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At least 235 records · Page 13Linked to original sources
PubMed1997

Decreased capacitance response with age in lower limbs of humans--a potential error in the study of cardiovascular reflexes in ageing.

The cardiovascular regulation in humans depends to a major extent on sympathetic reflexes originating from volume receptors in the arterial as well as the cardiopulmonary region. With experimental approaches, such as lower body negative pressure (LBNP) and tilting, signs of reduced efficiency with ageing have been shown. However, a confounding factor may be an age-related decline in venous capacitance response of the lower limbs, reducing the decrease in central blood volume and thus the deactivation of baro/cardiopulmonary receptors. This potential error was addressed in the present study. Central hypovolaemic stress was produced by LBNP 60 cmH2O in 10 young (mean age 23, range 20-25 years) and 10 old males (mean age 65, range 61-70 years). Changes in tissue volume of the calf were studied by strain gauge volumetric technique. Transmission of negative pressure to the calf muscle was studied in two young and two old volunteers. The haemodynamic response to hypovolaemic circulatory stress was attenuated in the old as compared with the young subjects, with a less marked increase in heart rate and peripheral resistance. Further, in the old subjects, the decrease in systolic blood pressure, pulse pressure and forearm blood flow was attenuated. Transmission of negative pressure to the calf was equal in both groups. The capacitance response was reduced with age from 2.27 +/- 0.14 to 1.64 +/- 0.13 mL 100 mL-1 (P < 0.005). However, the net capillary fluid filtration was unchanged. The reduced capacitance function might partly explain the declining reflex responses with age in humans, and thus seems to be of considerable importance when studying cardiovascular sympathetic reflex responses in ageing.

Adult↗
PubMed1998

Zaprinast, a type V phosphodiesterase inhibitor, dilates capacitance vessels in anaesthetised rats.

The effects of zaprinast (a type V phosphodiesterase inhibitor) on mean arterial pressure, heart rate, cardiac output, mean circulatory filling pressure, arterial and venous resistances were compared to those of sodium nitroprusside in three groups, each of intact or ganglion-blocked, Inactin-anaesthetised rats. In intact rats, zaprinast (1.5, 3.0 mg kg(-1) min(-1)) and sodium nitroprusside (8.0, 64.0,microg kg(-1) min(-1)) dose-dependently reduced mean arterial pressure and arterial resistance, but did not alter cardiac output and venous resistance. Both increased heart rate, with the effect of zaprinast less than that of sodium nitroprusside. Mean circulatory filling pressure was elevated by both doses of zaprinast but only the high dose of sodium nitroprusside. In rats given mecamylamine (3.7 micromol kg(-1), i.v. bolus) and noradrenaline (7.3 nmol kg(-l) min(-1)), zaprinast and sodium nitroprusside elicited dose-dependent reductions in mean arterial pressure, arterial and venous resistances, and mean circulatory filling pressure. Both increased cardiac output, with the effect of zaprinast greater than that of sodium nitroprusside at the low dose. Zaprinast but not sodium nitroprusside reduced heart rate. Our results indicate that zaprinast, similar to sodium nitroprusside, dilates both resistance and capacitance vessels in ganglion-blocked rats infused with noradrenaline to restore vasomotor tone. Zaprinast but not sodium nitroprusside has a direct, negative chronotropic effect on the heart.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2002

Role of short-term regulatory mechanisms on pressure response to hemodialysis-induced hypovolemia.

