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PubMed1999

Effects of P2 purinoceptor agonists on membrane potential and intracellular Ca2+ of human cardiac endothelial cells.

Vasoactive agonists like adenosine-5'-triphosphate (ATP) increase intracellular Ca2+ ([Ca2+]i) in vascular endothelial cells with an initial peak due to inositol 1,4,5-triphosphate-mediated Ca2+ release from intracellular stores followed by a sustained plateau that is dependent on the presence of extracellular Ca2+, thus leading to an increased synthesis and release of prostacyclin and nitric oxide. We studied the effects of nucleotides on membrane potential and [Ca2+]i in confluent human microvascular cardiac endothelial cells obtained from patients with dilated cardiomyopathy. The whole-cell configuration of the patch-clamp technique and a confocal laser scanning microscope employing fluo-3 as a Ca2+ indicator were used. Both uridine-5'-triphosphate (UTP) and 2-methylthioadenosine-5'-triphosphate (2MeSATP) induced depolarizations in human microvascular cardiac endothelial cells and increased [Ca2+]i with a rank order of potency 2MeSATP>ATP=UTP (EC50 values (in microM) were 0.084 2MeSATP, 0.67 ATP and 1.1 UTP). This suggests that both P2u and P2y purinoceptors are present on human microvascular cardiac endothelial cells. Maximal [Ca2+]i responses of confluent human microvascular cardiac endothelial cell monolayers to UTP were lower when compared to 2MeSATP. Nucleotide-induced increases in [Ca2+]i consisted of a transient peak, which was also observed in the absence of extracellular Ca2+, and a sustained [Ca2+]i plateau. This plateau, which was not observed in all monolayers studied, was not markedly influenced by increasing extracellular [K+]. Previous incubation with thapsigargin abolished ATP-induced increases of [Ca2+]i. It is concluded that human microvascular cardiac endothelial cells express both P2y and P2u purinoceptors. P2 purinoceptor agonists release Ca2+ from intracellular thapsigargin-sensitive stores and stimulate capacitative Ca2+ influx pathways. K+ efflux through Ca2+-dependent K+ (K(Ca)) channels does not play a major role in the regulation of nucleotide-induced Ca2+ influx in human microvascular cardiac endothelial cells, which might be related to an impaired function of the cells.

Adenosine Triphosphate↗

PubMed1987

Atrial natriuretic peptide: a new factor in blood pressure control.

The hypothesis of a natriuretic factor-originally an intriguing possibility and now an experimentally documented reality-has occupied the minds of scientists for more than 30 years. It has attracted not only experts in salt and water metabolism but also those interested in hypertension, because of the well known link between sodium homeostasis and blood pressure regulation. There are at least two distinct types of natriuretic substances: one is an inhibitor of the Na+K+ATPase and has been proposed to contribute to a rise in blood pressure; the other, now isolated from atrial tissue, is vasodilatory, natriuretic, diuretic, and has been demonstrated to decrease blood pressure. Our knowledge of regulation and function of this ANP has increased rapidly since its detection. Its role in blood pressure regulation is now fairly well understood. As depicted in Fig. 1, both synthesis and release of ANP are induced by atrial and ventricular wall stretch. In hypertension, distension of the left atrium and ventricle may be of particular importance for ANP release. The endocrine function of myocardial cells is stimulated in response to wall stretch in the ventricle. ANP is synthesized and stored as a 126 amino acid prohormone. Enzymatic processing of this prohormone to the circulating forms ANP 1-98 and ANP 99-126 takes place within the myoendocrine cells. The biological effects of ANP 1-98 are as yet unknown. ANP 99-126 acts at multiple sites to reduce blood pressure. One may distinguish between acute and more chronic effects. The acute effects include shift of fluid to the extravascular compartment and vasorelaxation. This shift is indicated by the rapidly developing rise in haematocrit, which is observed in intact as well as in nephrectomized rats and therefore not due to diuresis alone. The reduction of blood volume in addition to an increase in venous capacitance may be responsible for the reduced cardiac output. The latter may cause a reflex activation of the sympathetic nervous system and an increase in peripheral resistance, thereby overriding the vasodilator effects of the peptide. ANP appears to have a 'de-pressor' effect rather than a direct vasodilator effect. A lowering of peripheral resistance in response to ANP is not observed in normotensives, but is readily seen in at least certain forms of hypertension associated with an increased vascular tone. This most likely explains the discrepancy in the haemodynamic responses to ANP in normotensives and hypertensives.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1980

Plethysmographic registration of volume changes in a hand vein. Effects of serotonin and of a specific antagonist.

