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PubMed2004

Effects of iptakalim hydrochloride, a novel KATP channel opener, on pulmonary vascular remodeling in hypoxic rats.

To investigate whether pulmonary artery remodeling could be prevented or not in hypoxic pulmonary hypertensive rats by treatment, the effects of iptakalim hydrochloride, a novel KATPCO, were evaluated. Iptakalim hydrochloride was orally administered at the doses of either 1.5 mg/kg/day or 0.75 mg/kg/day before their 4-week exposure to hypoxia (10% oxygen). It was demonstrated that iptakalim hydrochloride could reverse all pathological indices of pulmonary arterial remodeling and significantly reduce right ventricular hypertrophy in hypoxic rats. The reversal of hypoxic indices was dose-dependent, in which the higher dose of iptakalim hydrochloride reversed pathological indices more effectively than the lower dose did. This was further confirmed electrophysiologically using whole cell patch-clamp technique, which revealed that the outward potassium currents could be enhanced by iptakalim hydrochloride, and the decrease of K+ current density and increase of membrane capacitance could be reversed by chronic iptakalim hydrochloride treatment. These findings implied that iptakalim hydrochloride could play its role through activating plasmalemmal K+ channels of pulmonary arterial SMCs. The results indicated that iptakalim hydrochloride had anti-remodeling properties of pulmonary artery in hypoxic pulmonary hypertensive rats. It is therefore suggested that KATPCOs might be promising in the treatment of patients with hypoxic, and even possibly other forms of, pulmonary hypertension.

Analysis of Variance↗
PubMed1991

Effects of alpha,beta-methylene ATP on resistance and capacitance blood vessels of the cat intestinal circulation; a comparison with other vasoconstrictor agents and sympathetic nerve stimulation.

The autoperfused intestinal circulation of pentobarbitone anaesthetized cats was used to study the effects of alpha,beta-methylene ATP (1-100 micrograms i.a.) on pre-capillary resistance vessels and post-capillary capacitance (venous) blood vessels in comparison with other vasoconstrictor agents (also given i.a.) and the effects of sympathetic nerve stimulation (0.25-16 Hz). All cats were treated with atropine and propranolol. alpha,beta-Methylene ATP, noradrenaline and sympathetic nerve stimulation all caused dose- or frequency-dependent constriction of both resistance and capacitance vessels. alpha,beta-Methylene ATP was particularly active on capacitance vessels causing a greater constriction than either noradrenaline or sympathetic nerve stimulation. In comparison, angiotensin II and vasopressin caused a selective constriction of resistance vessels and prostaglandin F2 alpha a selective constriction of capacitance vessels. The results demonstrate that functional P2x purinoceptors are present on both arterial and venous blood vessels of the cat intestinal circulation.

Adenosine Triphosphate↗
PubMed1999

A non-capacitative pathway activated by arachidonic acid is the major Ca2+ entry mechanism in rat A7r5 smooth muscle cells stimulated with low concentrations of vasopressin.

1. Depletion of the Ca2+ stores of A7r5 cells stimulated Ca2+, though not Sr2+, entry. Vasopressin (AVP) or platelet-derived growth factor (PDGF) stimulated Sr2+ entry. The cells therefore express a capacitative pathway activated by empty stores and a non-capacitative pathway stimulated by receptors; only the former is permeable to Mn2+ and only the latter to Sr2+. 2. Neither empty stores nor inositol 1,4,5-trisphosphate (InsP3) binding to its receptors are required for activation of the non-capacitative pathway, because microinjection of cells with heparin prevented PDGF-evoked Ca2+ mobilization but not Sr2+ entry. 3. Low concentrations of Gd3+ irreversibly blocked capacitative Ca2+ entry without affecting AVP-evoked Sr2+ entry. After inhibition of the capacitative pathway with Gd3+, AVP evoked a substantial increase in cytosolic [Ca2+], confirming that the non-capacitative pathway can evoke a significant increase in cytosolic [Ca2+]. 4. Arachidonic acid mimicked the effect of AVP on Sr2+ entry without stimulating Mn2+ entry; the Sr2+ entry was inhibited by 100 microM Gd3+, but not by 1 microM Gd3+ which completely inhibited capacitative Ca2+ entry. The effects of arachidonic acid did not require its metabolism. 5. AVP-evoked Sr2+ entry was unaffected by isotetrandrine, an inhibitor of G protein-coupled phospholipase A2. U73122, an inhibitor of phosphoinositidase C, inhibited AVP-evoked formation of inositol phosphates and Sr2+ entry. The effects of phorbol esters and Ro31-8220 (a protein kinase C inhibitor) established that protein kinase C did not mediate the effects of AVP on the non-capacitative pathway. An inhibitor of diacylglycerol lipase, RHC-80267, inhibited AVP-evoked Sr2+ entry without affecting capacitative Ca2+ entry or release of Ca2+ stores. 6. Selective inhibition of capacitative Ca2+ entry with Gd3+ revealed that the non-capacitative pathway is the major route for the Ca2+ entry evoked by low AVP concentrations. 7. We conclude that in A7r5 cells, the Ca2+ entry evoked by low concentrations of AVP is mediated largely by a non-capacitative pathway directly regulated by arachidonic acid produced by the sequential activities of phosphoinositidase C and diacylglycerol lipase.