BACKGROUND: A large inter-subject variability exists in the arterial pressure response to hemodialysis-induced blood volume (BV) withdrawal. We investigated the hypothesis that this variability is due to the inter-subject differences in the short-term reflex capacity to compensate for hypovolemia. METHODS: Mean arterial pressure (MAP), heart rate (HR) and the percentage reduction in BV (%R-BV) were recorded in 32 subjects during their regular hemodialysis sessions. On the basis of absolute MAP changes between the beginning and the end of the session with respect to %R-BV at the end of the session, three distinct pressure responses were identified: (1) hypotension-prone response; (2) unstable response with delayed hypotension; and (3) hypotension-resistant response. For each kind of response, one patient was selected and a computer model of the cardiovascular system including the main short-term reflex compensatory mechanisms was used to analyze data collected over five consecutive sessions. The %R-BV and HR were used as model inputs, while simulated arterial pressure was fitted to the measured MAP by the tuning model parameters representing the efficiency in the control of venous capacity, microvascular resistance and heart inotropism. RESULTS: The model-based analysis related the hypotension-prone response to a lack of efficacy in capacity and resistance regulation. In the unstable response with delayed hypotension, the control of venous capacity was not effective and resistance control alone kept the pressure stable only for a limited %R-BV reduction (<5%). In the hypotension-resistant response, an efficient compensation of capacitance vessels was evidenced, and the slightly increasing arterial pressure was referred to a prevalence of cardiopulmonary pathway in the compensatory process. CONCLUSIONS: The model ascribes differences in pressure response to differences in the effectiveness of reflex compensatory mechanisms.

Adult↗
PubMed1998

[The capacitance function of vessels of the anterior vena cava region during depressor stimulus effects on the blood circulation system].

Depressing neurogenic and humoral (acetylcholine, papaverine and histamine) effects against the background of dilatation of arterial vessels were shown to exert different results: the former stimuli led to blood output from the veins, whereas humoral stimuli enhanced the depot role of the veins in animals. The smallest possible doses of acetylcholine did sometimes reduce the vessels' capacity.

Acetylcholine↗
PubMed1998

[Changes in resistance and capacitance functions of skeletal muscle vessels during the amplitude-frequency modulation of the perfusion blood flow].

Changes of venous outflow, pre- and postcapillary resistance of the skeletal muscle vessels were found to depend on values of amplitude and frequency of the perfusion blood flow in cats. Three types of the responses were distinguished: either increase, or decrease, or absence of them. The findings suggest a possibility to affect haemodynamic parameters with the aid of amplitude-frequency deviations in the organ blood flow.

Animals↗
PubMed1997

Haemodynamic effects of adrenomedullin in human resistance and capacitance vessels.

AIMS: The haemodynamic effects of adrenomedullin and calcitonin gene-related peptide (CGRP) were studied in resistance and capacitance vessels of healthy volunteers. METHODS: Adrenomedullin and CGRP were infused into the brachial artery of eight healthy subjects on two separate occasions at doses between 0.3-30 pmol min(-1). Forearm blood flow was measured using venous occlusion plethysmography. Venodilatation to adrenomedullin and CGRP was assessed in a further eight subjects by infusing the peptides at doses between 0.3-10 pmol min(-1) into a dorsal hand vein preconstricted with noradrenaline. Venodilator responses were measured as percentage reduction in noradrenaline preconstriction. RESULTS: Adrenomedullin and CGRP at a dose of 30 pmol min(-1), produced an increase in forearm blood flow of 288 +/- 42% and 252 +/- 30% respectively (mean +/- s.e. mean, P<0.001). At doses between 3 and 10 pmol min(-1) adrenomedullin was significantly more potent than CGRP. The vasodilatation to both peptides was of similar duration with a biological half-life of approximately 18 min. Adrenomedullin reversed constriction in dorsal hand veins by 84 +/- 2% (P<0.001) at a dose of 10 pmol min(-1). CGRP produced a similar effect reversing constriction by 72 +/- 12% at the same dose (P<0.01). In veins, adrenomedullin was also more potent than CGRP at doses between 0.3 and 3 pmol min(-1). CONCLUSIONS: The lowest dose of adrenomedullin producing significant arteriolar dilatation was calculated to produce plasma levels similar to those found in heart failure. These findings suggest that in pathophysiological conditions such as heart failure circulating levels of adrenomedullin may be within a range capable of influencing vascular resistance directly.

Adrenomedullin↗
PubMed2000

Constriction to ETB receptor agonists, BQ-3020 and sarafotoxin s6c, in human resistance and capacitance vessels in vivo.