The influence of serotonin on a selected dorsal hand vein can be evaluated by changes in tangential wall tension, volume, and pressure. A plethysmographic method has been used to record the changes in venous capacitance at constant pressure after IV injection of small doses of serotonin. R 41 468, a specific serotonin antagonist, has been given orally (10, 20, or 40 mg) or intravenously (2.5 or 10 mg) to healthy volunteers. A reduction or a complete blockade of activity of serotonin was observed after all doses of R 41 468. Duration and strength of the antagonism were dose-dependent. This pharmacologic in vivo model allows investigations into substances with an effect on vascular smooth muscles.

Blood Pressure↗

PubMed1989

Cardiovascular circulatory adjustments and renal function in acute heart failure.

This study aims to clarify the neurohumoral regulation of cardiovascular circulatory adjustments and to analyze changes in renal function and their relationship to cardiovascular hemodynamics in the early stage of heart failure. Cardiac and peripheral (calf segment) hemodynamics, neurohumoral factors and renal function were investigated in totally 139 patients with acute myocardial infarction (AMI). Capacitance vessel constriction was observed in patients with uncomplicated AMI (Killip-I, Forrester HS-I) and constriction of capacitance and resistance vessels in patients complicated by heart failure (Killip II, Forrester HS-II) or cardiogenic shock (Killip III-IV, Forrester HS-IV). Augmented sympathoadrenal discharge significantly related to the degree of pump dysfunction (elevation of heart rate, central venous pressure, pulmonary capillary wedge pressure (PCWP) and decrease of stroke volume index (SVI] and activation of the renin-angiotensin-aldosterone system significantly related to fall in tissue perfusion pressure (mean blood pressure and calf vascular resistance) would be a possible mechanism for these compensatory mechanisms. However these would contribute to excessive vasoconstriction in limbs resulting in exercise intolerance or renal glomerular function impairment. The derangement of creatinine clearance, serum creatinine (Scr), blood urea nitrogen and beta 2-microglobulin were related to Killip classification, and it was clarified that PCWP tended to elevate more in patients with preexisting renal function disturbance, and when cardiac output (CO) depressed much lower, reduction of CO per se caused more severe prerenal renal insufficiency. That is, there were significant correlations between renal function parameters and cardiovascular hemodynamics. The Cardio-Renal Subset (CRS) was originally developed according to the initial SVI and Scr, and it was demonstrated that the CRS would be of definite predictive value in early identification of high risk patients.

Acute Disease↗

PubMed1996

Beneficial actions of nitrates in cardiovascular disease.

