased in P (84 +/- 6) and E (89 +/- 7), compared with NP (64 +/- 5) animals. Compliance, the ratio of the change in volume to change in pressure in the range of 6-12 mmHg (ml.kg-1.mmHg-1), was greater in P (4.4 +/- 0.3) than NP (3.5 +/- 0.3) animals. Hexamethonium blockade did not affect MCFP, capacitance, or compliance. We conclude that the effect of blood volume expansion on the circulation in pregnancy cannot be predicted from knowledge of MCFP-blood volume relationships in the nonpregnant animal, because capacitance and compliance are altered. Estrogen administration to nonpregnant animals reproduces some of these effects.

Animals↗
PubMed2006

Intravenous anesthetics inhibit capacitative calcium entry in pulmonary venous smooth muscle cells.

BACKGROUND: The authors have previously demonstrated that propofol attenuates capacitative calcium entry (CCE) via the protein kinase C signaling pathway in pulmonary artery smooth muscle cells (PVSMCs). The current goals were to determine whether CCE exists in PVSMCs; to assess the roles of the protein kinase C, tyrosine kinase (TK), and rho-kinase signaling pathways in regulating CCE; and to investigate the extent and cellular mechanisms by which intravenous anesthetics (thiopental, midazolam, ketamine, and propofol) alter CCE. METHODS: Primary cultures of fura-2-loaded canine PVSMCs were placed in a dish (37 degrees C) on an inverted fluorescence microscope. Intracellular Ca2+ concentration ([Ca2+]i) was measured as the 340/380 fluorescence ratio in individual PVSMCs. Thapsigargin, a sarcoplasmic reticulum Ca2+-adenosine triphosphatase inhibitor, was used to deplete intracellular Ca2+ stores after removing extracellular Ca2+. CCE was then activated by restoring extracellular Ca2+ (2.2 mm). RESULTS: Thapsigargin caused a transient increase in [Ca2+]i (160 +/- 6%). Restoring extracellular Ca2+ caused a rapid peak increase in [Ca2+]i (155 +/- 7% of baseline), followed by a sustained increase in [Ca2+]i (129 +/- 5% of baseline), i.e., CCE was stimulated in PVSMCs. Neither protein kinase C activation nor inhibition had an effect on CCE. rho-Kinase inhibition also had no effect on CCE, whereas TK inhibition attenuated both peak and sustained CCE. Thiopental, midazolam, ketamine, and propofol each attenuated both peak and sustained CCE. TK inhibition abolished the thiopental-, midazolam-, and ketamine-induced, but not the propofol-induced, decreases in CCE. CONCLUSION: Capacitative calcium entry is present in canine PVSMCs. Thiopental, midazolam, and ketamine attenuate CCE primarily via the TK signaling pathway. Propofol attenuates CCE via a TK-independent mechanism.

Anesthetics, Intravenous↗
PubMed2005

Hypoxic modulation of Ca2+ signaling in human venous endothelial cells. Multiple roles for reactive oxygen species.

The effects of hypoxia (pO2 approximately 25 mm Hg) on Ca2+ signaling stimulated by extracellular ATP in human saphenous vein endothelial cells were investigated using fluorimetric recordings from Fura-2 loaded cells. In the absence of extracellular Ca2+, ATP-evoked rises of cytosolic Ca2+ concentration ([Ca2+]i) because of mobilization from the endoplasmic reticulum (ER). These responses were reduced by prior exposure to hypoxia but potentiated during hypoxia. Hypoxia itself liberated Ca2+ from the ER, but unlike the effects of ATP this effect was not inhibited by blockade of the inositol trisphosphate receptor. By contrast, ryanodine blocked the effects of hypoxia but not those of ATP. Antioxidants abolished the effects of hypoxia but potentiated the effects of ATP. Inhibition of NADPH oxidase also augmented ATP-evoked responses but was without effect on hypoxia-evoked rises of [Ca2+]i. However, either uncoupling mitochondrial electron transport or inhibiting complex I markedly suppressed the actions of hypoxia yet exerted only small inhibitory effects on ATP-evoked rises of [Ca2+]i. Both hypoxia and ATP were able to activate capacitative Ca2+ entry. Our results indicate that hypoxia regulates intracellular Ca2+ signaling via two distinct pathways. First, it modulates agonist-evoked liberation of Ca2+ from the ER primarily through regulation of reactive oxygen species generation from NADPH oxidase. Second, it liberates Ca2+ from the ER via ryanodine receptors, an effect requiring mitochondrial reactive oxygen species generation. These findings suggest that local O2 tension is a major determinant of Ca2+ signaling in the vascular endothelium, a finding that is likely to be of both physiological and pathophysiological importance.

