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At least 433 records · Page 24Linked to original sources
PubMed1998

Time-dependent modulation of capacitative Ca2+ entry signals by plasma membrane Ca2+ pump in endothelium.

In vascular endothelial cells, depletion of intracellular Ca2+ stores elicited capacitative Ca2+ entry (CCE) that resulted in biphasic changes of intracellular Ca2+ concentration ([Ca2+]i) with a rapid initial peak of [Ca2+]i followed by a gradual decrease to a sustained plateau level. We investigated the rates of Ca2+ entry, removal, and sequestration during activation of CCE and their respective contributions to the biphasic changes of [Ca2+]i. Ca2+ buffering by mitochondria, removal by Na+/Ca2+ exchange, and a fixed electrical driving force for Ca2+ (voltage-clamp experiments) had little effect on the CCE signal. The rates of entry of Mn2+ and Ba2+, used as unidirectional substitutes for Ca2+ entry through the CCE pathway, were constant and did not follow the concomitant changes of [Ca2+]i. Pharmacological inhibition of the plasma membrane Ca2+ pump, however, abolished the secondary decay phase of the CCE transient. The disparity between the biphasic changes of [Ca2+]i and the constant rate of Ca2+ entry during CCE was the result of a delayed, Ca(2+)-dependent activation of the pump. These results suggest an important modulatory role of the plasma membrane Ca2+ pump in the net cellular gain of Ca2+ during CCE.

Animals↗
PubMed1982

beta-Adrenergic dilator effects in consecutive vascular sections of skeletal muscle.

Humoral and neurogenic beta-adrenergic dilatation that influenced the resistance function, the capillary exchange function, and to some extent the capacitance function was demonstrated in the vascular bed of cat skeletal muscle. The beta-adrenergic effects were mainly confined to the microcirculation, causing dilatation of the precapillary sphincters and the resistance vessels of small calibre. The microcirculatory effects were pronounced in response to epinephrine, but blood-borne and nerve-released norepinephrine also evoked marked effects. The beta-adrenergic inhibition of vascular tone in the microcirculation may serve in the intact organism to improve tissue nutrition by facilitating capillary diffusion exchange. It further seems to regulate transcapillary hydrodynamic exchange, partly by controlling the precapillary sphincters and the capillary hydrostatic pressure. The blood-borne catecholamines, especially epinephrine, also markedly affected total regional vascular resistance and thereby blood flow by dilator interaction with the concomitant alpha-adrenergic vasoconstrictor response.

Animals↗
PubMed1985

Abdominal vascular responses to changes in carbon dioxide tension in the cephalic circulation of anaesthetized dogs.

Dogs were anaesthetized with chloralose, the regions of both carotid sinuses were vascularly isolated and perfused with arterial blood and both cervical vagosympathetic trunks were cut above the nodose ganglia. The cephalic circulation was perfused through the brachiocephalic and left subclavian arteries with blood which was equilibrated with various levels of CO2. The abdomen was vascularly isolated, perfused through the aorta at constant flow and drained through the inferior vena cava at constant pressure. Changes in vascular resistance were determined from changes in abdominal aortic perfusion pressure and changes in capacitance from the integral of the changes in venous outflow. An increase in PCO2 in the cephalic perfusate resulted in an increase in abdominal vascular resistance and a decrease in capacitance. However, when carotid sinus pressure was high, the response of resistance to an increase in cephalic PCO2 was abolished and that of capacitance was significantly reduced. The reflex responses of both vascular resistance and capacitance to a change in carotid sinus pressure were enhanced when the cephalic PCO2 was raised. However, the effect on the reflex capacitance response from stimulation of baroreceptors was obtained only when PCO2 was changed below 5 kPa whereas the effect on resistance occurred at higher values of PCO2. The interaction between the effects of changes in cephalic PCO2 and the carotid sinus reflex and the differential effect on resistance and capacitance vessels have been explained in terms of the known difference in the sensitivities of these vessels to sympathetic nerve activity.

Abdomen↗
PubMed1986

[Role of alpha- and beta-adrenoreceptors in the formation of shifts in the vascular function of the intestine during acute cooling of the body].