Nitroglycerin and the long-acting nitrates have been used in cardiovascular medicine for >100 years. Nitrates are widely utilized for the various anginal syndromes and are also used in congestive heart failure and patients with left ventricular dysfunction. The potential mechanisms for relief of myocardial ischemia with nitrates are multiple. The nitrovasodilators are a related group of drugs that result in the formation of nitric oxide (NO) within vascular smooth muscle cells. NO stimulates the enzyme guanylate cyclase, which results in increases in cyclic guanosine monophosphate and vasodilation. In the presence of atherosclerosis, endothelial dysfunction is ubiquitous and associated with decreased NO availability, probably due to increased destruction of NO by free radical anions. Nitrovasodilators, including the nitrates, supply exogenous NO to the vascular wall and improve the vasodilator state. When nitrates are administered, endothelial-dependent stimuli cause relaxation rather than constriction in the setting of endothelial dysfunction. Nitrates also have antiplatelet effects, and recent evidence confirms that these drugs decrease platelet aggregation and thrombosis formation. This may play an important role in the therapy of acute unstable myocardial ischemia, including unstable angina and myocardial infarction. Nitrate hemodynamic effects have been long known. They are primarily modulated through a decrease in myocardial work that results from smaller cardiac chambers operating with lower systolic and diastolic pressures. These changes are caused by a redistribution of the circulating blood volume away from the heart to the venous capacitance system, with a fall in venous return to the heart. The afterload or arterial effects of nitrates are also useful in decreasing myocardial oxygen consumption. Considerable evidence confirms a variety of mechanisms whereby nitrates increase coronary blood flow, including epicardial coronary artery dilation, stenosis enlargement, enhanced collateral size and flow, improvement of endothelial dysfunction, and prevention or reversal of coronary artery vasoconstriction. These effects help increase nutrient coronary blood flow to zones of myocardial ischemia. Recent data with the nitroglycerin patch confirm that myocardial ischemia is decreased after nitrate administration. Nitroprusside, another nitrovasodilator, is a commonly used intravenous agent for lowering arterial pressure and left ventricular filling pressure. This drug is highly effective for the treatment of acute or severe hypertension and congestive heart failure. However, there are data suggesting that nitroprusside may be deleterious in the presence of acute myocardial ischemia, perhaps by shunting blood away from zones of jeopardized myocardial blood flow. Therefore, nitroprusside cannot be recommended to treat myocardial ischemia; intravenous nitroglycerin should be used in this context.

Cardiovascular Diseases↗

PubMed1996

Smooth muscle cell cycle and proliferation. Relationship between calcium influx and sarco-endoplasmic reticulum Ca2+ATPase regulation.

The role of Ca2+ influx in the regulation of the sarco-endoplasmic reticulum Ca2+ATPases (SERCA) associated with intracellular Ca2+ pools was investigated during smooth muscle cell (SMC) proliferation induced by platelet-derived growth factor (PDGF). We first defined that the previously described up-regulation of the SERCA2a isoform found in vascular SMC after a 24-h stimulation with PDGF (Magnier, C. , Papp, B., Corvazier, E., Bredoux, R., Wuytack, F., Eggermont, F., Maclouf, J., and Enouf, J. (1992) J. Biol. Chem. 267, 15808-15815) was precisely associated with SMC entry into S phase as it appeared linked with [3H]thymidine incorporation. This was further confirmed by testing the effect of transforming growth factor-beta1, which inhibited both aortic SMC proliferation associated with G1 cell cycle arrest and PDGF-induced SERCA2a up-stimulation. Then, we tested the role of Ca2+ influx by using SR 33805, a new Ca2+ channel blocker, which was characterized with regard to the voltage Ca2+ channel blocker nifedipine and the capacitative entry Ca2+ blocker SKF 96365. SR 33805 was found to be the most potent inhibitor of both PDGF-induced SMC proliferation and the associated rise in intracellular Ca2+ concentration with IC50 values of 0.2 +/- 0.1 and 0.31 +/- 0. 04 microM, respectively. Finally, by examining in parallel both SERCA2a and SERCA2b isoforms, in terms of activity and expression, we could determine that PDGF-induced stimulation of total SERCA activity (detected by formation of the phosphorylated intermediate, E approximately P) and of SERCA2a expression (Western blotting) were abolished when extracellular Ca2+ entry was prevented by SR 33805. This study demonstrates that SERCA2a up-regulation is: 1) related to the G1/S transition step of cell cycle and 2) dependent on Ca2+ entry during PDGF-induced SMC proliferation.

Animals↗

PubMed1991

The effects of flosequinan on regional blood flow in normal man.