Animals↗
PubMed1977

Effects of prazosin on forearm resistance and capacitance vessels.

The effects of oral prazosin on the peripheral circulation were evaluated in 10 subjects, including 7 patients with chronic congestive failure due to coronary heart disease. To achieve this purpose the actions of 30 to 50 micrograms/kg body weight prazosin were assessed on both the forearm arteriolar and venous beds simultaneously with the use of the limb plethysmographic technique. Prazosin produced marked decline of forearm venous tone (FVT) from 44.5 +/- 12.3 to 14.3 +/- 3.1 mm Hg/ml (p less than 0.01) concomitant with marked decrease in forearm vascular resistance (FVR) from 70.2 +/- 11.4 to 48.4 +/- 4.9 mm Hg/ml/100 gm/min (p less than 0.05) which persisted for at least 60 mins without change in heart rate. These findings, demonstrating that prazosin induces systemic venodilation and peripheral arteriolodilation, indicate potential benefits of the oral drug for relief of pulmonary congestion and elevations of cardiac output in patients with chronic congestive heart failure.

Adult↗
PubMed1990

Effects of serotonin on vascular tone of isolated human placental chorionic veins.

Vasomotor effects of serotonin (5-hydroxytryptamine; 5-HT) were studied in isolated human placental chorionic veins in vitro. 5-HT produced marked contraction with a maximum of 89 +/- 5.05% of the K(+)-induced contractions. This response was specifically and competitively antagonized by ketanserin at doses of 10(-9) and 10(-8) M (pA2 = 9.65). Ketanserin, at concentrations up to 10(-7) M, induced noncompetitive inhibition of the contractions. These findings show a marked vasoconstrictor effect of 5-HT on the capacitance vessels of the human placenta, which suggests that this amine could play an important role as a mediator of fetal circulation. The possible therapeutic effect of ketanserin as a vasodilator to improve blood flow in the uteroplacental unit, is also discussed, based on the ability of this drug to block competitively 5-HT effects on chorionic veins.

Chorion↗
PubMed1988

[Vascular effects of nicergoline].

The vascular effects of nicergoline, a post-synaptic alpha receptor antagonist, were studied using a total haemodilution non pulsatile normothermic cardiopulmonary bypass with a bubble oxygenator during cardiac surgery. Anaesthesia was induced with fentanyl 30 micrograms.kg-1 and diazepam 0.25 mg.kg-1 and maintained with incremental doses of fentanyl. All the patients were intubated using pancuronium bromide (0.1 mg.kg-1) and artificially ventilated (FIO2 = 1). Nine patients randomly selected received 10 ml of saline (group 1) and 11 other 5 mg nicergoline (group 2) into the venous line of the extracorporeal circuit. Pump flow remained constant during 10 min. Arteriolar resistance was assessed by mean arterial pressure recording and venous capacitance by the level of venous reservoir. Statistical analysis was carried out using analysis of variance and the Newman-Keuls test. In group 1, arteriolar resistance increased by 17.0 +/- 21.8% at 10 min (not significant), whereas in group 2 it decreased by 22.8 +/- 8.1% at 2 min (p less than 0.05) and then increased slowly. It then remained 18% lower than in group 1 at 10 min. In group 1, venous capacitance decreased regularly by 1 ml.kg-1.min-1 during 10 min (-10.0 +/- 6.2 ml.kg-1 at 10 min), whereas in group 2 it decreased up to the 6th min (-4.2 +/- 3.3 ml.kg-1) and then remained stable, with a 5.4 ml.kg-1 difference with group 1 at 10 min (p less than 0.05). Therefore, nicergoline seemed to cause venoconstriction during cardiopulmonary bypass, possibly through a baroreflex mechanism.

