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At least 379 records · Page 21Linked to original sources
PubMed1999

Kininergic system and arterial hypertension following chronic exposure to inorganic lead.

Rats were exposed for 10 months to 60 ppm of Pb (as acetate) in drinking water. Systolic and diastolic blood pressure and cardiac inotropism were increased by the metal, which reduced arterial blood flow and unaffected heart rate. The activities of plasma angiotensin I-converting enzyme (ACE) and kininase II were strongly augmented by Pb, suggesting markedly increased and decreased levels of plasma angiotensin II and bradykinin, respectively. Moreover, the Pb-exposed rats showed a lower increase of the plasma kallikrein and kininase I activities. These results are discussed in the context of the complex relationships linking the renin-angiotensin-aldosterone (RAA), kallikrein-kinin and other autacoidal, neurohumoral (e.g., catecholaminergic) and transductional systems (e.g., nitric oxide (NO)). Pb was confirmed to induce arterial hypertension and cardiovascular alterations at plasma levels similar to those observed in the general population or in subjects with short occupational exposure.

Animals↗
PubMed1999

Regulatory role of bradykinin in the coronary and cerebral circulations and in systemic hemodynamics.

Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa). Such a potentiation was prevented and reversed only by nitroarginine or 1,10-phenanthroline (PHE) (which also reduced basal jugular NO levels) and did not involve the BK1 or BK2 receptors. Either HIST or 5-HT potentiated (likely involving the H1 and 5-HT2 receptors, respectively) the activating effect of BK on kininase I (K1), thus increasing the availability of L-arginine for the synthesis of NO. In patients with migraine, venous NO and K1 activity were higher during HIST desensitization than in basal conditions; moreover, HIST reduced the activities of prekallikrein (pre-KAL), kallikrein (KAL) and kininase II (K2) in the venous blood of these patients, in which the intensity of pain was related to the levels of plasma NO, and the administration into the humeral artery during circulatory arrest of BK alone (but not HIST) or BK and HIST together caused a strong pain attack. BK was confirmed to interact selectively with other autacoids in regulating systemic and local hemodynamics through the system of NO.

Acetylcholine↗
PubMed2000

Selective activation of E-type prostanoid(3)-receptors reduces myocardial infarct size. A novel insight into the cardioprotective effects of prostaglandins.

Prostaglandins (PGs) and other eicosanoids are members of a large family of lipid mediators (autacoids). In 1978, Lefer and colleagues (Science 200, 52-55 [1978]) reported that prostacyclin reduces the myocardial tissue injury caused by coronary artery occlusion and reperfusion in the cat. Since this discovery, more than 50 papers have reported on the cardioprotective effects of vasodilator PGs, including prostacyclin. The cardioprotective effects of PGs are due in part to (1) a reduction in afterload, (2) an increase in coronary blood flow, (3) the inhibition of platelet function, and (4) the inhibition of the activation and extravasation of polymorphonuclear granulocytes. All of these effects are secondary to the activation of EP (E-type prostanoid)(2)-receptors, which activate G(s)-protein and, hence, adenylate cyclase. In addition, the protection of organs such as the heart by PGs has been attributed to a cytoprotective effect of these agents, the mechanism of which is largely unknown. We recently have discovered that certain E-type PGs, which do not activate EP(2)-receptors, also reduce myocardial infarct size, without causing a fall in blood pressure (EP(2)-receptor-mediated effects). Having provided a brief introduction into the role of eicosanoids in ischaemia-reperfusion injury of the heart, this review focuses on the recent discovery that selective agonists of EP(3)-receptors reduce myocardial infarct size, without causing haemodynamic side effects. The mechanisms of the cardioprotective effects of these agents are discussed, as are the therapeutic implications.

Animals↗
PubMed2002

Cardiovascular effects of cannabinoids.

The prototypic endocannabinoid, anandamide, and synthetic analogues have been shown to elicit pressor and depressor effects, bradycardia, vasorelaxation, and inhibition of neurotransmission in the central and peripheral nervous systems. Cannabinoid-mediated inhibition of neurotransmission is mediated by inhibition of voltage-gated Ca(2+) channels and adenylyl cyclase and activation of inwardly rectifying K(+) channels. The precise mechanisms underlying the vasorelaxant actions of cannabinoids are currently unclear, but might involve both receptor-dependent and -independent and endothelium-dependent and -independent pathways. Mechanisms proposed have included the release of endothelial autacoids, activation of myoendothelial gap junctions, activation of the Na(+) pump, activation of K(+) channels, inhibition of Ca(2+) channels, and activation of vanilloid receptors, leading to the release of sensory neurotransmitters. Pathophysiologically, the vasodilator actions of endocannabinoids have been implicated in the hypotension associated with both septic and haemorrhagic shock, but their physiological significance remains to be determined.