1. The effects of 100 mg and 200 mg flosequinan on limb, hepatic and renal blood flow were investigated in 14 healthy male volunteers in a placebo controlled double-blind randomised three-way crossover study. 2. Heart rate, blood pressure, forearm blood flow and venous capacitance measured by volume plethysmography, were recorded sequentially over 4 h, after oral dosing. 3. Apparent hepatic and renal blood flows were estimated 2 h post-dose by indocyanine green dye clearance and clearance of 125-iodohippuran respectively. 4. Flosequinan produced dose-dependent reductions in resting diastolic blood pressure, accompanied by a rise in heart rate. 5. Forearm blood flow increased to a maximum 4 h after 200 mg and this was accompanied by a fall in forearm vascular resistance. 6. Hepatic blood flow increased, compared with placebo, after 200 mg flosequinan, accompanied by a fall in hepatic vascular resistance. Renal blood flow remained unchanged but renal vascular resistance fell significantly, compared with placebo, following both doses of the drug. 7. In normal man blood flow to the limb, hepatic and renal vascular beds is preserved despite dose-dependent reductions in blood pressure following single doses of flosequinan.

Double-Blind Method↗

PubMed1989

Mechanical control of coronary artery inflow and vein outflow.

To analyze the origin of the coronary artery inflow and the coronary vein outflow, we measured the intramyocardial artery flow and the epicardial small vein flow by means of a laser Doppler velocimeter with an optical fiber. The functional characteristics of the intramyocardial capacitance vessels were investigated by analyzing the responses of coronary vein flow after stepwise changes in coronary artery pressure during long diastole. Then the effect of the intramyocardial capacitance vessels on coronary artery inflow and vein outflow was evaluated. Intramyocardial artery flow was found to be almost exclusively diastolic with frequent systolic reverse flow, whereas peripheral coronary vein flow was almost systolic exclusively. The intramyocardial capacitance vessels have two functional components, unstressed volume and ordinary capacitance. When the unstressed volume was saturated, the intramyocardial displacable blood volume impeded the coronary artery inflow, but promoted vein outflow.

Animals↗

PubMed1992

A case of vasovagal syncope with convulsions--the effects of midodrine hydrochloride.

A 42-year-old female had suffered from repeated syncope. She had vasovagal syncope with convulsions from vasodilatation and cardiac standstill which lasted for 9.8 sec. The 60 degrees head-up tilt test, nitroglycerin injection and isoproterenol infusion provoked vasovagal reaction. Although a beta blocker was not effective in preventing tilt-induced hypotension and bradycardia, midodrine hydrochloride (alpha-1 stimulant) or atropine prevented it. In this patient, insufficient constriction of capacitance vessels might have played an important role in activation of an inhibitory reflex from cardiopulmonary mechanoreceptors which caused hypotension and bradycardia.

Adult↗

PubMedDate not supplied

Sympathetic influence on the nasal mucosa.

The tone of the resistance vessels determines the capillary flow and the tone of the capacitance vessels --the nasal patency. Lower impulse frequencies in the sympathetic nerves affect mainly the capacitance vessels, while higher frequencies affect both types of vessel. The existence of both alpha- and beta-adrenoreceptors and their distribution offer pharmacological ways to affect mainly one type of the vessels.

Electric Stimulation↗

PubMed1982

A comparative plethysmographic study of the venoconstrictor effect of dihydroergotamine and dihydroergotoxine on the deep veins of the calf in healthy subjects and patients suffering from varicosis.

The venoconstrictor effect of dihydroergotamine and dihydroergotoxine was compared in ten volunteers and in tne patients suffering from varicosis of the leg veins. The dihydrogenated ergot alkaloids were administered subcutaneously in a dose of 0.5 mg each. The influence on the capacitance reaction was determined by occlusion plethysmography of the calf. In addition, the arterial resistance was measured in the same region. Dihydroergotamine reduces the capacitance reaction in volunteers only at the high occlusion pressure levels 8.0 and 10.7 kPa after a lag of 40 min, whereas dihydroergotoxine does not show any significant influence. On the other hand, dihydroergotamine and dihydroergotoxine lead to a significant decrease in capacitance reaction in the patients after 20 and 60 min, respectively. However, the effect if dihydroergotamine (2.1 ml/100 ml tissue) is significantly greater than that of dihydroergotoxine (1.2 ml/100 ml tissue) and nearly normalizes the increased capacitance reaction. The two drugs increase the arterial resistance more clearly in the volunteers than in the patients, and dihydroergotoxine more often than dihydroergotamine tends to decrease resistance when the pre-existent resistance value is low.

