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PubMed1994

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption.

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

Analysis of Variance↗
PubMed1985

Mechanisms of nitrate action in patients with severe left ventricular failure: conceptual problems with the theory of venosequestration.

Nitroglycerin and other organic nitrates exert a number of favorable effects on the circulation of patients with severe congestive heart failure, and these effects mediate the short- and long-term hemodynamic and clinical improvement that follows treatment with these drugs. Although these agents are potent dilators of systemic venous capacitance vessels, present evidence indicates that they do not exert their beneficial hemodynamic and clinical effects by decreasing venous return to the heart. Rather, their ability to dilate pulmonary and systemic resistance vessels offsets any decrease in cardiac output that might be expected to occur from a decrease in venous return. Of equal importance, the increase in output of the left side of the heart that results from drug-induced pulmonary and systemic vasodilation prevents any decrease in venous return to the right side of the heart that might be expected to accompany an increase in systemic venous capacitance. The net effect of these two interacting forces is not only to keep cardiac output and venous return constant but also to translocate blood volume from the pulmonary circulation and left ventricle to the systemic vessels. In addition, nitrates also relieve subendocardial ischemia and favorably alter pressure-volume relationships in the left ventricle. These observations support the conclusion that the complex cardiovascular responses to organic nitrates in patients with congestive heart failure cannot be adequately summarized by the single concept of preload reduction.

Arteries↗
PubMed1986

Pharmacological studies with SK&F 94120, a novel positive inotropic agent with vasodilator activity.

The pharmacological properties of SK&F 94120 on the cardiovascular system have been studied in laboratory animal species. The compound was shown to have positive inotropic activity on hearts from guinea-pig, cat, dog and marmoset in-vitro and in cat and dog in-vivo. These responses in-vivo occurred in association with minimal changes in heart rate. Positive inotropic activity was not caused by SK&F 94120 in rat or hamster hearts in-vitro, thereby indicating a species dependence in myocardial response. SK&F 94120 was shown to have vasodilator activity in cats in-vivo. Detailed studies carried out on anaesthetized cats indicated that the compound caused a balanced dilatation of both resistance and capacitance blood vessels. Haemodynamic studies in anaesthetized cats indicated that, as a consequence of the positive inotropic and vasodilator actions, SK&F 94120 causes significant increases in cardiac output and stroke volume. Studies in conscious dogs showed the compound to be active as a positive inotrope after oral administration. The above properties suggest that this compound possesses useful haemodynamic properties for the treatment of congestive heart failure.

Animals↗
PubMed2003

The volatile anesthetic isoflurane inhibits the histamine-induced Ca2+ influx in primary human endothelial cells.

UNLABELLED: Although isoflurane is a known vasodilator, the mechanism of isoflurane-induced vasodilation is not clear. One of the most important systems in this context is the nitric oxide (NO)-mediated vasodilation. The activity of this system is regulated by the agonist-induced Ca(2+) influx rather than Ca(2+) release from internal stores. A number of reports have studied the effect of volatile anesthetics on the cytoplasmic calcium concentration signaling in mammalian endothelial cells. However, similar studies using human endothelial cells are lacking. In this study, therefore, we investigated whether isoflurane affects the histamine-induced Ca(2+) influx in primary cultures of human endothelial cells. Using confocal laser scanning microscopy and cells loaded with the Ca(2+) indicator Fluo-3, we studied the effect of isoflurane on the plateau phase of the histamine-induced Ca(2+) influx, which is considered to be due to capacitative Ca(2+) entry. In addition, we measured the ion flux through capacitative Ca(2+) channels directly by using Mn(2+) ions, which, on entering the cell, quench the Fura-2 fluorescence. The results of these two methods were in close agreement and showed a dose-dependent inhibition of the capacitative Ca(2+) entry by isoflurane. Isoflurane apparently depresses NO-mediated vasodilation when the observed inhibition is not compensated for downstream of the endothelial NO synthase activation. IMPLICATIONS: In response to vasoactive agents, endothelial cells produce nitric oxide (NO), which relaxes the underlying smooth muscle cells. Inhaled anesthetics inhibit this system by an unknown mechanism. Using primary human endothelial cells, we showed that the anesthetic isoflurane depresses a Ca(2+) influx, which is responsible for the activation of the endothelial NO synthase.