Animals↗
PubMed2003

Endothelial nitric oxide synthase: the Cinderella of inflammation?

A hallmark of inflammation is increased vascular permeability. Increases in vascular permeability and the migration of inflammatory cells are linked to complex interactions of inflammatory mediators with the vascular endothelium. Normally, endothelial nitric oxide synthase (eNOS) produces a tonic amount of nitric oxide (NO), which is responsible for the homeostasis between the endothelium and surrounding tissues. However, most agonists that act on endothelial cells cause a series of post-translational modifications that influence eNOS activity. Furthermore, stimulation by shear stress, autacoids or growth factors either induces eNOS or shifts it to a more active state, which produces a burst of NO. Here, we highlight recent findings about eNOS and propose how new pharmacological tools can be used to dissect the involvement and contribution of eNOS to inflammatory responses.

Animals↗
PubMed1997

Nitric oxide supplementation or synthesis block--which is the better approach to treatment of heart disease?

Nitric oxide (NO) released from endothelium mediates the vasodilatation caused by numerous autacoids. Nitric oxide can also be exogenous in that some drugs used in cardiovascular disease are NO donors (e.g. glyceryl trinitrate, sodium nitroprusside and isosorbide mononitrate used in angina). However, the notion that NO is a cardiac protectant, whose mimicry or supplementation is desirable, has recently been questioned by data that suggest it is an innocent bystander in some conditions, and even a pathological mediator of dysfunction in others. This important issue is discussed by Mike Curtis and Ravinder Pabla who suggest it is necessary to reappraise the role of NO modulation in cardiac pharmacotherapy.

Heart Diseases↗
PubMed2003

Coupling to Gs and G(q/11) of histamine H2 receptors heterologously expressed in adult rat atrial myocytes.

The predominant histamine receptor subtype in the supraventricular and ventricular tissue of various mammalian species is the H2 receptor (H2-R) subtype, which is known to couple to stimulatory G proteins (Gs), i.e. the major effects of this autacoid are an increase in sinus rate and in force of contraction. To investigate histamine effects in H2-R-transfected rat atrial myocytes, endogenous GIRK currents and L-type Ca2+ currents were used as functional assays. In H2-R-transfected myocytes, exposure to His resulted in a reversible augmentation of L-type Ca2+ currents, consistent with the established coupling of this receptor to the Gs-cAMP-PKA signalling pathway. Mammalian K+ channels composed of GIRK (Kir3.x) subunits are directly controlled by interaction with betagamma subunits released from G proteins, which couple to seven-helix receptors. In mock-transfected atrial cardiomyocytes, activation of muscarinic K+ channels (IK(ACh)) was limited to Gi-coupled receptors (M2R, A1R). In H2-R-overexpressing cells, histamine activated IK(ACh) via Gs-derived betagamma subunits since the histamine-induced current was insensitive to pertussis toxin. These data indicate that overexpression of Gs-coupled H2-R results in a loss of target specificity due to an increased agonist-induced release of Gs-derived betagamma subunits. When IK(ACh) was maximally activated by GTP-gamma-S, histamine induced an irreversible inhibition of the inward current in a fraction of H2-R-transfected cells. This inhibition is supposed to be mediated via a G(q/11)-PLC-mediated depletion of PIP2, suggesting a partial coupling of overexpressed H2-R to G(q/11). Dual coupling of H2-Rs to Gs and Gq is demonstrated for the first time in cardiac myocytes. It represents a novel mechanism to augment positive inotropic effects by activating two different signalling pathways via one type of histamine receptor. Activation of the Gs-cAMP-PKA pathway promotes Ca2+ influx through phosphorylation of L-type Ca2+ channels. Simultaneous activation of Gq-signalling pathways might result in phosphoinositide turnover and Ca2+ release from intracellular stores, thereby augmenting H2-induced increases in [Ca2+]i.

Animals↗
PubMed1994

Essential fatty acid deficiency profiles in idiopathic immunoglobulin A nephropathy.