The 1st phase of acute cooling of cats from 37 degrees C to 25 degrees C characterized by an increase of the integral, pre- and postcapillary resistance of the small intestine vascular bed as well as the capillary pressure, revealed a greater role of the alpha-adrenoreceptors in the resistance, capacitance and exchange functions of the vascular bed, whereas the 2nd phase with its diminishing of the above parameters involved rather the beta-adrenoreceptors of the vessels. Blockade of the beta-adrenoreceptors led to a greater reduction of capillary filtration coefficient. Adrenergic mechanisms of the vascular functions control in hypothermia, are discussed.

Animals↗
PubMed2004

Measuring transient systemic conductance and capacitance responses using a modified Brooksby-Donald technique in anesthetized, autonomically intact rabbits.

BACKGROUND: The Brooksby-Donald approach uses two flow probes to measure the inflow and outflow from an organ or vascular bed; the difference in flow can be time-integrated to assess changes in venous capacitance. OBJECTIVES: To measure changes in subdiaphragmatic venous capacitance and arterial conductance in acutely instrumented rabbits, and to document the acute vascular responses to intravenous injections of pharmacological agents. METHODS: In artificially ventilated, fentanyl-anesthetized New Zealand female rabbits, ultrasonic flow probes were attached to the descending thoracic aorta and inferior vena cava to measure subdiaphragmatic inflow and outflow. Systemic arterial and venous pressures were measured. Conductance was calculated as aortic flow divided by the difference between systemic arterial and venous pressures. Changes in capacitance were assessed by integrating flow differences. Nitroglycerin (NG), isoproterenol hydrochloride, phenylephrine hydrochloride (PE) and vasopressin (VP) were administered intravenously in stepwise injections, and transient conductance and capacitance responses were determined. RESULTS: NG significantly increased conductance and capacitance, while isoproterenol hydrochloride had significant effects only on conductance. Both VP and PE significantly decreased conductance and capacitance. CONCLUSIONS: The modified Brooksby-Donald approach used in the present study was validated by the observed concordant increases in conductance and capacitance caused by NG, and decreases caused by VP and PE. This approach may be useful to characterize specific comparative conductance-capacitance properties of various vasoactive agents.

Analysis of Variance↗
PubMed1999

Capacitative calcium entry in smooth muscle cells from preglomerular vessels.

Calcium entry via voltage-gated L-type channels is responsible for at least half of the increase in cytosolic calcium ([Ca(2+)](i)) in afferent arterioles following agonist stimulation. We sought the presence of capacitative calcium entry in fresh vascular smooth muscle cells (VSMC) derived from rat preglomerular vessels. [Ca(2+)](i) was measured using fura-2 ratiometric fluorescence. Vasopressin V1 receptor agonist (V1R) (10(-7) M) increased [Ca(2+)](i) by approximately 100 nM. A calcium channel blocker (CCB), nifedipine or verapamil (10(-7) M), inhibited the response by approximately 50%. V1R in the presence of CCB increased [Ca(2+)](i) from 106 to 176 nM, confirming that calcium mobilization and/or entry may occur independent of voltage-gated channels. In nominally Ca(2+)-free buffer, V1R increased [Ca(2+)](i) from 94 to 129 nM, denoting mobilization; addition of CaCl(2) (1 mM) further elevated [Ca(2+)](i) to 176 nM, indicating a secondary phase of Ca(2+) entry. Similar responses were obtained when CCB was present in calcium-free buffer or when EGTA was present. In nominally Ca(2+)-free medium, the sarcoplasmic reticulum Ca(2+)-ATPase inhibitors (SRCAI), thapsigargin and cyclopiazonic acid (CPA), increased [Ca(2+)](i) from 97 to 128 and 143 nM, respectively, and to 214 and 220 nM, respectively, when 1 mM extracellular Ca(2+) was added. In the presence of verapamil, the results with CPA acid were nearly identical. In Ca(2+)-free buffer, the stimulatory effect of V1R or SRCAI on the Ca(2+)/fura signal was quenched by the addition of Mn(2+) (1 mM), demonstrating divalent cation entry. These studies provide evidence for capacitative (store- operated) calcium entry in VSMC freshly isolated from rat preglomerular arterioles.

Animals↗
PubMed2003

Isometric exercise increases the size of forearm veins in patients with chronic renal failure.

