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At least 667 records · Page 37Linked to original sources
PubMed2004

Differential activation of potassium channels in cerebral and hindquarter arteries of rats during simulated microgravity.

The purpose of this study was to test the hypothesis that differential autoregulation of cerebral and hindquarter arteries during simulated microgravity is mediated or modulated by differential activation of K(+) channels in vascular smooth muscle cells (VSMCs) of arteries in different anatomic regions. Sprague-Dawley rats were subjected to 1- and 4-wk tail suspension to simulate the cardiovascular deconditioning effect due to short- and medium-term microgravity. K(+) channel function of VSMCs was studied by pharmacological methods and patch-clamp techniques. Large-conductance Ca(2+)-activated K(+) (BK(Ca)) and voltage-gated K(+) (K(v)) currents were determined by subtracting the current recorded after applications of 1 mM tetraethylammonium (TEA) and 1 mM TEA + 3 mM 4-aminopyridine (4-AP), respectively, from that of before. For cerebral vessels, the normalized contractility of basilar arterial rings to TEA, a BK(Ca) blocker, and 4-AP, a K(v) blocker, was significantly decreased after 1- and 4-wk simulated microgravity, respectively. VSMCs isolated from the middle cerebral artery branches of suspended rats had a more depolarized membrane potential (E(m)) and a smaller K(+) current density compared with those of control rats. Furthermore, the reduced total current density was due to smaller BK(Ca) and smaller K(v) current density in cerebral VSMCs after 1- and 4-wk tail suspension, respectively. For hindquarter vessels, VSMCs isolated from second- to sixth-order small mesenteric arteries of both 1- and 4-wk suspended rats had a more negative E(m) and larger K(+) current densities for total, BK(Ca), and K(v) currents. These results indicate that differential activation of K(+) channels occur in cerebral and hindquarter VSMCs during short- and medium-term simulated microgravity. It is further suggested that different profiles of channel remodeling might occur in VSMCs as one of the important underlying cellular mechanisms to mediate and modulate differential vascular adaptation during microgravity.

Animals↗
PubMed1985

Peripheral circulatory effects of insulin in diabetes.

Peripheral circulatory effects of insulin were studied in the diabetic patients with and without autonomic neuropathy. Forearm blood flow, calf venous volume and calf venous distensibility were measured by strain gauge plethysmography. In the diabetic patients with autonomic neuropathy, mean blood pressure fell from 96 +/- 5 to 88 +/- 5 mmHg after an intravenous injection of 4 U of monocomponent insulin (p less than 0.001). Forearm vascular resistance decreased from 53.99 +/- 8.29 to 45.88 +/- 7.76 mmHg X ml-1 X 100ml-1 X min-1 after insulin (p less than 0.01). Insulin increased calf venous volume from 1.20 +/- 0.19 to 2.23 +/- 0.44 ml/100ml (p less than 0.05) and calf venous distensibility from 0.039 +/- 0.004 to 0.082 +/- 0.016 ml/mmHg (p less than 0.05). In contrast, in the diabetic patients without autonomic neuropathy, there were no significant changes in the mean blood pressure, forearm vascular resistance, calf venous volume and calf venous distensibility. Symptoms of hypoglycaemia did not occur in any patient. These results suggest that insulin has a vasodilator action on both resistance and capacitance vessels, which may be one of the main factors in insulin-induced hypotension.

Adult↗
PubMed2005

Evolution and modulation of age-related medial elastocalcinosis: impact on large artery stiffness and isolated systolic hypertension.

Arteriosclerosis, characterized by remodeling and stiffening of large elastic arteries is the most significant manifestation of vascular aging. The increased stiffening is believed to originate from a gradual mechanical senescence of the elastic network, alterations in cross-linking of extracellular matrix components, fibrosis and calcification of elastic fibers (medial elastocalcinosis). The stiffening of large arteries reduces their capacitance and accelerates pulse wave velocity, thus contributing to a widening of pulse pressure and to the increased prevalence of isolated systolic hypertension with age. Current antihypertensive drugs were mainly designed to reduce peripheral resistance and are not adequate to alter the pathological process of vascular stiffening or even to selectively reduce systolic blood pressure in isolated systolic hypertension. This review puts forward the concept that elastocalcinosis is a valuable therapeutic target and presents evidence that this process can be prevented and reversed pharmacologically.

