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At least 1,189 records · Page 66Linked to original sources
PubMed2004

Cannabinoid pharmacology in the cardiovascular system: potential protective mechanisms through lipid signalling.

Cannabinoids include not only plant-derived compounds (of which delta9-tetrahydrocannabinol is the primary psychoactive ingredient of cannabis), but also synthetic agents and endogenous substances termed endocannabinoids which include anandamide (2-arachidonoylethanolamide) and 2-arachidonoylglycerol. Cannabinoids act on specific, G-protein-coupled, receptors which are currently divided into two types, CB1 and CB2. Relatively selective agonists and antagonists for these receptors have been developed, although one agent (SR141716A) widely used as an antagonist at CB1 receptors has non-cannabinoid receptor-mediated effects at concentrations which are often used to define the presence of the CB1 receptor. Both cannabinoid receptors are primarily coupled to Gi/o proteins and act to inhibit adenylyl cyclase. Stimulation of CB1 receptors also modulates the activity of K+ and Ca2+ channels and of protein kinase pathways including protein kinase B (Akt) which might mediate effects on apoptosis. CB, receptors may activate the extracellular signal-regulated kinase cascade through ceramide signalling. Cannabinoid actions on the cardiovascular system have been widely interpreted as being mediated by CB1 receptors although there are a growing number of observations, particularly in isolated heart and blood vessel preparations, that suggest that other cannabinoid receptors may exist. Interestingly, the currently identified cannabinoid receptors appear to be related to a wider family of lipid receptor, those for the lysophospholipids, which are also linked to Gi/o protein signalling. Anandamide also activates vanilloid VR1 receptors on sensory nerves and releases the vasoactive peptide, calcitonin gene-related peptide (CGRP), which brings about vasodilatation through its action on CGRP receptors. Current evidence suggests that endocannabinoids have important protective roles in pathophysiological conditions such as shock and myocardial infarction. Therefore, their cardiovascular effects and the receptors mediating them are the subject of increasing investigative interest.

Animals↗
PubMed1981

Relative activities of atenolol and metoprolol on the cardiovascular system of man.

The effects or oral atenolol (100 mg once/day) and metoprolol (100 mg once/day, 100 mg twice/day and 300 mg once/day) have been compared with placebo on the heart rate and systolic blood pressure responses to exercise in 5 healthy volunteers. The drugs were given for 5 days in a double blind randomised fashion with each volunteer receiving each dose of drug. Measurements were made after the first dose on day 1 and after 5 days of dosing. The results on both heart rate and systolic blood pressure showed that overall (over a 24 h period) after acute (day 1) or after chronic (5 days) dosing, atenolol 100 mg once/day, metoprolol 100 mg twice/day and 300 mg once/day, were equivalent as beta-adrenoceptor blocking doses. Thus milligram for milligram atenolol and metoprolol do not produce equivalent blockade on the cardiovascular system of man.

Adolescent↗
PubMed1976

[Age-specific characteristics of functional disorders of the cardiovascular system and respiration in experimental atherosclerosis].

Results of investigations into age-specific peculiarities inherent in the contractile function of the cardiac ventricular myocardium, hemodynamics of the lesser circulation, oxygen supply of the organism in young (6--12 months old) and old (3 1/2--4 1/2 year old) rabbits in normalcy and with experimental atherosclerosis are reported. The contractility of the left ventricle myocardium in old animals was down as compared to the normal in young ones. Induction of atherosclerosis impairs this important function of the myocardium to a still greater degree. In old animals hemodynamics of the lesser circulation is characterized by a rising systolic pressure in the right ventricle and of the tension-time index (TTI) as contrasted against the young one in normalcy and with atherosclerosis. Against this background an additional action on the organism is attended by more pronounced pathological manifestations, i.e. in reactions of the cardiovascular system (including the lesser circulation). The initial manifestations of hypoxia recorded in older animals, as compared to the younger ones in normality, become more intensive in cases of induced atherosclerosis. There is reduced consumption of oxygen, oxygen saturation of arterial and, especially, mixed venous blood, as well as oxygen tension in the arterial blood. The recorded changes are of significance in clarifying the caused and conditions conducive to the development of atherosclerosis and to the intensification of its manifestations in an old organism.

Age Factors↗
PubMed2004

Effects of thyroid hormone on the cardiovascular system.

Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias - namely, atrial fibrillation - whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism ("subclinical hypothyroidism") or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring ("subclinical hyperthyroidism"), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease.

Cardiovascular Diseases↗
PubMed1983

Aristotle's "triventricular" heart and the relevant early history of the cardiovascular system.

Aristotle said that the human heart has three ventricles--right, left, and middle--a concept that has often been viewed as an astonishing error. But was it? Aristotle did not miscount ventricles. In the third century BC, all cardiac chambers were called "ventricles," meaning "cavities." The "ears" (auricles) were distinguished from the "cavities" (ventricles) by Herophilus of Alexandria (c 300 BC) and by Rufus and Ephesus (a contemporary of Jesus Christ). Aristotle regarded the right atrium as a venous dilatation, not as a part of the heart. Aristotle's "right ventricle" was our right ventricle. His "left ventricle" was our left atrium. His "middle ventricle" was our left ventricle. Because he did not count the right atrium, Aristotle considered the human heart to be three-chambered or "triventricular," consisting of the right ventricle, the left atrium, and the left ventricle. This report summarizes the relevant early history of the cardiovascular system.

Anatomy↗