Cardiac Surgical Procedures↗
PubMed1997

Bronchial blood vessel dimensions in asthma.

The extent to which the bronchial vasculature contributes to airway wall thickening in large and small airways in patients with asthma is unknown. The aim of this study was to quantify the number and the area occupied by blood vessels in the airway submucosa of patients with and without asthma. We used the monoclonal antibody Factor VIII to measure the blood vessels between the airway basement membrane and the outer border of the smooth muscle. In large cartilaginous airways in patients with fatal asthma, the number and area of large blood vessels were increased and the number and area of small blood vessels were decreased, compared with that in patients with nonfatal asthma and control subjects. However, the total number of blood vessels and the total area occupied by blood vessels per square millimeter in the airway submucosa were similar in patients with fatal asthma or nonfatal asthma and in control subjects in all airway size groups. Blood vessels were distended to a mean value of 80% of their estimated maximal area. The increased number of larger vessels in patients with fatal asthma raises the possibility that vascular congestion associated with an acute severe asthma attack may distend blood vessels. The finding of similar numbers of blood vessels per square millimeter of submucosa in control subjects and in patients with asthma suggests that blood vessels increase in number in patients with asthma only in proportion to increased airway wall area. It is unlikely that submucosal vessels could act as capacitance vessels and significantly alter inner airway wall thickness.

Adult↗
PubMed1984

Cardiovascular studies in rats with respect to some functional and structural relationships of relevance in hypertension and ordinary aging.

Five current lines of cardiovascular studies in rats are outlined, mainly dealing with some functional and structural relationships of particular relevance for hypertension and ordinary aging: 1. Characteristics of the smooth muscles and their neurogenic control in 'Windkessel' arteries, conduit arteries, precapillary resistance vessels and venous capacitance vessels from normotensive rats (WKY) with comparisons to rats with primary hypertension (SHR). 2. Different types of structural renovascular adaptation, comparing aging with advancing SHR hypertension, with 'high-pressure' and 'low-pressure' kidneys in one-clip, two-kidney renal hypertension, and with hypertrophied kidneys in uni-nephrectomized normotensive rats. 3. Relationships between 'structural autoregulation', wall distensibility, vascular reactivity and smooth muscle sensitivity in SHR and WKY hindquarter resistance vessels along with aging. 4. Relationships between wall thickness, luminal dimension and contractility in left ventricles from SHR and WKY during aging, and when one-clip, two-kidney hypertension is superimposed. 5. Interference with the capacity of the neurohormonal mechanisms counteracting blood loss in rats when on chronic low-salt diet.

Aging↗
PubMed2003

Ca2+-independent phospholipase A2 is a novel determinant of store-operated Ca2+ entry.

Store-operated cation (SOC) channels and capacitative Ca(2+) entry (CCE) play very important role in cellular function, but the mechanism of their activation remains one of the most intriguing and long lasting mysteries in the field of Ca(2+) signaling. Here, we present the first evidence that Ca(2+)-independent phospholipase A(2) (iPLA(2)) is a crucial molecular determinant in activation of SOC channels and store-operated Ca(2+) entry pathway. Using molecular, imaging, and electrophysiological techniques, we show that directed molecular or pharmacological impairment of the functional activity of iPLA(2) leads to irreversible inhibition of CCE mediated by nonselective SOC channels and by Ca(2+)-release-activated Ca(2+) (CRAC) channels. Transfection of vascular smooth muscle cells (SMC) with antisense, but not sense, oligonucleotides for iPLA(2) impaired thapsigargin (TG)-induced activation of iPLA(2) and TG-induced Ca(2+) and Mn(2+) influx. Identical inhibition of TG-induced Ca(2+) and Mn(2+) influx (but not Ca(2+) release) was observed in SMC, human platelets, and Jurkat T-lymphocytes when functional activity of iPLA(2) was inhibited by its mechanism-based suicidal substrate, bromoenol lactone (BEL). Moreover, irreversible inhibition of iPLA(2) impaired TG-induced activation of single nonselective SOC channels in SMC and BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid)-induced activation of whole-cell CRAC current in rat basophilic leukemia cells. Thus, functional iPLA(2) is required for activation of store-operated channels and capacitative Ca(2+) influx in wide variety of cell types.