AIMS: The aim of the study was to examine the effects of the ETB receptor selective agonists sarafotoxin S6c (SFTX6c) and BQ-3020 on the forearm resistance and capacitance vessels in healthy subjects in vivo. METHODS: The local response to intra-arterial or intravenous infusion of SFTX6c (5 pmol min-1) or BQ-3020 (50 pmol min-1) was assessed, on separate occasions, in eight healthy men (aged 20-28 years). Data (mean +/- s.e.mean) were examined by ANOVA. Results are expressed as percentage change from baseline at 90 min. RESULTS: SFTX6c and BQ-3020 reduced forearm blood flow, following local intra-arterial infusion (-25 +/- 7% and -27 +/- 7%, respectively; P < 0.001) and reduced hand vein diameter, following local intravenous infusion (-30 +/- 8% and -16 +/- 7%, respectively; P < 0.001). CONCLUSIONS: We have shown that locally active infusions of the selective ETB receptor agonists SFTX6c and BQ-3020 cause arterial constriction and venoconstriction in healthy human blood vessels in vivo. These results indicate that ETB receptor stimulation may mediate vasoconstriction in humans.

Adolescent↗
PubMedDate not supplied

Autonomic control of the venous system in health and disease: effects of drugs.

The venous system contains approximately 70% of the blood volume. The sympathetic nervous system is by far the most important vasopressor system in the control of venous capacitance. The baroreflex system responds to acute hypotension by concurrently increasing sympathetic tone to resistance, as well as capacitance vessels, to increase blood pressure and venous return, respectively. Studies in experimental animals have shown that interference of sympathetic activity by an alpha1- or alpha2-adrenoceptor antagonist or a ganglionic blocker reduces mean circulatory filling pressure and venous resistance and increases unstressed volume. An alpha1- or alpha2-adrenoceptor agonist, on the other hand, increases mean circulatory filling pressure and venous resistance and reduces unstressed volume. In humans, drugs that interfere with sympathetic tone can cause the pooling of blood in limb as well as splanchnic veins; the reduction of cardiac output; and orthostatic intolerance. Other perturbations that can cause postural hypotension include autonomic failure, as in dysautonomia, diabetes mellitus, and vasovagal syncope; increased venous compliance, as in hemodialysis; and reduced blood volume, as with space flight and prolonged bed rest. Several alpha-adrenoceptor agonists are used to increase venous return in orthostatic intolerance; however, there is insufficient data to show that these drugs are more efficacious than placebo. Clearly, more basic science and clinical studies are needed to increase our knowledge and understanding of the venous system.

Aging↗
PubMed1997

Capacitative calcium entry is inhibited in vascular endothelial cells by disruption of cytoskeletal microfilaments.

The role of an intact cytoskeleton for store-operated ('capacitative') Ca2+ influx was investigated in single cultured vascular endothelial cells. Capacitative Ca2+ entry was measured as changes of cytoplasmic Ca2+ concentration ([Ca2+]i) induced by depletion of Ca2+ stores with thapsigargin. In cells pretreated with cytochalasin D, an agent that disrupts the microfilament network of the cytoskeleton, as confirmed with FITC-phalloidin staining, capacitative Ca2+ entry was inhibited. Cytochalasin D did not affect basal [Ca2+]i nor ATP-induced increases of [Ca2+]i, indicating that release of Ca2+ from intracellular stores through the inositol-phosphate pathway was intact. These results suggest that microfilaments are an integral part of the mechanism for capacitative Ca2+ entry. The necessity for an intact cytoskeleton favors a conformational coupling model for store-operated Ca2+ influx.

Adenosine Triphosphate↗
PubMed2002

Capacitative Ca(2+) entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C.