Aminoquinolines↗
PubMed1999

Potentiation of Ca2+ signaling in endothelial cells by 11,12-epoxyeicosatrienoic acid.

Incubation of endothelium with an increased epoxyeicosatrienoic acid (EET) concentration specifically augments the endothelium-dependent relaxation ascribed to endothelium-derived hyperpolarizing factor in porcine coronary arteries (Weintraub et al., Circ Res 1997;81:258-267). Experiments were designed to test whether such sustained increased levels of EETs in the environment of endothelial cells alters Ca2+ signaling. Changes in cytosolic Ca2+ were monitored in cultured porcine aortic endothelial cells (PAECs) and in the human endothelial EA.hy926 cell line after incubation (or not) with 5 microM 11,12-epoxyeicosatrienoic acid (EET). Although the mobilization of intracellular Ca2+ induced by 2 microM thapsigargin was not affected significantly, EET treatment augmented the capacitative Ca2+ entry evoked by the Ca(2+)-ATPase) inhibitor in both cell types. Similar observations were obtained by using histamine as a stimulant in EA.hy926 cells. As assessed in PAECs, 2 micrograms/ml triacsin C, a known inhibitor of the incorporation of EETs into phospholipids, did not significantly affect the potentiating action of EETs on Ca2+ signaling in response to thapsigargin. However, in solvent-control cells, triacsin C significantly reduced both the mobilization of Ca2+ from intracellular stores and the capacitative Ca2+ entry provoked by thapsigargin. Thus the EET-potentiating effect overcomes the inhibitory action of triacsin C on Ca2+ signaling in endothelial cells. Taken together, these results demonstrate that sustained increases in EETs may amplify Ca2+ signaling. However, contrary to the EET-induced augmentation of endothelium-dependent relaxation in the porcine coronary artery, resistance of this novel action of EETs to triacsin C suggests that the mechanism involved does not depend on incorporation into phospholipids.

8,11,14-Eicosatrienoic Acid↗
PubMed1991

Effects of isradipine on peripheral hemodynamic reflex responses in mild-to-moderate essential hypertension.

In a randomized double-blind, placebo-controlled, crossover study of isradipine (5 mg twice daily), effects on peripheral hemodynamic reflex responses were studied in nine patients (mean age 48 years) at baseline and after six weeks of active treatment. Assessments included vital signs, resting blood flow in the calf and finger (using an electrocardiograph-triggered venous occlusion plethysmograph), reflex responses during isometric exercise and cold pressor resistance, and venous capacitance in the forearm and calf. Isradipine lowered systolic and diastolic blood pressure as well as mean arterial pressure in patients with mild-to-moderate essential hypertension without reflex tachycardia or venoconstriction. All of the reflex responses studied were attenuated. It is concluded that vasodilatation of the peripheral circulation induced by isradipine contributes partially to the blood pressure-lowering effect.

Adult↗
PubMed1997

Immunoglobulin light chain alters mesangial cell calcium homeostasis.

