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At least 865 records · Page 48Linked to original sources
PubMed1999

Troglitazone inhibits the capacitative Ca2+ entry in endothelial cells.

To investigate the effects of troglitazone on the capacitative Ca2+ entry, we monitored changes in cytosolic Ca2+ concentrations ([Ca2+]i) induced by thapsigargin in fura-2-loaded porcine endothelial cells in situ and in primary culture. In aortic valve endothelial cells in situ, thapsigargin induced sustained elevation of [Ca2+]i. Both troglitazone and SKF 96365 inhibited the steady state increase in [Ca2+]i in a concentration-dependent manner. At 30 microM, troglitazone and SKF 96365 inhibited the [Ca2+]i elevation to 19.4 +/- 3.6% and 43.9 +/- 4.5%, respectively. In aortic endothelial cells in primary culture, both troglitazone (10 microM) and SKF 96365 (100 microM) completely inhibited the thapsigargin-induced [Ca2+]i increase. The EC50 value of troglitazone (1.4 +/- 0.1 microM) was lower than that of SKF 96365 (10.0 +/- 3.3 microM). We suggest that troglitazone would be a useful tool to investigate the capacitative Ca2+ entry.

Adenosine Triphosphate↗
PubMed1992

Differing actions of endothelin-1 on canine systemic resistance and capacitance vessels.

In anesthetized open-chest dogs, an intravenous bolus injection of endothelin-1 (ET-1, 400 pmol/kg) caused transient hypotension (initial hypotensive phase; phase 1), followed by a continuous elevation of blood pressure (late hypertensive phase; phase 2). The constriction and dilation of the systemic capacitance and resistance vessels were evaluated from the change in mean circulatory pressure (MCP) and in total peripheral resistance (TPR) in phases 1 and 2. To examine the modification of the action of ET-1 on the blood vessels by the baroceptor reflex or by the endothelium-derived relaxing factor (EDRF) released by ET-1 in phase 1, we performed experiments in dogs under total spinal anesthesia (TSA group), methylene blue-treated dogs (MB group) as well as in the untreated dogs (control group). ET-1 decreased the TPR significantly, and increased the MCP significantly in phase 1 in the control (n = 8) and TSA (n = 8) groups; there was no difference between the groups. ET-1 had no significant effect on TPR but increased the MCP significantly in MB group (n = 8) during phase 1. The percentage increase of MCP in the MB group significantly exceeded that of the control group. ET-1 increased both the TPR and MCP significantly in phase 2 in the control group (n = 8). This study indicated that the vasoconstrictor action of ET-1 on the systemic capacitance vessels in phase 1 did not result from a baroceptor reflex, and that the vasodilator action of ET-1 on the systemic resistance vessels may be at least in part mediated via EDRF released by ET-1. We suggest that the vasoconstrictor action of ET-1 on the systemic capacitance vessels is strong, but the vasodilator action of EDRF on the systemic capacitance vessels is weak.

Animals↗
PubMed2005

Trans- and cis-resveratrol increase cytoplasmic calcium levels in A7r5 vascular smooth muscle cells.

The effects of trans- and cis-resveratrol on cytosolic Ca2+ concentration ([Ca2+]i) were studied using fura-2 in vascular smooth muscle cells (A7r5). Both isomers of resveratrol caused a sustained elevation in [Ca2+]i, cis-resveratrol being significantly more effective than the trans-isomer. The resveratrol-induced increase in [Ca2+]i was significantly potentiated by the previous application of low concentrations of thapsigargin, partially inhibited by nifedipine or Ni2+, and not affected by SKF 96365. In the absence of extracellular Ca2+, both isomers of resveratrol induced a transient, slow increase in [Ca2+]i, which was inhibited by the previous depletion of intracellular stores with thapsigargin and completely blocked by preincubation with TMB-8, an inhibitor of intracellular calcium release. Reintroduction of Ca2+ in the external solution after the resveratrol-induced release of Ca2+ activated the Ca2+ influx through store-operated calcium channels. The resveratrol-induced increase in [Ca2+]i in the absence of extracelullar Ca2+ partially reduced the increase in [Ca2+]i evoked by the subsequent application of thapsigargin. Our results suggest that trans- and cis-resveratrol induce a depletion of Ca2+ from the same intracellular stores released by thapsigargin and subsequent capacitative influx of Ca2+. Additionally, a direct activation of transmembrane Ca2+ influx through another type of channel may be also implicated.