1. Agonists increase endothelial cell intracellular Ca(2+), in part, by capacitative entry, which is triggered by the filling state of intracellular Ca(2+) stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca(2+) stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which affects the gating of membrane channels. As an axis involving the IP(3) receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the effects of the putative IP(3) receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca(2+) entry. 2. Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart. 3. 2APB (30 - 300 microM) inhibited Ca(2+) entry induced by both agonists (ATP 1 microM, bradykinin 0.1 microM) and receptor-independent mechanisms (thapsigargin 1 microM, ionomycin 0.5 and 5 microM). 2APB did not diminish endothelial cell ATP-induced production of IP(3) nor effect in vitro binding of [(3)H]-IP(3) to an adrenal cortex binding protein. Capacitative Ca(2+) entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca(2+) release phase was unaffected. 4. Similarly to 2APB, xestospongin C (3 - 10 microM) inhibited ATP-induced Ca(2+) release and capacitative Ca(2+) entry. Further, xestospongin C inhibited capacitative Ca(2+) entry induced by thapsigargin (1 microM) and ionomycin (0.5 microM). 5. The data are consistent with a mechanism of capacitative Ca(2+) entry in vascular endothelial cells which requires (a) IP(3) receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca(2+) release and entry pathways.

Actins↗
PubMed1997

Effects of natriuretic peptides and nitroprusside on venous function in trout.

Active venous regulation of cardiovascular function is well known in mammals but has not been demonstrated in fish. In the present studies, the natriuretic peptides (NP) rat atrial natriuretic peptide (ANP) and trout ventricular natriuretic peptide (VNP), clearance receptor inhibitor SC-46542, and sodium nitroprusside (SNP) were infused into unanesthetized trout fitted with pressure cannulas in the ventral aorta, dorsal aorta, and ductus Cuvier, and a ventral aorta (VA) flow probe was used to measure cardiac output (CO). In another group, in vivo vascular (venous) capacitance curves were obtained during ANP or SNP infusion. The in vitro effects of NP on vessels and the heart were also examined. ANP, VNP, and SC-46542 decreased central venous pressure (PVen), CO, stroke volume (SV), and gill resistance (RG), whereas systemic resistance (RS) and heart rate (HR) increased. Dorsal aortic pressure (PDA) transiently increased and then fell even though RS remained elevated. ANP decreased mean circulatory filling pressure (MCFP), increased vascular compliance at all blood volumes, and increased unstressed volume in hypovolemic fish. ANP had no direct effect on the heart. ANP responses in vivo were not altered in trout made hypotensive by prior treatment with the angiotensin-converting enzyme inhibitor lisinopril. SNP reduced ventral aortic pressure (PVA), PDA, and RS, increased CO and HR, but did not affect PVen, SV, or RG. SNP slightly decreased MCFP but did not affect compliance or unstressed volume. In vitro, large systemic arteries were more responsive than veins to NP, whereas SNP relaxed both. These results show that, in vivo, NP decrease venous compliance, thereby decreasing venous return, CO, and arterial pressure. Conversely, SNP hypotension is due to decreased RS. This is the first evidence for active regulation of venous capacitance in fish, which probably occurs in small veins or venules. The presence of venous baroreceptors is also suggested.

Animals↗
PubMed2002

Reciprocal regulation of capacitative and non-capacitative Ca2+ entry in A7r5 vascular smooth muscle cells: only the latter operates during receptor activation.