Adult↗

PubMed1994

[The heart in systolic hypertension].

Among the various forms of systolic hypertension, the primary hyperkinetic heart syndrome (overactivity of the cardiac beta-receptors) and the systolic hypertension in the elderly are the more interesting ones. The former, although involving subjects in the second or third decade of life, is a separate entity from the hyperdynamic phase of primary hypertension. Beta-adrenergic blockade, even at very long-term, is able to normalize all the major features of the syndrome (systolic hypertension, high cardiac output and systolic ejection rate, and variability of the repolarization phase of the electrocardiogram related to changes in the cardiac adrenergic tone). Beta-blockade is not curative and the syndrome reappears as soon as treatment is interrupted. It is a sort of clinical experimental model allowing the following deductions: high cardiac output is able to cause systolic hypertension; its persistence does not promote the development of an elevated systemic vascular resistance; although exposed to some of the stimuli that promote cardiac hypertrophy, such as increased stress of the ventricular wall, very prolonged adrenergic stimulation, activation of the renin system, the syndrome does not evolve towards ventricular hypertrophy. Regarding isolated systolic hypertension in the elderly, the so called de novo and "burned out" hypertension, are currently indicated as the two forms that characterize patients in the seventh and eighth decades of life. Both are interpreted as due to a loss of capacitance of the arterial system. It follows that the great vessels do not propel blood during diastole, thus increasing the hemodynamic burden on the left ventricle, prolonging diastole and delaying relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart↗

PubMed1992

Conclusions on the measurement of arterial wall thickness: anatomic, physiologic and methodologic considerations.

AIM: To discuss the use of new ultrasonic techniques that make it possible to visualize elastic (carotid) and muscular (radial) capacitance arteries non-invasively. RESULTS OF DATA REVIEW: Measurements of carotid wall thickness and the detection of atheromas are related to arterial pressure, to other risk factors and to the risk of subsequent complications. The use of high-frequency ultrasound (7.5-10 MHz), measurements of far wall thicknesses in areas free of atheromas at end-diastole (by ECG gating or pressure waveform recording) and descriptions of the size and characteristics of atherosclerotic plaques allow a non-invasive assessment of vascular hypertrophy and atherosclerosis in hypertensive patients. CONCLUSIONS: Careful attention to methodologic and physiologic factors is needed to provide accurate information about the anatomy of the dynamically pulsating arterial tree.

Arteries↗

PubMed1983

Documentation of a venous resistance in the baboon.

In the steady state, blood flow out of the heart must be the same as blood flow into the heart. Thus, flow in the cardiovascular system should depend not only on cardiac determinants of flow--pericardial pressure, afterload, heart rate, and contractility--but also on systemic venous determinants of flow as well. We studied the venous determinants of flow in nine baboons. The mean systemic pressure, the upstream driving pressure for venous return, was 10 mm Hg higher than the right atrial pressure. Flow generated by this upstream pressure was modulated by a venous resistance. This resistance acted as if it were interposed between the upstream capacitance vessels and the right atrium. These determinants of venous return in the baboon would be inadequately described by classical concepts of cardiovascular physiology. We suspect that classical concepts would be inadequate in man as well.

Animals↗

PubMed1988

Computation of haemodynamic power and input impedance in the ascending aorta of patients undergoing open heart surgery.

Ascending aortic blood pressure and flow were successfully measured shortly after sternotomy in 16 patients undergoing coronary artery bypass graft surgery. Total haemodynamic power in the aorta was 953.9(444.7) mJ.s-1 (mean (SD], of which 11.65% was pulsatile. Quadrature components accounted for 50.8% of the pulsatile power. The mean (SD) term of the input impedance spectrum was 149.3(51.1) X 10(6) kg.m-4.s-1 and the characteristic impedance was 81.6(3.88) X 10(6) kg.m-4.s-1. Arterial pulsations are thought to be important for adequate tissue perfusion and the movement of tissue fluids and lymph. It is suggested that atheroma may increase the workload of the heart by diminishing the capacitative coupling between the aorta and the peripheral resistance vessels as well as pathological changes in other organs by impeding the lateral transmission of energy into the tissues.