Aged↗
PubMed1996

OPC-18790, a novel positive inotropic agent, has both arterial and venous vascular dilating actions in the dog.

OPC-18790, (+/-)6-[3-(3,4-dimethoxybenzylamino)-2- hydroxypropoxy]-2(1H)-quinolinone, is a novel positive inotropic agent with a moderate vasodilating action. We examined the vasodilating action of OPC-18790 in detail in the pentobarbital-anesthetized dogs using a colored microsphere technique for resistance vessels and a mean circulatory filling pressure method for capacitance vessels. Intravenously (i.v.) infused OPC-18790 increased the first derivative of left ventricular pressure (LVdP/dt max), cardiac output, heart rate and decreased total peripheral resistance but did not affect mean blood pressure. OPC-18790 significantly increased arterial blood flow distribution to heart and decreased vascular resistance in heart. OPC-18790 at 300 micrograms/kg i.v. and nitroglycerin at 50 micrograms/kg i.v. did not affect mean circulatory filling pressure in intact anesthetized dogs, but both compounds decreased mean circulatory filling pressure in spinally anesthetized dogs. OPC-18790 also decreased resistance to venous return but nitroglycerin did not. These results suggest that OPC-18790 has both arterial and venous vasodilating actions in addition to its positive inotropic action. These actions may produce an improvement of cardiohemodynamics in heart failure.

Animals↗
PubMed1980

[Pathogenesis of renal hypertension (author's transl)].

99 patients with a chronic renal disease (glomerulonephritis, pyelonephritis, polycystic kidneys) with a GFR reduced to 2/3 normal and without anaemia were subjected to detailed haemodynamic investigation. The earliest haemodynamic abnormality was found even before the blood pressure became elevated. This consisted in a rise of the cardiac output. Ist most likely cause was an increase in the circulating blood volume. As the arteriolar and capacitance vessels adjusted to it, the blood pressure remained unchanged and the central venous pressure slightly decreased. Blood pressure rises, when this vascular adjustment subsides. At this moment the raised blood volume will drop to normal. These changes do not correlate with the minor fluctuations of the PRA which obviously are not responsible for the subsidance of the vascular adjustment and for the rise of blood pressure.

Blood Pressure↗
PubMed2006

Haemodynamics and wall remodelling of a growing cerebral aneurysm: a computational model.

We have developed a computational simulation model for investigating an often postulated hypothesis connected with aneurysm growth. This hypothesis involves a combination of two parallel and interconnected mechanisms: according to the first mechanism, an endothelium-originating and wall shear stress-driven apoptotic behavior of smooth muscle cells, leading to loss of vascular tone is believed to be important to the aneurysm behavior. Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state. All resistance and capacitance vessels under basal conditions exhibit some degree of smooth muscle contraction that determines the diameter, and hence tone, of the vessel. The second mechanism is connected to the arterial wall remodeling. Remodeling of the arterial wall under constant tension is a biomechanical process of rupture, degradation and reconstruction of the medial elastin and collagen fibers. In order to investigate these two mechanisms within a computationally tractable framework, we devise mechanical analogues that involve three-dimensional haemodynamics, yielding estimates of the wall shear stress and pressure fields and a quasi-steady approach for the apoptosis and remodeling of the wall. These analogues are guided by experimental information for the connection of stimuli to responses at a cellular level, properly averaged over volumes or surfaces. The model predicts aneurysm growth and can attribute specific roles to the two mechanisms involved: the smooth muscle cell-related loss of tone is important to the initiation of aneurysm growth, but cannot account alone for the formation of fully grown sacks; the fiber-related remodeling is pivotal for the latter.

Biomechanical Phenomena↗
PubMed1999

[Electrically enhanced damaged tissues healing. Part II: direct and pulse current in soft tissue healing].