This study examined the hypothesis that certain immunoglobulin light chains directly altered mesangial cell calcium homeostasis. Intracellular Ca2+ concentration (intracellular [Ca2+]) signaling was determined in suspensions of rat mesangial cells using the acetoxymethyl ester of fura 2 with a calcium removal/replacement protocol. Pretreatment of cultured rat mesangial cells with a glomerulopathic kappa-light chain (gle) produced reversible dose- and time-dependent attenuation of ATP- and thrombin-evoked [Ca2+] transients (189 +/- 24 vs. 126 +/- 10 nM, P < 0.05 with ATP; 198 +/- 5 vs. 117 +/- 3 nM, P < 0.05 with thrombin) and capacitative calcium influx (199 +/- 14 vs. 142 +/- 17 nM, P < 0.05 for ATP; 252 +/- 19 vs. 198 +/- 18 nM, P < 0.05 for thrombin). Mesangial cells treated with gle and supplemented with myo-inositol (450 microM) did not demonstrate the attenuation of the ATP-evoked [Ca2+] transient and capacitative calcium influx. Gle also decreased mean [Ca2+] transient (80 +/- 7 vs. 56 +/- 1 nM, P < 0.05) and capacitative calcium influx (306 +/- 10 vs. 241 +/- 4 nM, P < 0.05) in response to thapsigargin, a Ca2+-adenosinetriphosphatase inhibitor. This inhibition was not reversed by exogenous myo-inositol. Another kappa-light chain (10 microg/ml) did not affect mesangial cell calcium signaling. Deranged mesangial cell calcium homeostasis by certain light chains may play a central pathogenetic role in glomerulosclerosis associated with deposition of immunoglobulin light chains.

Adenosine Triphosphate↗
PubMed1987

Efficacy of O-(beta-hydroxyethyl)-rutosides at high dosage in counteracting the unwanted activity of oral contraceptives on venous function.

In a double-blind study the effect of a high dosage of O-(beta-hydroxyethyl)-rutosides (HR) was tested in women taking oral contraceptives and suffering from venous insufficiency of the lower limbs. Ten patients were treated for 28 days with HR (3 g/day) and ten with a placebo. In basal conditions and after therapy, the symptoms of venous disorders and the venous function, by means of strain gauge plethysmography, was evaluated in both groups. The results showed an increase of venous capacitance and a reduction of venous tone in the subjects treated including those without symptoms in the lower limbs. The HR treatment resulted in a significant improvement of the venous function parameters and of the symptoms in lower limbs.

Adult↗
PubMed2004

Dynamic changes in expression of myosin phosphatase in a model of portal hypertension.

Myosin phosphatase is a target for signaling pathways that modulate calcium sensitivity of force production in smooth muscle. Myosin phosphatase targeting subunit 1 (MYPT1) isoforms are generated by cassette-type alternative splicing of exons in the central and 3' portion of the transcript. Exclusion of the 3' alternative exon, coding for the leucine zipper (LZ)-positive MYPT1 isoform, is associated with the ability to desensitize to calcium (relax) in response to NO/cGMP-dependent signaling. We examined expression of MYPT1 isoforms and smooth muscle phenotype in normal rat vessels and in a prehepatic model of portal hypertension characterized by arteriolar dilation. The large capacitance vessels, aorta, pulmonary artery, and inferior vena cava expressed predominantly the 3' exon-out/LZ-positive MYPT1 isoform. The first-order mesenteric resistance artery (MA1) and portal vein (PV) expressed severalfold higher levels of MYPT1 with predominance of the 3' exon-included/LZ-negative isoform. There was minor variation in the presence of the MYPT1 central alternative exons. Myosin heavy and light chain splice variants in part cosegregated with MYPT1 isoforms. In response to portal hypertension induced by PV ligature, abundance of MYPT1 in PV and MA1 was significantly reduced and switched to the LZ-positive isoform. These changes were evident within 1 day of PV ligature and were maintained for up to 10 days before reverting to control values at day 14. Alteration of MYPT1 expression was part of a complex change in protein expression that can be generalized as a modulation from a phasic (fast) to a tonic (slow) contractile phenotype. Implications of vascular smooth muscle phenotypic diversity and reversible phenotypic modulation in portal hypertension with regards to regulation of blood flow are discussed.

Animals↗
PubMed1989

Effects of topical treatment with H1 and H2 antagonists on clinical symptoms and nasal vascular reactions in patients with allergic rhinitis.