Animals↗
PubMed1985

[Resistance, exchange and capacitance vessels of the skeletal musculature in acute hypoxic hypoxia].

In cats under conditions of autoperfusion of hemodynamically isolated m. gastrocnemius, acute hypoxia (10% O2 in nitrogen) increased the precapillary and decreased the postcapillary resistance, reduced the capillary hydrostatic pressure and induced shifts of the capillary filtration coefficient (CFC) by 30% on the average. In cross-circulation performed for analysis of the neurogenic component in the vascular responses, analogous changes of the above parameters were revealed, the CFC decreasing, however. In denervated vascular bed of the m. gastrocnemius, the acute hypoxia decreased the precapillary and increased the postcapillary resistance, the hydrostatic pressure and the CFC increasing. In decentralized vessels of skeletal muscle, hypoxia induced prevalence of filtration while absorption of fluid prevailed in perfusion of the preparation with donor's arterial blood and in recipient's hypoxia.

Acute Disease↗
PubMed1996

Neuroimaging for differentiating vascular from Alzheimer's dementias.

Recent advances in the clinical and neuroimaging features of vascular dementia (VAD) versus Alzheimer type dementia (DAT) are described. The lacunar type of VAD, which is often accompanied by silent strokes and a progressive course, is easily confused with DAT. Measurements of cerebral blood flow (CBF) and metabolism (CMR) displayed as brain maps, identify VAD from DAT because of the multifocal and often subcortical nature of the infarcts in VAD, which are strikingly different from the diffuse cortical reductions of CBF and CMR in DAT. Thus, neuroimaging is important for establishing the diagnosis in these two most common forms of dementia in the elderly. A dramatic method for separating VAD from DAT is by utilizing the noninvasive acetazolamide test and xenon contrast CT scanning for measuring the cerebral vasomotor capacitance. In DAT the vasodilator reserve is increased due to the law of initial values. In VAD it is absent or severely blunted so that the differences between the two underlying causes of the dementias become readily apparent.

Aged↗
PubMed1976

Pharmacological mechanisms for left ventricular unloading in clinical congestive heart failure. Differential effects of nitroprusside, phentolamine, and nitroglycerin on cardiac function and peripheral circulation.

We compared cardiocirculatory actions of the commonly employed systemic vasodilators, intravenous (iv) nitroprusside (NP), iv phentolamine (PH), and sublingual nitroglycerin (NTG), causing left ventricular (LV) unloading in 29 chronic coronary subjects with congestive failure to determine whether they produce disparate responses in LV function by different relaxing actions on systemic resistance and capacitance beds. Each drug equally lowered systemic arterial pressures to a small extent, whereas heart rate rose slightly with NTG. Cardiac catheterization showed a decline in end-diastolic pressure with NTG (19 to 8 mm Hg) which was greater (P less than 0.05) than with NP and PH (21 to 11). Cardiac index increased (P less than 0.05) during NP (2.68 to 2.93 liters/min per m2) and PH (2.60 to 3.02) but was unchanged (2.83) by NTG. Stroke work increased with PH, ejection fraction rose with NP and PH, and mean ejection rate increased with each, whereas pressure-time per minute fell and end-diastolic volume decreased with each agent. Total systemic vascular resistance declined (P less than 0.001) during NP and PH (1,475 to 1,200 dynes sec cm-5) but was unchanged (1,487) by NTG. Plethysmographically, forearm vascular resistance (FVR) decreased (P less than 0.01) with NP and PH (61.6 to 39.1 mm Hg/ml per 100 g/min) but not (52.4) by NTG. The decreases in venous tone (VT) with NTG (18.2 to 9.3 mm Hg/ml) and NP (18.5 to 9.8) were greater (P less than 0.05) than with PH (18.8 to 13.1) FVR/VT percent changes of 0.96, 1.62, and 0.53 with NP, PH, and NTG indicated balanced systemic arteriolovenous relaxation by iv NP, greater arteriolar dilation with iv PH, and predominant venous dilation by sublingual NTG. Thus, vasodilators produce disparate modifications of LV function by their differing alterations of preload and impedance, which are dependent upon relative extents of relaxation of systemic resistance and capacitance vessels characteristic of each agent as used clinically.