Animals↗
PubMed1997

[Electron microscopy studies of vascular innervation of nasal mucosa in the human].

BACKGROUND: The distribution of neural structures in human nasal vasculature is still not completely understood. To date, immunocytochemical and histochemical studies of the innervation pattern and neurotransmitter distribution have only been performed using light microscopy. The aim of this study was to verify these results by electron microscopy and to obtain new knowledge of the innervation of the individual vessel types. The target was to determine the role of the different vessels in the swelling mechanism in human nasal mucosa. MATERIAL AND METHODS: Specimens were prefixed in glutaraldehyde and postfixed in osmium tetroxide. After dehydration they were embedded in araldite. Ultrathin sections were cut, contrasted with uranylacetate and lead citrate, and studied under EM. RESULTS: Nasal vasculature is controlled by a dense innervation. Amyelinated longitudinal nerve bundles and smaller axon conglomerates are detected in the arterial adventitia. Capacitance vessels (veins) in general show few nerve structures, which, in contrast to arteries, are also located between the smooth muscle cells. Cushion veins, however, reveal a stronger innervation pattern especially in their muscular swelling. In contrast to smaller arterioles, no axons can de demonstrated in capillaries. CONCLUSION: The density of innervation in arteries and cushion veins seems to indicate that these vessel types are the central neural control point for the swelling mechanism in human nasal mucosa. Capillary function, however, does not seem to be directly influenced by the autonomic nervous system.

Arteries↗
PubMed1982

Hemodynamic effects of diuretics in patients with marked peripheral edema and mild hypertension.

Hypertension develops in about 10% to 50% of patients with nephrosis or cirrhosis and peripheral edema, but the hemodynamic mechanism of the hypertension and its reversal by diuretic therapy has not been elucidated. In eight patients with marked edema and mild hypertension, diuretics (furosemide and spironolactone) decreased mean arterial pressure because of concurrent decrease in cardiac output and total peripheral resistance. Neither total blood volume nor plasma volume were decreased by the diuretics and the decrease in body weight was therefore attributed to the decrease in interstitial fluid volume. This, in turn, resulted in increased venous capacitance (as can be judged from the diuretic-induced decrease in the ratio of cardiopulmonary blood volume/total blood volume).

Adult↗
PubMed1992

Asthma. Tracheobronchial vasculature.

The tracheobronchial vasculature consists of a subepithelial capillary network and a deeper system of blood sinuses or capacitance vessels. There seem to be no arteriovenous anastomoses. Sympathetic nerves constrict the vasculature by the transmitters noradrenaline and neuropeptide-Y, parasympathetic nerves dilate it by acetylcholine and vasoactive intestinal polypeptide, and sensory nerves release neuropeptides including substance P that are dilator. Most inflammatory mediators are also vasodilator. In asthma there is mucosal vasodilation due to the direct action of mediators on vascular smooth muscle, neuropeptides released by axon reflexes in sensory nerve receptors, and possibly reflex vasodilation due to stimulation of sensory nerves. The vasodilation increases the thickness of the mucosa, both by vascular engorgement and by increased interstitial liquid volume. This mucosal thickening will narrow the airways and increase the rigidity of their walls. The vascular bed is also dilated by cold and hyperosmolality, and this change may be a component of the bronchoconstriction due to hyperventilation, inhalation of cold air and exercise. Changes in mucosal blood flow influence the uptake of chemical agents from the lumen, and the success of aerosol therapy in asthma may to some extent depend upon the influence of mucosal blood flow.

Animals↗
PubMed2002

Theoretical analysis of the noncardiac limits to maximum exercise.