The profiles of fatty acids (FAs) of plasma phospholipids (the compartment reflecting the essential FA status of tissue lipids), nonesterified FAs (the precursor pool for autacoid synthesis), urine protein excretion, and glomerular filtration rate were measured before and after supplementation with fish oil in 15 patients with immunoglobulin A nephropathy. In the FA profiles, there was deficient 18:3 omega 3 (alpha-linolenic acid), the parent compound of omega 3 polyunsaturated FA, and deficient chain elongation products of both omega 3 and omega 6 polyunsaturated FAs with replacement by saturated and monounsaturated short-chain, odd-chain, and branched-chain FAs, producing significant loss of omega 3 FA. These alterations indicate nutritional or functional (omega 3) and metabolic (omega 6) deficiencies. Additionally, the mean melting point of the FAs was significantly increased, implying an inherent decrease in cell membrane fluidity. Enhancement of 20: 5 omega 3 (eicosapentaenoic acid) and 22:6 omega 3 (docosahexaenoic acid) and suppression of 20:4 omega 6 (arachidonate) after supplementation with fish oil were accompanied by important decreases in proteinuria and improved glomerular filtration rate. Omega-3 polyunsaturated FAs may favorably influence immunoglobulin A nephropathy through a modulation of the pathologic actions of the omega 6 eicosanoids and other diverse actions on various mediators produced by an initial immune injury.

Adult↗
PubMed1999

Alteration of Na+ currents in dorsal root ganglion neurons from rats with a painful neuropathy.

Increased excitability of primary sensory neurons may be important for the generation of neuropathic pain from nerve injury. The currents underlying the action potentials of these neurons are largely carried by Na+, and changes in Na+ currents have been postulated to contribute to this increased excitability. Using patch clamp in whole-cell mode, we recorded Na+ currents from DRG neurons freshly isolated from rats with a chronic constriction injury (CCI), an animal model of neuropathic pain. We found significant changes in Na+ currents after CCI when cell size and Na+ channel properties were used to segregate DRG neurons. Most changes were concentrated in small neurons (< or = 25 microm diameter) and in the slow TTX-resistant current that is predominant in these cells. CCI produced two principal changes in these cells: it shifted the voltage-dependence of activation of the TTX-resistant current to more negative potentials and it reduced the average density of this current. The decrease in density appears to be primarily due to the decrease in the number of small neurons expressing this current. The net result is a change in both activation and steady-state inactivation properties of the total Na+ current to more negative potentials without a significant change in the density of total Na+ current. The change in activation properties of the TTX-resistant Na+ current are similar to those produced by some hyperalgesic autacoids, and may contribute to the increase in primary afferent excitability and hyperalgesia that occurs after this lesion.

Animals↗
PubMed1996

Local regulation of oviductal blood flow.

1. Blood flow to the oviduct is implicated in the genesis and maintenance of oviductal fluid, in this way contributing to the creation of an adequate medium for ovum/embryo physiology. Therefore, factors controlling the tone of the vessels supplying the oviduct would be expected to affect its luminal environment. In addition, cyclic changes in oviductal blood flow have been suggested to have mechanical functions in the transport of the ovum/embryo. 2. The vascular supply to the oviduct has a prominent adrenergic vasomotor control. A dense adrenergic innervation, together with the presence of a predominant population of alpha(1)-adrenoceptors, provides a contractile regulatory mechanism of oviductal blood flow. No evidence is available on the presence of beta-adrenoceptors. The scanty cholinergic innervation of mammalian oviduct is mainly confined to the vessels, where acetylcholine (ACh) has a vasodilatory effect by releasing endothelium-derived relaxing factors. 3. The presence of nerves containing neuropeptides has been shown in the oviduct. Specifically, a high density of neuropeptide Y- and vasointestinal peptide-containing nerve fibers has been found in relation to blood vessels, but their role in the neutral control of the oviduct blood flow remains to be established. To date, it is not known whether or not oviductal blood vessels receive perivascular nitrergic nerves. 4. Relaxing and contracting factors derived from endothelium also seem to have a modulatory role on oviductal vascular tone. Neurotransmitters or autacoids, such as ACh and histamine, acting on endothelial receptors, release nitric oxide (NO), which relaxes oviductal arteries through guanylyl cyclase activation and accumulation of cyclic GMP. In addition, the release of an endothelium-derived hyperpolarizing factor (EDHF), distinct from NO, by ACh has been shown in oviductal arteries. It acts through the opening of low-conductance Ca(2+)-activated K+ channels leading to hyperpolarization and relaxation. Furthermore, potent and long-lasting contractions induced by the endothelium-derived contractile factor, endothelin (ET), points to its role in the long-term regulation of oviductal vascular tone. 5. A particularly high density of 5-hydroxytryptamine (5-HT) and histamine, present in mast cells clustered in the vicinity of blood vessels, has been described in the oviduct. It is known that histamine elicits a relaxation of oviductal arteries that is partially endothelium-dependent and mediated by the activation of H1-receptors. The implication of histamine in both the increase in blood flow and edema around ovulation, as well as the existence of a functional antagonism between histamine and 5-HT in the regulation of oviductal blood flow, await further investigation. 6. Other factors, such as relaxing and contracting cyclooxygenase-derived products, may also participate in the modulation of blood flow to the oviduct. 7. An overall endocrine regulation of the oviductal vascular supply exists, acting by both direct effects on smooth muscle and modulation of neural and autocrine factors. This control enables cyclic changes in blood flow to the oviduct that are tightly coupled to the reproductive functions of the tube.