Methodology of soft tissues wounds, ulcers and pressure sores healing with direct current is described by the authors. Results of clinical trials and animal experiments are represented, as well as technical and using data. Electrical properties of damaged tissues (e. i. skin battery, vascular-interstitial closed circuits etc.) and probable electrical healing mechanisms are discussed. Effects of electrical current on batteries are described. Inductive and capacitive coupling of electric and magnetic fields, and high voltage electrostimulation for enhance tissue healing are also described in the article.

Animals↗
PubMed2001

Effect of simvastatin on vascular smooth muscle responsiveness: involvement of Ca(2+) homeostasis.

This report is focused on the study of simvastatin-induced relaxation of rat aorta through its effects on vascular smooth muscle and Ca(2+) signalling. The presence of endothelium affected only the simvastatin-induced relaxation of aortic rings precontracted with noradrenaline, but not by depolarization with KCl 80 mM. Blockade of Ca(2+) entry through voltage-operated Ca(2+) channels (VOCCs) by diltiazem abolished the endothelium-dependent and direct relaxation, whereas Ca(2+)-ATPase inhibition by cyclopiazonic acid (3 x 10(-5) M) only affected the endothelium-dependent relaxation. In KCl-depolarised arteries concentration-response curves for CaCl(2) were shifted to the right in the presence of simvastatin (3 x 10(-6) and 3 x 10(-5) M) or diltiazem (10(-6) and 10(-7) M). The transient contraction caused by noradrenaline in Ca(2+)-free medium, which is mainly due to intracellular Ca(2+) release, was inhibited by simvastatin (3 x 10(-5) M) or cyclopiazonic acid (3 x 10(-5) M) and the contraction induced by CaCl(2) (2 x 10(-3) M) added after noradrenaline was inhibited by diltiazem and simvastatin. All the reported effects of simvastatin were inhibited by the product of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, mevalonate (10(-3) M). These findings demonstrate that the vascular effects of simvastatin may involve both Ca(2+) release from intracellular stores, which could promote activation of endothelial factors, and blockade of extracellular Ca(2+) entry, which promote relaxations independent of the presence of endothelium. This action on Ca(2+) could be related to the inhibition of isoprenoid synthesis, which subsequently affects the function of G-proteins involved in communication among intracellular Ca(2+) pools and capacitative Ca(2+) entry.

Animals↗
PubMed1991

A capacitative Ca2+ influx is required for sustained fluid secretion in sublingual mucous acini.

The Ca2+ dependence of muscarinic-induced fluid and electrolyte secretion was studied using rat sublingual mucous gland preparations. During stimulation, secretions from vascularly perfused glands were totally inhibited when perfused with a Ca(2+)-free medium. Fluid secretion correlated with sustained losses of 42K+ and 36Cl- content and sustained increases in 22Na+ content and the intracellular free Ca2+ concentration ([Ca2+]i) in fura-2-loaded acini. The magnitudes of the initial agonist-induced changes in Na+, K+, and Cl- content and [Ca2+]i were unaltered in a Ca(2+)-free medium, whereas extracellular Ca2+ removal resulted in the recovery of these ions during the sustained phase to pre-stimulation levels. The recovery of Cl- content induced by Ca2+ depletion was totally blocked in the presence of bumetanide, an inhibitor of Na(+)-K(+)-2Cl- cotransport, while 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of anion exchange, did not influence Cl- recovery in a HCO(3-)-containing solution (25 mM NaHCO3, 5% CO2). The stimulated increase in [Ca2+]i was not inhibited by the addition of voltage-activated Ca2+ channel blockers (D 888, nifedipine, and diltiazem) or in a Na(+)-free medium. Studies using the quench of fura-2 by Mn2+ as an index of Ca2+ influx and thapsigargin, an inhibitor of microsomal Ca(2+)-ATPase, indicate that a capacitative Ca2+ entry pathway mediates Ca2+ entry during stimulation. The above data demonstrate that Ca2+ uptake, which is dependent on the refill status of the agonist-sensitive intracellular Ca2+ pool, is a prerequisite for sustained muscarinic-induced fluid and electrolyte secretion in the rat sublingual mucous gland.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Release of calcitonin gene-related peptide in the pig nasal mucosa by antidromic nerve stimulation and capsaicin.