OBJECTIVES: Delay in maturation or failure of maturation of Cimino-Brescia fistulae contributes to the significant vascular access-related morbidity of chronic hemodialysis patients. Increased size and capacitance of native veins before the formation of vascular access has been considered an important variable in the success rate of native fistulae. We evaluated whether a formal exercise program might alter the size of native veins. METHODS: The effect of exercise on venous size was evaluated in 5 patients with severe chronic renal failure [glomerular filtration rate, 30.6 +/- 5.3 mL/min (mean +/- SD)]. Five male patients with a mean age of 57 +/- 9 years underwent a 6-week forearm exercise training program, involving nondominant arms, that included isometric hand-grip contractions to 25 to 35% of MVC lasting 40 to 120 seconds and repetitive squeezing of squash and racquet balls. Both the volume and intensity of exercise training was increased weekly based on strength measured by hand-grip dynamometer and on the patients' indicated level of comfort. Cephalic vessel size in both the nondominant (trained) and dominant (control) arms, with and without a tourniquet, were obtained using Doppler ultrasound before and after the 6-week exercise training program. RESULTS: The size of the cephalic vein of the exercised arm increased significantly ( < 0.05) compared with the control arm when measured in both the absence (048 +/- 0.016 versus 0.024 +/- 0.023 cm ) and the presence of a tourniquet (0.056 +/- 0.022 versus 028 +/- 0.027 cm ). CONCLUSIONS: These findings indicate that a simple, incremental resistance, exercise-training program can cause a significant increase in the size of the cephalic vein commonly used in the creation of an arteriovenous fistula. The increase in size and resultant probable increase in blood flow might accelerate the maturation of native arteriovenous fistulae, thereby lessening the morbidity associated with vascular access.

Aged↗
PubMed2000

The cavernous body of the human efferent tear ducts: function in tear outflow mechanism.

PURPOSE: To determine the structure and function of a system of large blood vessels integrated in the bony canal between the orbit and the inferior nasal duct. METHODS: Thirty-one dissected lacrimal systems of adults were analyzed by using gross anatomy, histology, and electron microscopy as well as corrosion vascular casts. RESULTS: More than two thirds of the bony canal between orbit and inferior nasal duct is filled by a plexus of wide-lumened veins and arteries. The vascular system is embedded in the wall of the lacrimal sac and nasolacrimal duct and is connected to the cavernous tissue of the inferior turbinate. Three types of blood vessels can be distinguished inside the vascular tissue that surrounds the lumen of the lacrimal passage: barrier arteries, capacitance veins, and throttle veins. CONCLUSIONS: The surrounding vascular plexus of the lacrimal sac and nasolacrimal duct is comparable to a cavernous body. While regulating the blood flow, the specialized blood vessels permit opening and closing of the lumen of the lacrimal passage, effected by the bulging and subsiding of the cavernous body, and at the same time regulate tear outflow. Other functions such as drainage of absorbed tear fluid components and a role in immunologic response are under discussion as well. Malfunctions in the cavernous body may lead to disturbances in the tear outflow cycle, ocular congestion, or total occlusion of the lacrimal passages. Variations in the conditions for swelling of the cavernous tissue may have led to the (mistaken) description of valves in the lacrimal passage.

Adult↗
PubMed1993

Cardiovascular effects of nifedipine in the dog.

This study was designed to measure certain cardiovascular effects of 2 or 11 micrograms nifedipine/kg body weight given intravenously to dogs anesthetized with fentanyl-droperidol-pentobarbital. Parameters measured were: cardiac output, stroke volume, stroke work, systemic arterial pressure and vascular resistance, splenic weight (a measure of venous capacitance), and fractionation of cardiac output to many tissues. In response to doses of nifedipine, systemic vascular resistance decreased, cardiac output and flows to most organs increased, and heart rate, stroke work, and splenic capacitance were unchanged. The flow to the diaphragm increased more than that to other organs.

Animals↗
PubMed1992

Plasma disposition and hemodynamic effects of a single oral dose of isosorbide dinitrate in human males and females.