Fifteen asymptomatic subjects with allergic rhinitis participated in a double-blind, randomized, crossover, placebo-controlled study. The subjects were pretreated intranasally with a single dose of a selective H1 receptor antagonist, levocabastine, and/or selective H2 receptor antagonist, ranitidine, prior to a nasal allergen challenge. The nasal symptoms obtained at the challenge were assessed using a scoring technique 15 min after the allergen exposure. The nasal airway resistance was determined twice prior to and once after the allergen challenge using anterior rhinomanometry. The nasal mucosal blood flow was determined before and 15 min after allergen challenge using the 133Xe wash-out technique. After pretreatment with the H1 antagonist there was a statistically significant reduction in the number of sneezes and rhinorrhea compared to pretreatment with placebo. Pretreatment with the H2 receptor significantly decreased the rhinorrhea but not the sneeze. The nasal blockage was unaffected by both the H1 and the H2 antagonists. Pretreatment with the H1 and/or the H2 antagonists inhibited the reduction in the nasal mucosal blood flow induced by the allergen challenge to a significant degree. The present findings suggest that topical treatment with the highly selective histamine antagonist, levocabastine, inhibits allergen-induced reflex-mediated symptoms. H1 and H2 receptors do not appear to be involved in the regulation of the tone of the capacitance vessels. This indicates that a more complex mechanism participates in the induction of nasal blockage than the direct effect of histamine on H1 and H2 receptors on the capacitance vessels of the nasal mucosa alone. Both H1 and H2 receptors are of importance for the regulation of nasal mucosal blood flow during the allergic reaction.

Administration, Topical↗
PubMed1976

Mechanism of dilutional anemia in massive splenomegaly.

Twenty patients with anemia and massive splenomegaly were studied in order to elucidate the mechanism by which splenomegaly results in plasma volume expansion. In 18 patients, increased plasma volume accounted for most of the anemia. Fourteen patients had an exaggerated renin response to standing, mean 1967 +/- 613 (SE) ng angiotensin ll/100 ml plasma (p less than 0.05). The mean resting forearm blood flow was increased 3.47 +/- 0.32 (SE) ml/100 ml forearm tissue (p less than 0.001). The venous capacitance was normal, as contrasted to a marked decrease in venous capacitance in patients with anemia of comparable degree without splenomegaly. Cardiac indices were increased in 10 of 11 patients (range 4.1-8.1 liters/min/sq m). In nine of ten patients oxygen consumption was increased (range 147-231 ml/min/sq m). Splenectomy was performed on 14 patients. Splenic blood flow was elevated in four of four patients (range 750-2000 ml/min). Splenic A-V oxygen difference was exaggerated in seven of seven patients and in three of three patients splenic indocyanine-green dye dilution curve failed to show an early peak suggestive of A-V shunting in the spleen. Free portal pressure was elevated in 12 of 12 patients and decreased immediately after splenectomy. The intravascular albumin mass decreased in ten patients, was unchanged in three at 2-4 mo after splenectomy, and was accompanied by a rise in the plasma albumin concentration in nine. These data suggest that a flow-induced portal hypertension with expansion of the portal vascular space is an important early hemodynamic change. This finding, together with a decreased peripheral resistance, probably results in a decrease in effective intravascular volume, resulting in stimulation of the renin-angiotensin-aldosterone system and other renal hemodynamic changes necessary for salt and water retention. Splenectomy usually accomplishes a complete reversal of these abnormalities and correction of the anemia.

Anemia↗
PubMed1989

Endothelin is a potent long-lasting vasoconstrictor in men.