Adrenergic Fibers↗
PubMed2003

CGRP-mediated cardiovascular effect of nitroglycerin.

Organic nitrates, including nitroglycerin, produce vascular relaxation by releasing nitric oxide in vascular tissues near the plasma member of smooth muscle cells of veins and arteries. Calcitonin gene-related peptide (CGRP), a major transmitter in capsaicin-sensitive sensory nerves, is widely distributed in cardiovascular tissues and the release of CGRP is regulated by multiple autacoids including nitric oxide (NO). CGRP exerts complex cardiovascular effects including potent vasorelaxation and protective effects on myocytes and endothelial cells. Nitroglycerin activates sensory nerves fibres to release CGRP by generating NO and increasing cGMP level, and that the cardiovascular effects of nitroglycerin are partly mediated by endogenous CGRP.

Calcitonin Gene-Related Peptide↗
PubMed2003

Adenosine A1 and A2A receptor cross-talk during ageing in the rat myocardium.

Adenosine (Ado), a naturally occurring autacoid, exerts cardioprotective effects against myocardial ischemia and reperfusion injury, through activation of its receptors type 1 (A1) and 2A (A2A). Since ageing involves a complex change in these effects, we evaluated A1 and A2A gene expression in left (LV) and right ventricle (RV) from 2-, 5-, 12-, and 21-month-old Sprague-Dawley rats. LV end-diastolic (EDD) and end-systolic (ESD) internal dimensions (mm) and LV fractional shortening (FS, %) were measured by M-mode echocardiography. Senescence was associated with a reduction in FS (42+/-1, 38+/-2, 39+/-2 and 35+/-2, in 2-, 5-, 12- and 21-month-old rats; p<0.02) and increases in EDD (7.5+/-0.2, 8.1+/-0.2, 8.5+/-0.2 and 8.8+/-0.2; p<0.001) and ESD (4.2+/-0.1, 4.4+/-0.2, 4.7+/-0.2 and 5.1+/-0.2; p=0.002). Ado A1 mRNA levels were highest in 12 and 21-month-old animals in both ventricles (LV: p<0.001; RV: p=0.001). By contrast, Ado A2A gene expression was lower in the aged LV (p<0.001), but higher in the aged RV (p<0.001). These modifications of Ado receptor gene expression and especially the increase in A1 receptor mRNA may partially explain the stronger antiadrenergic effects of Ado in the senescent heart.

Aging↗
PubMed1987

Regulation of coronary artery tone in relation to the activation of signal transductors that regulate calcium homeostasis.

Muscle tone of coronary arteries is regulated by free calcium concentration in the myoplasm. Various agonists, autacoids and putative peptides modify the calcium concentration directly or through actions of second messengers (signal transductors), such as cyclic guanosine monophosphate (GMP), cyclic adenosine monophosphate (AMP), inositol 1,4,5-trisphosphate, diacylglycerol or calmodulin. For example, acetylcholine (in the presence of intact endothelium cells), alpha-human natriuretic peptide or nitrate compounds increase the amount of cyclic GMP and isoproterenol, prostacyclin (prostaglandin I2) or vasoactive intestinal polypeptide increases cyclic AMP. Both cyclic nucleotides reduce free calcium concentration. On the other hand, acetylcholine (in the presence or absence of endothelium cells), norepinephrine or thromboxane A2 increases inositol 1,4,5-trisphosphate and diacylglycerol, thus causing the increase in the free calcium concentration, whereas vasoactive intestinal peptide and alpha-human natriuretic peptide reduce them. Calmodulin acts as an internal calcium receptor for regulation of the contractile machinary. Regulation of calcium homeostasis in relation to the muscle tone in the coronary arteries including other vascular tissues is discussed together with the role of second messengers.