The goal of the present work was to determine the plasma disposition and hemodynamic effects of isosorbide dinitrate (ISDN) in human males and females. Fourteen healthy human volunteers took part in the study; seven males, 21.7 +/- 2.5 y (SD), and seven females, 20.7 +/- 3.4 y. Measurements of forearm blood flow (FBF), vascular conductance (FVC), and venous capacitance (Cv) were obtained by venous occlusion plethysmography, whereas blood pressure was measured by automatic sphygmomanometry. Blood samples were taken through a catheter placed in the antecubital vein at 0, 15, 30, 45, 60, 90, 120, 360, 480, 720, and 1440 min following a single 10 mg oral dose of ISDN. Plasma concentrations of ISDN and its mononitrate metabolites, isosorbide-2-mononitrate (2-ISMN) and isosorbide-5-mononitrate (5-ISMN), were determined by large bore capillary column gas-liquid chromatography. Hemodynamic measurements were made at corresponding experimental times up to 480 min. No differences were observed in the disposition of ISDN, 2-ISMN or 5-ISMN between the male and female volunteers. In addition, the plasma concentrations of ISDN and its mononitrate metabolites did not consistently correlate with the hemodynamic changes of the individual subjects. Diastolic blood pressure was significantly decreased for a 0.5 h period starting at 30 min, which was the time at which plasma ISDN concentrations peaked, and which preceded the time when the plasma concentrations of 2-ISMN and 5-ISMN were maximal. These observations indicate that, for a single 10 mg oral dose of ISDN, there were no gender-dependent differences in the plasma disposition of the parent drug or its mononitrate metabolites, and the vascular changes responsible for the decrease in diastolic blood pressure in these volunteers occurred in vascular beds other than those of skeletal muscle as represented by forearm blood flow.

Administration, Oral↗
PubMed1988

[Effect of structures of the ventral surface of the medulla oblongata on coupled vascular functions of the small intestine].

The effect of the ventrolateral medulla electrical stimulation of various intensity on resistance, capacitance and exchange functions was studied in the vascular bed of the small intestine. Brain activation with superliminal current applied to a point 2 mm rostral-wise of the middle of the twelfth cranial nerve rootlets has been shown to produce the strongest effect on the precapillary resistance of the vascular bed, whereas brain stimulation in a point 2 mm caudal-wise of this level produces a much stronger effect on the postcapillary small intestine resistance.

Animals↗
PubMed1985

[Plasma renin activity and prostaglandin E2 in hypotension induced by nicergoline].

The hypotensive actions of nicergoline, a new alpha 1-adrenoreceptor blocking agent, were studied in six dogs during stable anaesthesia under mechanical ventilation. Systemic haemodynamic parameters were measured before the infusion of nicergoline (500 micrograms X kg-1 in 5 min), and regularly after it during 2 h. Plasma renin activity (PRA), right atrial (V PGE2) and arterial (A PGE2) prostaglandin E2 concentrations measured by radio-immunoassay were collected before, and 10 and 20 min after nicergoline infusion. The mean aortic pressure fell to its lowest figure (-30%) at the 5th min, this being maintained for 45 min. Heart rate and cardiac output remained unchanged. Pulmonary wedge pressure (p less than 0.01) and central venous pressure (p less than 0.05) decreased. All parameters reached their control values in 120 min. PRA was unchanged. V PGE2 (p less than 0.01) and pulmonary extraction in PGE2 (V PGE2 - A PGE2/V PGE2) (p less than 0,05) increased whilst A PGE2 was unmodified. The fall in mean aortic pressure was linked (p less than 0.001) to the increase in V PGE2. Nicergoline infusion induced hypotension by reducing vascular tone of resistance and capacitance beds. Hypotension was related to the vasoplegia and to an inhibition of the rapid pressor control mechanisms. The reasons for the lack of renin release were unknown. V PGE2 release was stimulated by the hypotension. The increase in pulmonary extraction in PGE2 was involved in the maintenance of A PGE2 concentration. Nicergoline gave mild hypotension without reflex sympathetic activation. Its alpha-adrenoreceptor blocking properties were similar to those of prazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1986

Does dihydroergotamine reduce plasma volume?

Indications on a plasma volume reduction by dihydroergotamine (DHE) has been found in earlier studies. This study was made in order to further evaluate such a change. In animal experiments (sheep, n = 10) measurements were performed of red blood cell volume and plasma volume using radioactive labelling techniques. Red blood cell volume was unchanged but a plasma volume decrease of 10% was found after two hours and it persisted for 24 hours. In postoperative patients (n = 9), who had been given an infusion of ringer-glucose (5.5%) at a rate of 100 ml/hour, DHE caused an increase in diuresis but neither ADH (n = 9) nor aldosterone (n = 3) levels were changed. The data from the present study further support the earlier findings of a reduced plasma volume after DHE administration. The main effect of dihydroergotamine is on the vascular bed and especially on capacitance vessels (increased tonus). The reduced plasma volume by DHE seems to be one additional effect of DHE.

Aldosterone↗
PubMed1989

alpha 1-antagonists in the treatment of hypertension.