Endothelin, a 21-amino acid peptide synthesized by cultured porcine aortic endothelial cells, has recently been identified and shown to produce a potent and prolonged constriction of mammalian blood vessels in vitro. We have studied the effect of local infusion of this peptide on resistance and capacitance vessels of normal volunteers. Infusion of endothelin (5 pmol/min) reduced forearm blood flow by 39 +/- 7% from control observations. The maximum response was seen after approximately 55 min of infusion. After stopping the infusion, return of flow to basal values took approximately 120 min. This contrasts with the short onset and duration of action observed when angiotensin II was infused. During coinfusion studies, reversal by nicardipine (0.3-10 micrograms/min) occurred at similar concentrations in both endothelin-induced and angiotensin-induced flow reduction. This observation suggests that nicardipine nonspecifically antagonizes the flow-reducing effects of endothelin. A pattern of slow onset of constriction was found on local infusion of endothelin (5 pmol/min) into dorsal hand veins. During coinfusion of nicardipine (1.5 microgram/min), no reversal of endothelin-induced (5 pmol/min) constriction of dorsal hand veins occurred. The pharmacological profile of this peptide in the peripheral circulation of humans suggests that it may be involved in long-term regulation of vascular tone.

Adult↗
PubMed2004

A highly efficient electroporation method for the transfection of endothelial cells.

Several approaches have been described for improving transfection efficiencies of endothelial cells but the general observations have indicated that yields of transfected endothelial cells are low, irrespective of the techniques used. Here we describe a transfection procedure performed by means of electroporation, with efficiencies up to 85%, by optimizing several parameters such as the electroporation buffer, number of cells, voltage, capacitance and pulse length. The protocol was applied to three endothelial cell types (HUVECs, HUAECs and HMEC-1) commonly used in 'in vitro' angiogenic assays. We did not observe functional impairment between transfected and non-transfected cells in their adhesion to different components of the extracellular matrix, migration, or the development of capillary-like structures. Our experiments show that this electroporation procedure does not alter the physiology of endothelial cells and can be applied to functional studies, as exemplified by the successful transfection of the isoform 1 of calcipressin 1 (CALP1L).

Biological Assay↗
PubMed1999

Effect of hypercholesterolaemia on voltage-operated calcium channel currents in rabbit arterial smooth muscle cells.

Cholesterol is a major component of cell membranes and influences membrane fluidity. Watanabe heritable hyperpercholesterolaemic rabbits (WHHL) possess defective receptors for low density lipoprotein leading to increased plasma cholesterol, accumulation of cholesterol in the arterial wall and atherosclerosis. In this study calcium channel currents (IBa) were compared using conventional whole cell voltage clamp techniques in ear artery cells isolated from control New Zealand White rabbits (NZ) with those from WHHL. IBa were larger in cells isolated from NZ than from WHHL, however cell capacitance was also greater in NZ cells. Consequently, there was no significant difference in current density between NZ and WHHL cells either in the absence of drug or in the presence of the calcium channel agonist (+)202 791. Current voltage-relationships, kinetics of fast inactivation and steady-state inactivation of IBa also did not differ significantly between WHHL and NZ. These findings suggest that hypercholesterolaemia in WHHL has no direct effect on calcium channel current density or voltage-modulation in arterial smooth muscle cells.

Animals↗
PubMed2001

Partial HIF-1alpha deficiency impairs pulmonary arterial myocyte electrophysiological responses to hypoxia.

Chronic hypoxia depolarizes and reduces K+ current in pulmonary arterial smooth muscle cells (PASMCs). Our laboratory previously demonstrated that hypoxia-inducible factor-1 (HIF-1) contributed to the development of hypoxic pulmonary hypertension. In this study, electrophysiological parameters were measured in PASMCs isolated from intrapulmonary arteries of mice with one null allele at the Hif1a locus encoding HIF-1alpha [Hif1a(+/-)] and from their wild-type [Hif1a(+/+)] littermates after 3 wk in air or 10% O2. Hematocrit and right ventricular wall and left ventricle plus septum weights were measured. Capacitance, K+ current, and membrane potential were measured with whole cell patch clamp. Similar to our laboratory's previous results, hypoxia-induced right ventricular hypertrophy and polycythemia were blunted in Hif1a(+/-) mice. Hypoxia increased PASMC capacitance in Hif1a(+/+) mice but not in Hif1a(+/-) mice. Chronic hypoxia depolarized and reduced K+ current density in PASMCs from Hif1a(+/+) mice. In PASMCs from hypoxic Hif1a(+/-) mice, no reduction in K+ current density was observed, and depolarization was significantly blunted. Thus partial deficiency of HIF-1alpha is sufficient to impair hypoxia-induced depolarization, reduction of K+ current density, and PASMC hypertrophy.