When right atrial pressure (Pra) is greater than zero (atmospheric pressure), cardiac output is determined by the intersection of two functions, cardiac function and return function, which is used here to mean the determinants of venous return. When Pra < or = 0, flow is only determined by circuit function. The objective of this analysis was to determine the potential changes in return function that need to occur to allow the maximum cardiac output during exercise when Pra < or = 0 or is constant. The analysis expands on the model of Green and Jackman and includes the effects of changes in circuit parameters, including venous resistance, changes in capacitance, and muscle contractions. The analysis is based on the model of the circulation proposed by Permutt and co-workers, which assumes that the systemic circulation has two lumped compliant regions in parallel with independent inflow and outflow resistances. Changes in total flow in this model can come about by changes in the distribution of flow between the regions, recruitment of unstressed vascular volume, and changes in the regional venous resistances. The data for the analysis are from previous animal studies and are normalized to a 70-kg man. The major conclusions are that, to achieve the high cardiac output that occurs at peak exercise, there need to be marked changes in the distribution of blood flow, recruitment of unstressed volume, and the venous resistance draining vascular beds. A consequence of the increase in peripheral flow is a marked increase in pressure in the veins of the working muscle. Muscle contractions are potentially a very important mechanism for transiently decreasing this pressure and preventing excessive filtration of plasma during exercise.

Animals↗
PubMed1991

Diastolic coronary resistance and capacitance are independent of the duration of diastole.

Systolic myocardial contraction may produce changes in coronary resistance and capacitance that persist throughout a normal diastole. In addition, coronary resistance and capacitance as determined in the arrested heart may not accurately describe normal diastolic behavior. To evaluate these possibilities, an identification method capable of characterizing the input impedance of the coronary circulation in as little as 150 ms was developed. Using this method, coronary dynamics were measured during early and late diastoles in the beating heart with tone intact as well as during adenosine-induced maximal vasodilation. Coronary dynamics were also measured in the arrested heart during maximal vasodilation. With vasomotor tone intact, the parameters of a lumped model of the coronary circulation showed no variation from early to late diastole. During maximal vasodilation, model parameters also showed no variation from early to late diastole. Parameters in the arrested heart were not statistically different from those of the beating heart during maximal vasodilation. However, model parameters determined during maximal vasodilation were significantly different from those determined with tone intact. These results suggest that although coronary resistance and capacitance are dependent on vasomotor tone, they remain constant throughout diastole and remain similar in the arrested heart.

Animals↗
PubMed2005

Sphingosylphosphorylcholine-induced vasoconstriction of pulmonary artery: activation of non-store-operated Ca2+ entry.

OBJECTIVE: Sphingosylphosphorylcholine (SPC) is an important lipid mediator that has been implicated in vascular disease. As it has not been studied in the pulmonary circulation, we examined its mechanisms of action in rat small intrapulmonary arteries (IPA). METHODS: IPA were mounted on a myograph for recording tension and intracellular Ca2+ concentration ([Ca2+]i). Ca2+ sensitisation was examined in alpha-toxin permeabilized IPA, and by Western blot analysis of MYPT1 phosphorylation. RESULTS: SPC induced a slow but powerful vasoconstriction in IPA associated with an elevation in [Ca2+]i, with an EC50 for vasoconstriction of 12+/-2 microM. Removal of extracellular Ca2+ increased the EC50 to 76+/-33 microM (p<0.01) and abolished the rise in [Ca2+]i. Endothelial denudation or inhibition of NO synthase with L-NAME enhanced vasoconstriction. Treatment with pertussis toxin or the PLC inhibitor U731223 had no effect on SPC-induced vasoconstriction. The Rho kinase inhibitor Y27632 reduced SPC-induced vasoconstriction by approximately 70% and abolished both SPC-induced Ca2+ sensitisation in permeabilized IPA and the associated increase in MYPT1 phosphorylation; Ca2+ sensitisation was substantially inhibited by GDPbetaS. La3+ and 2-APB, at concentrations previously shown to block capacitative Ca2+ entry in IPA, suppressed SPC-induced vasoconstriction to the same extent as removal of extracellular Ca2+; residual tension was abolished by Y27632. Diltiazem was relatively ineffective. 2-APB also abolished the SPC-induced rise in [Ca2+]i. However, treatment with thapsigargin to empty intracellular stores had no effect on the elevation of [Ca2+]i induced by SPC. CONCLUSION: We present evidence that SPC is a powerful vasoconstrictor of IPA and the novel finding that SPC-induced vasoconstriction in IPA is dependent on activation of a Ca2+ entry pathway with a similar sensitivity to La3+ and 2-APB as capacitative Ca2+ entry, although its activation is not dependent on emptying of PLC/IP3 or thapsigargin-sensitive intracellular stores.

Amides↗