In A7r5 vascular smooth muscle cells, Arg(8)-vasopressin (AVP) stimulates phospholipase C leading to activation of two distinct Ca(2+) entry pathways. The capacitative Ca(2+) entry (CCE) pathway is activated by depletion of Ca(2+) stores, is permeable to Mn(2+), Ba(2+) and Ca(2+), and is selectively blocked by Gd(3+)(1 microM). A7r5 cells also express a non-capacitative Ca(2+) entry (NCCE) pathway, which is activated by arachidonic acid that is released by the sequential activities of phospholipase C and diacylglycerol lipase. This pathway is permeable to Sr(2+), Ba(2+) and Ca(2+) and selectively blocked by (R,S)-(3,4-dihydro-6,7-dimethoxy-isochinolin-1-yl)-2-phenyl-N,N-di[2-(2,3,4-trimethoxyphenyl)ethyl]acetamid mesylate ("LOE-908"). We use these selective tools to show that AVP, via the same signalling pathway that leads to activation of NCCE, also inhibits CCE and that the inhibition is not due to depolarization of the plasma membrane. Using the selective inhibitors to resolve the contributions of each Ca(2+) entry pathway during stimulation with AVP, we establish that reciprocal regulation of CCE and NCCE by arachidonic acid ensures that only NCCE is active in the presence of AVP, whereas CCE is active only after its removal. NCCE and CCE are therefore activated in a strict temporal sequence: NCCE first and then CCE. Because Ca(2+) passing through different Ca(2+) entry pathways can selectively regulate different responses, reciprocal regulation of CCE and NCCE may allow a stimulus to first evoke a response and then recruit actively a different response when the stimulus is removed.

Amino Acid Sequence↗
PubMedDate not supplied

A nonlinear model for myogenic regulation of blood flow to bone: equilibrium states and stability characteristics.

A simple compartmental model for myogenic regulation of interstitial pressure in bone is developed, and the interaction between changes in interstitial pressure and changes in arterial and venous resistance is studied. The arterial resistance is modeled by a myogenic model that depends on transmural pressure, and the venous resistance is modeled by using a vascular waterfall. Two series capacitances model blood storage in the vascular system and interstitial fluid storage in the extravascular space. The static results mimic the observed effect that vasodilators work less well in bone than do vasoconstrictors. The static results also show that the model gives constant flow rates over a limited range of arterial pressure. The dynamic model shows unstable behavior at small values of bony capacitance and at high enough myogenic gain. At low myogenic gain, only a single equilibrium state is present, but a high enough myogenic gain, two new equilibrium states appear. At additional increases in gain, one of the two new states merges with and then separates from the original state, and the original state becomes a saddle point. The appearance of the new states and the transition of the original state to a saddle point do not depend on the bony capacitance, and these results are relevant to general fluid compartments. Numerical integration of the rate equations confirms the stability calculations and shows limit cycling behavior in several situations. The relevance of this model to circulation in bone and to other compartments is discussed.

Arteries↗
PubMed1999

Dynamic regulation of [Ca2+]i by plasma membrane Ca(2+)-ATPase and Na+/Ca2+ exchange during capacitative Ca2+ entry in bovine vascular endothelial cells.

The dynamic regulation of Ca2+ extrusion by the plasma membrane Ca(2+)-ATPase (PMCA) and Na+/Ca2+ exchange (NCX) was investigated in single cultured calf pulmonary artery endothelial (CPAE) cells using indo-1 microfluorimetry to measure cytoplasmic Ca2+ concentration ([Ca2+]i). The quantitative analysis of the recovery from an increase of [Ca2+]i elicited by activation of capacitative Ca2+ entry (CCE) served to characterize kinetic parameters of these Ca2+ extrusion systems in the intact cell. In CPAE cells the PMCA is activated in a Ca(2+)- and time-dependent manner. Full activation of the pump occurs only after [Ca2+]i has been elevated for at least 1 min which results in an increase of the affinity of the pump for Ca2+ and an increase in the apparent maximal extrusion rate (Vmax). Application of calmodulin antagonists W-7 and calmidazolium chloride (compound R 24571) revealed that calmodulin is a major regulator of PMCA activity in vivo. Sequential and simultaneous inhibition of PMCA and NCX suggested that both contribute to Ca2+ extrusion in a non-additive fashion. The activity of one system is dynamically adjusted to compensate for changes in the extrusion rate by the alternative transporter. It was concluded that in vascular endothelial cells, the PMCA functions as a calmodulin-regulated, high-affinity Ca2+ removal system. The contribution by the low-affinity NCX to Ca2+ clearance became apparent at [Ca2+]i > approximately 150 nM under conditions of submaximal activation of the PMCA.

Animals↗