Animals↗
PubMed1994

Effects of a novel dihydropyridine calcium antagonist on venous capacitance in Wistar-Kyoto rats.

Calcium antagonists are potent dilators of resistance vessels but do not dilate capacitance vessels. CD832 is a novel dihydropyridine calcium antagonist which has a nitrate moiety in its chemical structure. The authors examined the effects of CD832 on venous capacitance in anesthetized rats. Venous capacitance was assessed by measuring mean circulatory filling pressure (MCFP) at three levels of blood volume. Nitroglycerin decreased and phenylephrine increased MCFP. CD832 did not alter MCFP. After treatment with hexamethonium to prevent reflex venoconstriction, CD832 significantly decreased MCFP but nicardipine (another dihydropyridine calcium antagonist) did not. The magnitude of hypotension caused by CD832 and nicardipine was comparable. The results suggest that CD832 is a unique calcium antagonist which has a venodilator effect.

Animals↗
PubMed2004

Overexpression of TRPC1 enhances pulmonary vasoconstriction induced by capacitative Ca2+ entry.

Transient receptor potential (TRP) cation channels are a critical pathway for Ca2+ entry during pulmonary artery (PA) smooth muscle contraction. However, whether canonical TRP (TRPC) subunits and which TRP channel isoforms are involved in store depletion-induced pulmonary vasoconstriction in vivo remain unclear. This study was designed to test whether overexpression of the human TRPC1 gene (hTRPC1) in rat PA enhances pulmonary vasoconstriction due to store depletion-mediated Ca2+ influx. The hTRPC1 was infected into rat PA rings with an adenoviral vector. RT-PCR and Western blot analyses confirmed the mRNA and protein expression of hTRPC1 in the arterial rings. The amplitude of active tension induced by 40 mM K+ (40K) in PA rings infected with an empty adenoviral vector (647 +/- 88 mg/mg) was similar to that in PA rings infected with hTRPC1 (703 +/- 123 mg/mg, P = 0.3). However, the active tension due to capacitative Ca2+ entry (CCE) induced by cyclopiazonic acid was significantly enhanced in PA rings overexpressing hTRPC1 (91 +/- 13% of 40K-induced contraction) compared with rings infected with an empty adenoviral vector (61 +/- 14%, P < 0.001). Endothelial expression of hTRPC1 was not involved since the CCE-induced vasoconstriction was also enhanced in endothelium-denuded PA rings infected with the adenoviral vector carrying hTRPC1. These observations demonstrate that hTRPC1 is an important Ca(2+)-permeable channel that mediates pulmonary vasoconstriction when PA smooth muscle cell intracellular Ca2+ stores are depleted.

Adenoviridae↗
PubMed1991

[The effect of long-term venous hypertension on the macro- and microhemodynamics in the skeletal muscle].

Preliminary artificial venous hypertension of hindlimbs for 4-6 weeks was followed by comparison of resistive, capacitance and metabolic functions of the m. gastrocnemius' vessels performed in experimental and control cats with different levels of initial pressure of venous outflow. An increase of precapillary resistance, of the capillary filtration coefficient, a decrease of distensibility of the muscle venous bed, and constancy of postcapillary resistance and mean capillary pressure, were found in experimental animals. Mechanogenic responses of the muscle venous vessels to a rapid increase of the pressure in them were augmented in animals with chronic venous hypertension. The mechanisms of the effect of prolonged venous hypertension on functions of skeletal muscle's vessels, are discussed.

Animals↗