Aorta↗

PubMed2004

Passive regulation of cardiac output during exercise by the elastic characteristics of the peripheral circulation.

A change in cardiac output induced by a change in cardiac performance is accompanied by opposite changes in cardiac filling pressure owing to the resistive and capacitive properties of blood vessels. The inverse relationship between cardiac output and cardiac filling pressure provides a passive (hydraulic) regulatory mechanism that functions to keep cardiac output constant during rest and exercise.

Adaptation, Physiological↗

PubMed1982

Effects of alpha -adrenergic blockade during acute anemia.

Studies were carried out in seven anesthetized paralyzed dogs to examine the importance of alpha -adrenergic tone in the cardiovascular responses during acute anemia. Data were obtained 1) at normal hematocrit (Hct), 2) during anemia produced by isovolemic hemodilution with dextran (Hct, 13-15%), 3) during anemia after alpha -blockade (alpha -bl) with phenoxybenzamine (3 mg/kg), and 4) following volume expansion during anemia with a red blood cell dextran solution. Cardiac output (QT), limb and total body oxygen uptake (VO2), and limb blood flow (QL) were determined. Both QT and QL increased during anemia (P less than 0.01), whereas limb resistance (RL) and total peripheral resistance (TPR) were decreased (P less than 0.01). No further change in either RL or TPR occurred with alpha -blockade anemia, but both QT and QL decreased (P less than 0.01). Whole-body VO2 increased during anemia and then declined with alpha -bl and anemia. Following volume expansion during anemia with alpha -bl, QT, QL, and whole-body VO2 increased. We conclude that alpha -adrenergic sympathetic tone to capacitance vessels is essential for the cardiac output increased during anemia, but has little or no effect on resistance vessels and hence distribution of peripheral blood flow.

Acute Disease↗

PubMed1994

Sites of vasodilation by inhaled nitric oxide vs. sodium nitroprusside in endothelin-constricted isolated rat lungs.

We localized the sites of vasodilation of inhaled nitric oxide (NO), a selective pulmonary vasodilator, and sodium nitroprusside (SNP) in isolated rat lungs. The sites were determined by analyzing the arterial, venous, and double-occlusion data with a two-resistor (small arteries and veins) three-capacitor (large arteries, large veins, and capillaries) model of the pulmonary vascular bed. Inhaled NO (170 and 670 ppm) and SNP (22.5 and 45.0 micrograms) decreased the small-artery resistance by 7.4 +/- 1.6, 17.2 +/- 2.2, 14.2 +/- 2.8, and 21.4 +/- 3.4% and the small-vein resistance by 13.5 +/- 3.2, 20.3 +/- 3.4 (SNP of 22.5 micrograms not significant), and 9.3 +/- 3.3%, respectively, in blood-perfused lungs (n = 12). Similar results were observed in Krebs-perfused lungs (n = 12). Capillary compliance was unaffected by inhaled NO and SNP. SNP increased the large-artery capacitance by 40.0 +/- 8.6 and 69.3 +/- 9.7%, whereas inhaled NO had no effect. SNP increased the large-vein capacitance by 31.0 +/- 8.7 and 48.0 +/- 10.7%, whereas inhaled NO had no effect in blood-perfused lungs. However, in Krebs-perfused lungs inhaled NO and SNP (45.0 micrograms only) increased the large-vein capacitance by 43.3 +/- 11.9, 41.4 +/- 14.2, and 44.2 +/- 11.0%. In conclusion, in blood-perfused isolated rat lungs inhaled NO and SNP dilate small-resistance arteries and veins, whereas SNP but not inhaled NO dilates larger capacitance arteries and veins. Furthermore, blood appears to prevent the downstream vasodilation by inhaled NO on larger capacitance pulmonary veins.

Administration, Inhalation↗