Arteries↗
PubMed1998

The role of nitric oxide in hepatic metabolism.

Nitric oxide (NO) may regulate hepatic metabolism directly by causing alterations in hepatocellular (hepatocyte and Kupffer cell) metabolism and function or indirectly as a result of its vasodilator properties. Its release from the endothelium can be elicited by numerous autacoids such as histamine, vasoactive intestinal peptide, adenosine, ATP, 5-HT, substance P, bradykinin, and calcitonin gene-related peptide. In addition, NO may be released from the hepatic vascular endothelium, platelets, nerve endings, mast cells, and Kupffer cells as a response to various stimuli such as endotoxemia, ischemia-reperfusion injury, and circulatory shock. It is synthesized by nitric oxide synthase (NOS), which has three distinguishable isoforms: NOS-1 (ncNOS), a constitutive isoform originally isolated from neuronal sources; NOS-2 (iNOS), an inducible isoform that may generate large quantities of NO and may be induced in a variety of cell types throughout the body by the action of inflammatory stimuli such as tumor necrosis factor and interleukin (IL)-1 and -6; and NOS-3 (ecNOS), a constitutive isoform originally located in endothelial cells. Another basis for differentiation between the constitutive and inducible enzymes is the requirement for calcium binding to calmodulin in the former. NO is vulnerable to a plethora of biologic reactions, the most important being those involving higher nitrogen oxides (NO2-), nitrosothiol, and nitrosyl iron-cysteine complexes, the products of which (for example, peroxynitrite), are believed to be highly cytotoxic. The ability of NO to react with iron complexes renders the cytochrome P450 series of microsomal enzymes natural targets for inhibition by NO. It is believed that this mechanism provides negative feedback control of NO synthesis. In addition, NO may regulate prostaglandin synthesis because the cyclooxygenases are other hem-containing enzymes. It may also be possible that NO-induced release of IL-1 inhibits cytochrome P450 production, which ultimately renders the liver less resistant to trauma. It is believed that Kupffer cells are the main source of NO during endotoxemic shock and that selective inhibition of this stimulation may have future beneficial therapeutic implications. NO release in small quantities may be beneficial because it has been shown to decrease tumor cell growth and levels of prostaglandin E2 and F2 alpha (proinflammatory products) and to increase protein synthesis and DNA-repair enzymes in isolated hepatocytes. NO may possess both cytoprotective and cytotoxic properties depending on the amount and the isoform of NOS by which it is produced. The mechanisms by which these properties are regulated are important in the maintenance of whole body homeostasis and remain to be elucidated.

Animals↗
PubMed1999

Proposal of a new PAF pharmacophoric map by the AM1 method.

PAF is a powerful phospholipid-derived autacoid involved in many pathophysiological processes. Many PAF antagonists have been synthesized and assayed for therapeutic purposes. We have synthesized derivatives (5-7), structurally related to WEB 2086 (1), which were rationally designed based on a planar PAF receptor model previously described by Bures et al. (1994; J. Chem. Inf. Comput. Sci. 24, 218-223). However, pharmacological studies revealed that derivatives (5-7) were inactive as PAF antagonists. AM1 quantum calculations of classical PAF antagonists (1-4), as well as of our derivatives (5-7), demonstrated that electronic features alone are unable to explain the lack of the activity of (5-7). These results induced us to propose a new tridimensional PAF receptor pharmacophoric map by analyzing all stable conformations obtained for derivatives (1-4). The interpoint distances (D1-D5) revealed that the lowest-energy conformers of (5-7) had similar geometries to derivatives (1-4). So, these aspects could not explain the inactivity of the compounds (6-7). The proposed model suggests that the best fit of antagonist compounds may involve the participation of a sulfur atom electron lone pair adequately oriented in relation to the plane of a N-aromatic ring present in the compounds investigated.