The overflow of calcitonin gene-related peptide like-immunoreactivity (CGRP-LI) in the nasal venous effluent upon antidromic stimulation of the maxillary division of the trigeminal nerve with 6.9 Hz for 3 min or upon capsaicin (0.3 mumol bolus injection) were analysed in the nasal mucosa of sympathectomized pentobarbital anaesthetized pigs. The overflow of CGRP-LI upon antidromic stimulation displayed a slower appearance in the venous effluent than the overflow upon bolus injection of capsaicin. The vascular effects as revealed by the arterial blood flow, the venous blood flow, the blood volume of the nasal mucosa, i.e., the filling of the capacitance vessels and the superficial mucosal blood flow as revealed by the laser-Doppler signal were also studied. Antidromic stimulation of the trigeminal nerve as well as capsaicin bolus injection induced a marked vasodilation which was parallel to the overflow of CGRP. However, capsaicin bolus injection also resulted in a marked increase in the mean arterial blood pressure which may be due to reflex activation of sympathetic fibers. In conclusion, we have demonstrated that chemical stimulation with capsaicin as well as antidromic stimulation of nasal sensory nerves in sympathectomized animals induces both vasodilation and overflow of CGRP-LI in vivo. This indicates that CGRP may contribute to the sensory regulation of the microcirculation in the nasal mucosa.

Animals↗
PubMed1985

Effects of felodipine on resistance and capacitance vessels in patients with essential hypertension.

The acute cardiovascular effects of oral felodipine (0.05 mg/kg and 0.1 mg/kg) were studied using radionuclide methods in 14 hypertensive patients. Eight were previously untreated and 6 had been treated with atenolol 100mg daily for a least 1 month. The maximal effects were observed 60 minutes after the first oral dose and no greater effect was observed with the higher dose. Felodipine caused a reduction in systemic vascular resistance, with a fall in blood pressure and an increase in cardiac output and left ventricular ejection fraction. Those responses were presumably mediated by the reduction in afterload, as they were not modified by pretreatment with atenolol. There were no changes in venous capacitance and the overall pattern of response was similar to that noted with hydralazine. Thus, in hypertensive subjects felodipine acts as a potent arteriolar vasodilator. The results suggest the drug may be an effective means of controlling hypertension, particularly when given in combination with other antihypertensive therapy.

Adult↗
PubMed2005

Vascular involvement in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.

A 26-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) was admitted to our hospital for further cardiovascular examination. A muscle biopsy demonstrated strongly succinate dehydrogenase-reactive blood vessels. Pulse wave contour analysis revealed that both capacitive and oscillatory compliance were markedly reduced in this patient compared with 45 normal age-matched control subjects. Hepatocyte growth factor was remarkably elevated in this patient over that of 10 normal control subjects. These findings suggest that a MELAS patient has not only pathologic but also functional vascular involvement. If so, patients with MELAS need systemic vascular assessment.

Adult↗
PubMed2001

Iodinated radiographic contrast media inhibit the capacitative calcium entry into smooth muscle cells of the swine renal artery.

RATIONALE AND OBJECTIVES: To investigate whether nonionic, iodinated, radiographic contrast media (RCM) could modulate calcium release from or calcium entry into smooth muscle cells of the swine renal artery. METHODS: Intracellular calcium concentrations of isolated myocytes loaded with the calcium-sensitive dye fluo-3 were analyzed using a fluorescence imaging system. Calcium signals were compared with isometric contractions of vascular segments in an organ bath. The effects of the triiodinated monomer iomeprol were compared with those of a mannitol solution. RESULTS: Stimulation of alpha-receptors by phenylephrine caused a biphasic calcium signal. Transient liberation of calcium from intracellular stores triggered the sustained entry of extracellular calcium (capacitative entry). Iomeprol and mannitol slightly inhibited the initial transient spike to the same extent. The calcium influx was reversibly inhibited by RCM by about 50%. Up to a concentration of 40 mmol/L, the inhibition induced by iomeprol was significantly higher than that induced by mannitol (P < 0.05-0.01). In isolated arterial segments, relaxation of the contraction phase depending on the calcium influx was significantly higher with the RCM than with mannitol (P < 0.01). CONCLUSIONS: Vasodilatation by CM is associated with a reduction in the capacitative entry of calcium. The mechanism of this effect is not clear, but it can be ruled out that it is mainly due to the high osmolarity of these compounds.