A number of agents are now available to treat hypertension. One relatively new class of agents is the selective alpha 1-inhibitors, which have distinct advantages over earlier nonselective alpha-adrenergic receptor-blocking agents. Three alpha 1-inhibitors are reviewed in this article: prazosin, terazosin, and doxazosin. These alpha 1-inhibitors are similar in chemical structure and pharmacological action. alpha 1-Inhibitors lower blood pressure by reducing vascular tone in resistance and capacitance vessels. alpha 1-Inhibitors are similar in effectiveness in blood pressure lowering to other commonly used antihypertensive agents like the thiazide diuretic drugs and beta-blockers, which are efficacious as monotherapy in lowering pressure, as initial agents, or in combination with other antihypertensive agents in multidrug therapeutic regimens. alpha 1-Inhibitors are associated with a reasonably low incidence of serious adverse effects and are essentially free of any adverse metabolic effects. alpha 1-Inhibitors have been shown to beneficially effect blood lipids in several studies. The favorable lipid effect makes alpha 1-inhibitors especially appropriate to use in diabetic hypertensive and other patients with elevated serum lipid levels. The beneficial lipid effects may enhance the ability of alpha 1-inhibitors to prevent coronary heart disease, an outcome that has been difficult to demonstrate in thiazide-based trials.

Adrenergic alpha-Antagonists↗
PubMed1970

Responses of saphenous and mesenteric veins to administration of dopamine.

Others have observed that dopamine (3,4-dihydroxyphenylethylamine) constricts resistance vessels in skin, but dilates these vessels in the mesentery. We studied the effects of dopamine on cutaneous and mesenteric veins of dogs to see if this agent also produced qualitatively different effects on the tone of capacitance vessels (veins) in these vascular beds. The lateral saphenous or the left colic vein was perfused at constant flow with blood from a femoral artery. Pressures at the tip of the perfusion cannula and at the tip of a catheter 15 cm downstream were recorded continuously. Increases in the pressure gradient between these two points indicated venoconstriction; decreases indicated venodilatation. Dopamine and norepinephrine injected into the perfusion tubing caused constriction of both veins. The constriction was antagonized by blockade of alpha receptors. A dilator action of dopamine was not seen, even after alpha receptor blockade or in the presence of increased venous tone produced by serotonin, norepinephrine, or nerve stimulation. Reserpine and cocaine did not alter responses to dopamine in the saphenous vein; this suggests that the venoconstrictor action of dopamine results mainly from a direct effect on alpha receptors and that uptake into sympathetic nerve endings may not be important in regulating the amount of dopamine available to receptors in the saphenous vein.

Adrenergic alpha-Antagonists↗
PubMed2000

Midodrine: a selective alpha-adrenergic agonist for orthostatic hypotension and dialysis hypotension.

Midodrine is an oral agent which acts as a selective peripherally-acting alpha-receptor agonist. Midodrine is a prodrug that is almost completely absorbed after oral administration and converted into its active drug de-glymidodrine in the systematic circulation, with a bioavailability of 93%. It has been used successfully in the treatment of neurogenic orthostatic hypotension and more recently, in the treatment of dialysis hypotension. It acts through vasoconstriction of the arterioles and the venous capacitance vessels, thereby increasing peripheral vascular resistance and augmenting venous return, respectively. It is a unique agent in the armamentarium against orthostatic hypotension since it has minimal cardiac and CNS effects. This article will review the literature on midodrine for conditions of autonomic dysfunction, with focus on recent studies on its use in haemodialysis patients.

Adrenergic alpha-Agonists↗
PubMed1989

[Blood supply of skeletal muscles in reactive hyperemia].

In 18 anesthetized cats, 60-sec occlusion of the m. gastrocnemius artery entailed a decrease in the muscle blood supply by 15-20 ml of the blood volume in the vessels whereas the post-occlusion increase in the blood flow restored the blood volume with 45% excess. The intravascular accumulation of the blood exerting a moderating effect upon the venous return while preserving the increased arterial inflow, can be regarded as an automatic way of limiting the hemodynamic excitation due to the postocclusion shifts and involved in systemic circulation. Papaverin interacts with the blood volume restoration and leads to insufficient restoration in the postocclusion period. This suggests that the postocclusion excessive restoration of the blood volume in muscle, as observed in control animals, can be due to an active vasodilatation of the capacitance portion of the intraorgan vascular bed.

Animals↗