Adult↗
PubMed1989

Effects of preoperative calcium channel and beta-adrenergic blockade on the vascular response to adrenergic agonists during cardiopulmonary bypass.

The present report compares the effects of isoproterenol (ISO), norepinephrine (NE), and phenylephrine (PH) on the mean arterial pressure (MAP) and reservoir volume (RV) during cardiopulmonary (CPB) in 16 patients undergoing coronary artery bypass grafting (CABG) who were treated preoperatively with oral nifedipine (10 to 40 mg, three times a day) and propranolol (40 to 60 mg, three times a day). The changes of RV and MAP were used as indices of the changes in venous capacitance and arterial resistance, respectively, produced by the adrenergic agonists. ISO, a beta-adrenergic agonist, decreased both MAP and RV. NE, which activates both alpha 1- and alpha 2- adrenoceptors, increased both MAP and RV, while PH, a selective alpha 1-adrenergic agonist, increased only MAP with no significant change in RV. The changes are qualitatively similar to those previously achieved in patients undergoing valve replacement who did not receive any blocker preoperatively. However, the decrease of MAP by ISO and its increase by NE were significantly less in the CABG group. It is concluded that preoperative preparation of patients undergoing CABG with beta-adrenergic blockers and calcium channel blockers can modify the effect of ISO and NE on the peripheral resistance, but they have no significant effect on the action of PH at the doses selected in this study.

Adult↗
PubMed1984

On the haemodynamic differences between sodium nitroprusside, nitroglycerin, and isosorbide nitrates. Comparison of their vasorelaxant effects in vitro and of their inactivation in vivo.

In organ bath studies, the sensitivity of isolated renal arteries and veins of the rabbit to sodium nitroprusside (SNP), nitroglycerin (GTN), and two isosorbide nitrates was compared. For isosorbide-dinitrate and isosorbide-5-mononitrate, a 7 to 20 times greater sensitivity of veins than of arteries was found explaining their known in vivo predilection for the capacitance vessels. To SNP and GTN, the immediate response was practically identical; a moderately greater sensitivity of the veins at threshold concentrations ( EC10 ), and a similar sensitivity of veins and arteries at the EC50 was observed with both drugs. However, on prolonged exposure (30 min), the relaxant response to GTN faded to a greater extent in arteries than in veins which may be a factor in the in vivo preference of GTN for the capacitance vessels. In anaesthetized rats, the hypotensive response to SNP and to GTN either infused i.v. or into the femoral artery, was compared. With GTN, the hypotensive response was the same by either route of administration. In contrast, the hypotensive response to SNP was considerably reduced on infusion into the femoral artery; an inactivation of SNP by 34% on passage through the hind-leg was calculated. The resulting decrease in venous over arterial blood levels of SNP could outweigh the somewhat greater sensitivity of veins than of arteries found in the organ bath, and may account for the balanced effect of SNP on resistance and capacitance vessels known to exist in vivo.

Animals↗
PubMedDate not supplied

[Modification of cardiovascular dynamics in orthostatic dysregulation in childhood by oxilofrin].