Analysis of Variance↗
PubMed1997

Redox control of ion channel activity in vascular endothelial cells by glutathione.

Oxidized glutathione (GSSG) is endogenously formed within vascular endothelial cells. The bioactivity of GSSG results in the oxidation of protein thiol groups, leading to changes in protein structure-function relationships. When ion channel protein thiols are the target of oxidation by GSSG, important changes in channel conductance, activity, and gating occur. In this review, we focus on two endothelial cell ion channels, the activities of which influence vascular cell signaling and the nitric oxide signaling pathway. The first channel is the GSSG-operated cation channel that depolarizes the endothelial cell, leading to inhibition of capacitative Ca2+ entry. The second channel is the inositol 1,4,5-triphosphate (IP3)-operated Ca2+ channel that is responsible for the agonist-stimulated release of Ca2+ from IP3-sensitive endoplasmic reticulum. GSSG acts to deplete IP3-sensitive Ca2+ stores, thereby attenuating the intracellular Ca2+ response to agonist stimulation. Together, these effects indicate that glutathione, which is formed endogenously within the cell, is a key physiological modulator of endothelial cell signaling.

Animals↗
PubMed1989

Vasodilator properties of atrial natriuretic factor: a comparison with nitroglycerin, nitroprusside, and phentolamine during cardiopulmonary bypass.

Thirty-five patients scheduled for coronary artery surgery were studied during hypothermic cardiopulmonary bypass (CPB) to compare the arteriolar and venodilator properties of a bolus dose of atrial natriuretic factor (ANF), 100 micrograms, with those of nitroglycerin, 200 micrograms, sodium nitroprusside, 120 micrograms, phentolamine, 3 mg, and placebo. A decrease observed in mean arterial pressure was used as an indicator of a decrease in systemic vascular resistance (arteriolar dilation), while a decrease in reservoir blood volume of the CPB circuit was considered to indicate an increase in venous capacitance (venodilation). All vasodilators decreased mean arterial pressure, and there was no difference in the maximal decrease of the pressure between the drugs. However, the decrease caused by ANF appeared later than that caused by the other vasodilators and lasted longer than with nitroglycerin and sodium nitroprusside. Nitroglycerin and sodium nitroprusside decreased reservoir blood volume, while ANF and phentolamine had no effect. It is concluded that ANF is an arteriolar dilator with a time profile of its effect differing from those of nitroglycerin, sodium nitroprusside, and phentolamine. ANF seems to have no venodilator activity in patients undergoing hypothermic CPB.

Atrial Natriuretic Factor↗
PubMed2001

Cardiovascular effects of vasopressin following V(1) receptor blockade compared to effects of nitroglycerin.

Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic subjects with impaired efferent sympathetic responses. Studies to compare the effects of AVP with the hemodynamic effects of nitroglycerin, an agent that primarily affects venous capacitance vessels, were also performed in normal subjects. Incremental infusions of AVP following V(1)-receptor blockade resulted in equivalent reductions in systemic vascular resistance (SVRI) in normal and in quadriplegic subjects. However, there were major differences in the effect on mean arterial pressure (MAP), which was reduced in quadriplegic subjects but did not change in normal subjects. This difference in MAP can be attributed to a difference in the magnitude of increase in cardiac output (CI), which was twofold greater in normal than in quadriplegic subjects. These observations are consistent with AVP-induced vasodilation of arterial resistance vessels with reflex sympathetic enhancement of CI and are clearly different from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP, CI, and indexes of cardiac preload, with only minor changes in SVRI.

Antidiuretic Hormone Receptor Antagonists↗