Adenosine Triphosphate↗
PubMed2000

Heart and lung support interaction--modeling and simulation.

Mechanical support of the lungs used to preserve life or during any kind of surgery may have an adverse effect on the cardiovascular system. Usually, positive pressure in alveoli diminishes lung perfusion, venous return and cardiac output. Positive pressure during the respiratory cycle is transfered into the thoracic space. The aim of this study was to assess how synchronization of the respirator with spontaneous breathing influences the distribution of pressure and ventilation in nonhomogeneous lungs and how it should influence hemodynamics. For this purpose a multicompartmental model of respiratory system mechanics was used in the electrical analog of a respirator-lung circuit, which enabled us to simultaneously simulate ventilatory support and spontaneous breathing. Mechanical properties of the respiratory system were modeled by lumped parameters: resistances and capacitances of constant values, independent of lung volume or inspiratory flow changes. A multicompartmental model of the respiratory system enabled us to simulate lung pathology characterized by non-homogeneity of the mechanical properties of the different parts of the lungs. The results of simulations presented in the paper enable us to conclude that lung volume increase, independent of the respirator-patient breathing synchronization, may be modeled as the increase in pulmonary vascular resistance and alveolar pressure increase, dependent on respirator-patient breathing synchronization, may be averaged by esophageous balloon measurements which show intrathoracic pressure changes.

Cardiovascular Physiological Phenomena↗
PubMed1981

[Embryonal histogenesis of endothelium].

Development of the mammalian vascular system is characterized by recapitulation of many morpho-functional signs peculiar to certain ancestral forms, as well as by certain aromorphous reorganizations reflecting in histogenesis of endothelium. Prior to the period of the common blood circulation in the mammalian embryos, the endothelium is developing within the endomesenchyme constructed by cells of a peculiar - endothelial - germ, but not of the endomesenchymal cells, as numerous investigators consider. The endothelium is developing as a capacitance tissue which presents by itself an epitheliomorphous duplex selective membrane, functionally connected with blood, tissue fluid and lymph in order metabolism and other functions of the organism's cells and tissues can be performed. Increase in cell number and their proendothelial derivatives at pretissue, tissue and hemoendothelial levels and successive union of recapitularities with the same name at the formation of the endothelial vessels add certain essential features to histogenesis of the endothelium and to its normal reactions. Polymerization and union of the recapitularities with the same name are the ways of integration; they are important ingredients of hereditarily determined differentiation. The latter is realized in the development of hemoendothelial offsprings which appear after the common blood circulation is started. The endothelial genesis in its capacitant form is complemented with blood cells incorporated, the means which is subjected to certain essential evolutional reorganizations. In its turn, this results in appearance of the double tissue hemoendothelial complex possessing features of an elementary organ.

Animals↗
PubMed1986

Comparison of the acute vascular effects of frusemide and bumetanide.

The acute peripheral vascular and diuretic effects of intravenous frusemide 10 mg and 20 mg were compared with those of bumetanide 250 micrograms and 500 micrograms in a group of 10 salt depleted volunteers. Significant reductions in forearm blood flow (FBF) were observed after frusemide 10 mg (-0.77 ml 100 ml-1 min-1 P less than 0.05) and 20 mg (-0.75 ml 100 ml-1 min-1 P less than 0.01 at 15 min). No changes were observed after bumetanide. The reductions in blood flow produced by frusemide were significantly different from those of bumetanide (P less than 0.05) at 15 min. Increases in venous capacitance (VC) and mean arterial blood pressure (MAP) were observed after frusemide but these differences were not statistically different from placebo or bumetanide. No increases were seen after bumetanide. Plasma aldosterone concentrations were unchanged after either drug but plasma renin activity (PRA) was increased after frusemide 10 mg (4.42 +/- 1.01----8.50 +/- 1.90 ng A I ml-1 h-1 P less than 0.01) and 20 mg (4.01 +/- 0.72----7.81 +/- 2.27 ng A I ml-1 h-1 P less than 0.05). No increases were observed after bumetanide and significant differences between bumetanide and frusemide were observed (P less than 0.01). This study demonstrates that the acute peripheral arterial effects of frusemide are not observed after comparable diuretic doses of bumetanide. The differences appear to be related to the ability of the drugs to stimulate acute renin release from the kidney.

Adult↗
PubMed1993

Regulation of cerebral blood flow--a brief review.