In 10 children with clinically and hemodynamically proven orthostatic dysregulation of the sympathetic type, non invasive hemodynamics using sphygmographic techniques as well as systolic time intervals were evaluated. Measurements were taken during 10 minutes in the supine and a 65 degrees position on a tilting table before and after acute administration of Oxilofrin, 20 mg as well as after 2 and 4 weeks of chronic treatment with 20 mg t.i.d. During orthostatic stress, Oxilofrin caused a significant increase in pulse pressure, cardiac output, stroke volume, and systolic ejection rate with a reduction in peripheral vascular resistance compared to control. Pre-ejection period and isovolumic contraction time, while prolonged on baseline orthostatic stress, were only slightly shortened by Oxilofrin. These hemodynamic actions of the drug are explained by a stimulation of adrenergic beta and alpha receptions with the consequence of decreasing venous capacitance and increased venous return, thus providing a useful hemodynamic profile for the treatment of orthostatic dysfunction.

Adolescent↗
PubMed1977

Responses of the cardiovascular system of the rat to alpha-and beta-adrenoceptor agonists.

1 The effects of intravenously infused phenylephrine and isoprenaline upon the cardiovascular system of the rat anaesthetized with pentobarbitone, have been investigated.2 Phenylephrine produces a dose-dependent rise in mean arterial blood pressure (MABP) that is due mainly to an increase in total peripheral vascular resistance (TPR), though at all doses tested cardiac output was invariably raised.3 The increase in cardiac output was due in each instance to an increase in stroke volume, heart rate being unchanged. This increase in cardiac output is probably brought about by effects of phenylephrine on the capacitance vessels rather than by an effect on the heart.4 Evidence is presented to show that the effects of phenylephrine are mediated largely by alpha-adrenoceptors, but that beta-adrenoceptors which affect TPR are also stimulated by the amine.5 Isoprenaline produces a dose-dependent fall in MABP that is due entirely to a fall in TPR since the cardiac output increases.6 Unlike phenylephrine, the increase in cardiac output obtained with isoprenaline was achieved by an increase in heart rate while stroke volume remained close to control values. It is contended that the augmented venous return required for the elevated cardiac output results in this case mainly from the isoprenaline-induced fall in TPR which enhances transfer of blood from arteries to the veins.7 Evidence is presented to show that the effects of isoprenaline are mediated mainly by beta-adrenoceptors.8 Under the present experimental conditions the adrenoceptor-mediated cardiovascular changes are little modified reflexly by the arterial baroreceptors.

Adrenergic alpha-Agonists↗
PubMed1977

Cardiovascular system simulation requirements.

Circulatory system characteristics are considered with respect to specifying model design parameters for simulators and pulse duplicators. The requirements are investigated to determine what characteristics and parameters are important in design and construction. The specific design depends on the functions of the device to be investigated. The single most important quantity is the modeled proximal capacitance or compliance of the large vessels. More detailed study specifications require more detailed models.

Blood↗
PubMed1993

Effects of angiotensin-converting enzyme inhibition with perindopril on hemodynamics, arterial structure, and wall rheology in the hindquarters of atherosclerotic mini-pigs.

The effects of ACE inhibition with perindopril on the atherosclerosis-induced impairment of arterial flow were investigated via histopathologic studies, hemodynamics, and vascular rheology of hindlimb arteries in 7 adult Pitman-Moore mini-pigs (7 months of age) fed for 4 months with an atherogenic diet and perindopril (at the daily oral dose of 4 mg, which induced a continuous 70% inhibition of serum ACE activity), versus 7 atherogenic and 7 control animals. Major fibroproliferative fatty lesions with medial intimalization were observed in the abdominal aorta. Atherosclerosis impaired the function of both capacitance and resistance hindlimb arteries. In atherogenic mini-pigs, blood pressure (BP) increased significantly due to increased hindlimb peripheral resistance (HPR) and aortic input impedance, although aortic blood flow was not affected. Altered aortic wall rheology revealed that the stiffness of the aorta was markedly increased due to increased wall tension and reduced viscoelasticity, the viscous component being reduced in the arterial wall. Perindopril significantly opposed these alterations by reducing BP, HPR and input impedance and by returning parietal stiffness to control values by increasing aortic compliance. Angiotensin converting enzyme (ACE) inhibition significantly prevented the development of atherosclerosis in the abdominal aorta by decreasing the cross-sectional area of lesions and the presence of lipid-laden cells, as well as by preventing alteration and fragmentation of elastic laminae. In conclusion, ACE inhibition with perindopril showed a significant preventive action on atherosclerosis-induced deleterious effects on vascular wall function and structure in mini-pig arteries.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Selective inhibition of L-type Ca2+ channels in A7r5 cells by physiological levels of testosterone.