Azepines↗
PubMed1997

A pharmacophore for high affinity PAF antagonists. II. Hydrophobicity study using the molecular lipophilicity potential.

Platelet-activating factor (PAF) is a powerful phospholipid-derived autacoid involved in many physiopathological mechanisms. Many PAF antagonists have been synthesized and evaluated as therapeutic candidates. In a previous report, we have described an electronic pharmacophore of PAF antagonists using the molecular electrostatic potential. In the present study, a molecular lipophilicity potential is used to compare the hydrophobic properties of 49 "heterocyclic sp2 nitrogen' highly potent PAF antagonists, belonging to six structurally different series (nine hetrazepines, five pyrrolo[1,2-c]thiazoles, 14 carboxamides, nine dihydropyridines, nine pyridinyl-thiazolidines and three imidazo[4,5-c]pyridines). Their common features consist of three hydrophilic (HYD2, HY14(3)B and HYD3) and two lipophilic zones (LIP3 and LIP4), defining the lipophilic pharmacophore of the antagonists. This pharmacophore is also characterized by several zone-to-zone distances: HYD3-HYD2 = 1.3 +/- 1.0 A, HY3B-HYD2 = 7.8 +/- 1.1, HYD3-HY3B = 5.1 +/- 1.1 A, LIP4-LIP3 = 5.4 +/- 1.1 A, LIP3-HYD2 = 11.3 +/- 1.6 A, LIP3-HY3B = 5.9 +/- 1.0 A, LIP3-HYD3 = 4.3 +/- 0.9 A, LIP4-HYD2 = 14.7 +/- 1.6 A, LIP4-HY3B = 8.1 +/- 1.2 A and LIP4-HYD3 = 3.9 +/- 1.1 A. These results represent a new step in the determination of a global pharmacophore for PAF antagonists.

Binding Sites↗
PubMed2003

Primary prevention in cardiovascular disease: moving out of the shadows of the truth about death.

AIM: This review identifies deficits in current educational efforts for the primary prevention of cardiovascular disease. DATA SYNTHESIS: Essential fatty acids in the foods we eat have a subtle but powerful influence on hundreds of different processes in the life and death of humans, understanding of which has been delayed by two attitudes in the biomedical community. One involves a bias towards expensive curative/treatment interventions that neglect prevention of initial nutritional causes of disease and death, and the other involves careless logic in interpreting evidence of causes of disease and death. Both attitudes interfere with translation of published science of essential fatty acids into effective prevention of cardiovascular deaths, a situation made worse by a widespread wish for simple descriptions of complex interactions in disease. Some clinical signs and risk factors may be only shadows of true causal factors. For example, attention to cholesterol ignored important evidence that nutritional imbalances in expenditure/intake of energy and in omega-3/omega-6 essential fatty acids cause cardiovascular disease. Balancing the few percentage of daily calories in omega-3/omega-6 nutrients is not a question of obesity or blood cholesterol. Effective prevention through education will require targeting the causal risk factors that are known beyond the shadow of a doubt, but seldom discussed by health professionals and the public. CONCLUSIONS: Death from coronary heart disease comes from acute ischemia and arrhythmia, often following long-term chronic inflammatory vascular damage that predisposes to acute fatal thrombosis and arrhythmia. The three processes involve excessive self-healing actions of natural n-6 autacoids (auto = self, akos = healing) produced from tissue essential fatty acids that come only from foods. Readily corrected nutritional imbalances in expenditure/intake of energy and in omega-3/omega-6 essential fatty acids are causal risk factors with plausible mechanisms contributing to fatal events which can be prevented.

Cardiovascular Diseases↗
PubMed2000

Studies on extracts of Elaeocarpus sphaericus fruits on in vitro rat mast cells.

Elaeocarpus sphaericus (Syn: E. ganitrus), in Ayurvedic Medicine commonly known as Rudraksha is known to have wide range of pharmacological activities. We reported previously the protective action of E. sphaericus in experimental bronchial asthma. The present study on rat mesenteric mast cell was undertaken to investigate the effect of E. sphaericus fruits on autacoid release. The petroleum ether (PE), benzene (BE), chloroform (CE), acetone (AE) and ethanol (EE) extracts of E. sphaericus fruits were found to have mast-cell stabilizing activity, substantiating the efficacy of E. sphaericus against bronchial asthma.

Animals↗