Cerebral blood flow is largely independent of perfusion pressure when autoregulation is intact. Cerebral circulation is regulated mainly by changes of vascular resistance. Resistance can be modulated by local-chemical and endothelial factors, by autacoids, and by release of transmitters from perivascular nerves. Local-chemical factors such as H(+)-, K(+)-, Ca(2+)-ions, adenosine, and osmolarity are involved in the regulation of cerebrovascular resistance during cortical activation and under pathological conditions such as hypoxia or ischaemia. Endothelial factors such as thromboxane A2, endothelin (ET), endothelium derived constrictor factor and endothelium derived relaxing (EDRF, identified as nitric oxide, NO) or hyperpolarizing (EDHF) factor, and prostacyclin (PGI2), can be released by physical stimuli such as shear stress or haemorrhage, by autacoids, by neurotransmitters, and by cytokines. Several of these factors (NO, PGI2, ET) can also be released from neurons and astrocytes thus enabling a coupling between parenchymal function and flow. Autacoids like histamine, bradykinin, eicosanoids, and free radicals influence cerebrovascular resistance, capacitance vessels and the permeability of the blood-brain barrier under pathological conditions. They are released by trauma, ischaemia, seizures and inflammation. Cerebral arteries are innervated by several systems. The sympathetic-noradrenergic fibres originate from the superior cervical ganglion. By releasing the constricting transmitters norepinephrine and neuropeptide Y this system extends the range of autoregulation. The parasympathetic cholinergic system with the dilating transmitters acetylcholine and vasoactive intestinal polypeptide may prevent ischaemia. Besides the intracerebral noradrenergic and serotonergic perivascular innervation with an unclear function, a trigeminal innervation has been described.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Differential involvement of N-type calcium channels in transmitter release from vasoconstrictor and vasodilator neurons.

1. The effects of calcium channel blockers on co-transmission from different populations of autonomic vasomotor neurons were studied on isolated segments of uterine artery and vena cava from guinea-pigs. 2. Sympathetic, noradrenergic contractions of the uterine artery (produced by 200 pulses at 1 or 10 Hz; 600 pulses at 20 Hz) were abolished by the N-type calcium channel blocker omega-conotoxin (CTX) GVIA at 1-10 nm. 3. Biphasic sympathetic contractions of the vena cava (600 pulses at 20 Hz) mediated by noradrenaline and neuropeptide Y were abolished by 10 nm CTX GVIA. 4. Neurogenic relaxations of the uterine artery (200 pulses at 10 Hz) mediated by neuronal nitric oxide and neuropeptides were reduced <50% by CTX GVIA 10-100 nm. 5. Capsaicin (3 microm) did not affect the CTX GVIA-sensitive or CTX GVIA-resistant neurogenic relaxations of the uterine artery. 6. The novel N-type blocker CTX CVID (100-300 nm), P/Q-type blockers agatoxin IVA (10-100 nm) or CTX CVIB (100 nm), the L-type blocker nifedipine (10 microm) or the 'R-type' blocker SNX-482 (100 nm), all failed to reduce CTX GVIA-resistant relaxations. The T-type channel blocker NiCl(2) (100-300 microm) reduced but did not abolish the remaining neurogenic dilations. 7. Release of different neurotransmitters from the same autonomic vasomotor axon depends on similar subtypes of calcium channels. N-type channels are responsible for transmitter release from vasoconstrictor neurons innervating a muscular artery and capacitance vein, but only partly mediate release of nitric oxide and neuropeptides from pelvic vasodilator neurons.

Animals↗
PubMed2006

Sex-related effects on venous compliance and capillary filtration in the lower limb.

Recent studies in humans have suggested sex differences in venous compliance of the lower limb, with lower compliance in women. Capillary fluid filtration could, however, be a confounder in the evaluation of venous compliance. The venous capacitance and capillary filtration response in the calves of 12 women (23.2 +/- 0.5 years) and 16 men (22.9 +/- 0.5 years) were studied during 8 min lower body negative pressure (LBNP) of 11, 22, and 44 mmHg. Calf venous compliance is dependent on pressure and was determined using the first derivative of a quadratic regression equation that described the capacitance-pressure relationship [compliance = beta1 + (2 x beta2 x transmural pressure)]. We found a lower venous compliance in women at low transmural pressures, and the venous capacitance in men was increased (P < 0.05). However, the difference in compliance between sexes was reduced and not seen at higher transmural pressures. Net capillary fluid filtration and capillary filtration coefficient (CFC) were greater in women than in men during LBNP (P < 0.05). Furthermore, calf volume increase (capacitance response + total capillary filtration) during LBNP was equivalent in both sexes. When total capillary filtration was not subtracted from the calf capacitance response in the calculation of venous compliance, the sex differences disappeared, emphasizing that venous compliance measurement should be corrected for the contribution of CFC.

Adult↗