Testosterone has marked beneficial cardiovascular effects, many of which have been attributed to a vasodilatory action. However, the molecular target of testosterone underlying this effect is subject to debate. In this study, we have used microfluorimetry as a noninvasive means of examining whether testosterone could exert dilatory effects via inhibition of voltage-gated Ca2+ entry in the model vascular smooth muscle cell line, A7r5. Rises of [Ca2+]i evoked by 50 mm K+ -containing solution were suppressed in a concentration-dependent manner by testosterone (IC50, 3.1 nm) and by the nonaromatizable analog, 5beta-dihydrotestosterone (IC50, 6.9 nm). The effects of testosterone were apparent in the presence of pimozide (to block T-type Ca2+ channels) but not nifedipine (to block L-type Ca2+ channels). Testosterone did not alter Ca2+ mobilization from intracellular stores by the prostaglandin analog U46619 or capacitative Ca2+ entry in cells pretreated with thapsigargin. Our results indicate that testosterone, at physiological concentrations, can selectively suppress Ca2+ entry into A7r5 cells via L-type Ca2+ channels. We suggest this effect is a likely mechanism underlying its vasodilatory actions and beneficial cardiovascular effects.

Animals↗
PubMed1998

Ca2+, annexins, and GTP modulate exocytosis from maize root cap protoplasts

Protoplasts isolated from root cap cells of maize were shown to secrete fucose-rich polysaccharides and were used in a patch-clamp study to monitor changes in whole-cell capacitance. Ca2+ was required for exocytosis, which was measured as an increase in cell capacitance during intracellular dialysis with Ca2+ buffers via the patch pipette. Exocytosis was stimulated significantly by small increases above normal resting [Ca2+]. In the absence of Ca2+, protoplasts decreased in size. In situ hybridization showed significant expression of the maize annexin p35 in root cap cells, differ-entiating vascular tissue, and elongating cells. Dialysis of protoplasts with maize annexins stimulated exocytosis at physiological [Ca2+], and this could be blocked by dialysis with antibodies specific to maize annexins. Dialysis with milli-molar concentrations of GTP strongly inhibited exocytosis, causing protoplasts to decrease in size. GTPgammaS and GDPbetaS both caused only a slight inhibition of exocytosis at physiological Ca2+. Protoplasts were shown to internalize plasma membrane actively. The results are discussed in relation to the regulation of exocytosis in what is usually considered to be a constitutively secreting system; they provide direct evidence for a role of annexins in exocytosis in plant cells.

Journal Article↗
PubMed1977

An aortic--left ventricular pulse duplicator used in testing prosthetic aortic heart valves.

A pulse duplicator for the testing of prosthetic valves has been produced which accurately simulates physiological pressure and flow wave forms in the left ventricle and ascending aorta. The model consists of two components--the ventricle and the artificial systemic circulation. The ventricle is a collapsible bag which is externally pressurized and produces an accurate ventricular pressure-time history. The artificial circulation is externally pressurized and produces an accurate ventricular pressure-time history. The artificial circulation is a development of the lumped parameter model of Westerhof13 in which the physiological input impedance is modeled by a characteristic resistance, a capacitance, and a peripheral resistance connected in series. The model allows for a wide range of heart rates, systolic-diastolic ratios, mean pressures, flow rates, and fluid viscosity. A Fourier analysis of the model pressure and flow waves shows excellent quantitative agreement with physiological data, as does the vascular input impedance. The Oxford aortic heart valve exhibited a regurgitation of 1.9 per cent and no measureable pressure drop or power loss.

Aorta↗