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PubMed2002

[Cardiovascular system of normal aged subjects. Cardiovascular senescence].

The cardiovascular system of the elderly is characterised by (i) an increased characteristic impedance of the big vessels, without hypertension; (ii) a cardiac index unchanged at rest and during submaximal exercising, despite a diminished VO2 max; (iii) a diastolic dysfunction with reduced rapid early filling (E wave at echo) and enhanced atrial systole (A wave); (iv) benign arrhythmias; (v) a reduced coronary reserve and an increased sensitivity to ischemia; (vi) an efficacy of converting enzyme inhibitors remaining unchanged, despite an altered renin-agiotensin system.

Aged↗
PubMed2002

Renin angiotensin system and gender differences in the cardiovascular system.

In the effort to explain gender-related differences of the cardiovascular system, the renin-angiotensin system experienced intensive exploration. Indeed, the development of hypertension as well as the progression of coronary artery disease and heart failure have two factors in common: (1) display distinct gender specific characteristics and (2) are enhanced by the renin-angiotensin system. It is therefore interesting to note that data from experimental animals, epidemiological surveys, and clinical investigations suggest that the components of the circulating as well as tissue-based renin-angiotensin system are markedly affected by gender. However, the issue is complicated by counter-regulatory effects of estrogen on the system with the substrate, on one hand, and the processing enzymes as well as the chief receptor, on the other hand. In fact, angiotensinogen is up-regulated particularly by oral administration of estrogen, whereas renin, angiotensin-converting enzyme (ACE), and AT-1 receptor are down-regulated by the hormone. While under well-defined experimental conditions the net effect of estrogen appears to result in suppression of the renin-angiotensin system, the clinical situation may be more complex. The judgment is further complicated by the difficulty in precisely measuring the activity of the system at the tissue level. Moreover, clinically relevant read-outs for the activity of the renin-angiotensin system may be regulated multifactorially or only indirectly affected by the system. Nevertheless, the undisputable, profound biochemical changes in the renin-angiotensin system related to the estrogen status allow speculation that such interaction explains some of the differences in the cardiovascular system of men and women.

Angiotensin I↗
PubMedDate not supplied

Serotonin (5HT) and its antagonists: involvement in the cardiovascular system.

The cardiovascular actions of serotonin and its antagonists are reviewed with a view to clarifying whether serotonin has a role in blood pressure control through actions on the peripheral vasculature. Serotonin has complex actions in the heart and vasculature but none of these actions is completely understood. There is no doubt, however, that serotonin has extensive interactions with the sympathetic nervous system. The nature of the serotonin receptor is also discussed. There is extensive evidence that more than one type of serotonin receptor exists. Biochemical studies in brain homogenates have delineated two sub-populations of serotonin receptors, named 5HT1 and 5HT2. It is not clear whether the same receptor types exist in the vasculature but various actions of serotonin on the vasculature have tentatively been ascribed to actions on 5HT1- and 5HT2-type receptors. It is clear that there is some functional overlap between serotonin-receptors and alpha-adrenoceptors. The mechanism by which this overlap could occur is unknown although we suggest it may result from a physical overlap of serotonin receptors and alpha-adrenoceptors. Compounds which antagonize serotonin have provided the means for investigating serotonin receptors but have not clarified the role of serotonin in blood pressure control; certainly they have comparatively little effect on blood pressure and this may simply reflect the lack of free circulating serotonin. In animal studies the new serotonin antagonist ketanserin appears to lower blood pressure via alpha-adrenoceptor blockade.

Animals↗
PubMed2006

Complex actions of sex steroids in adipose tissue, the cardiovascular system, and brain: Insights from basic science and clinical studies.

Recent publications describing the results of the Women's Health Initiative (WHI) and other studies reporting the impact of hormone therapy on aging women have spurred reexamination of the broad use of estrogens and progestins during the postmenopausal years. Here, we review the complex pharmacology of these hormones, the diverse and sometimes opposite effects that result from the use of different estrogenic and progestinic compounds, given via different delivery routes in different concentrations and treatment sequence, and to women of different ages and health status. We examine our new and growing appreciation of the role of estrogens in the immune system and the inflammatory response, and we pose the concept that estrogen's interface with this system may be at the core of some of the effects on multiple physiological systems, such as the adipose/metabolic system, the cardiovascular system, and the central nervous system. We compare and contrast clinical and basic science studies as we focus on the actions of estrogens in these systems because the untoward effects of hormone therapy reported in the WHI were not expected. The broad interpretation and publicity of the results of the WHI have resulted in a general condemnation of all hormone replacement in postmenopausal women. In fact, careful review of the extensive literature suggests that data resulting from the WHI and other recent studies should be interpreted within the narrow context of the study design. We argue that these results should encourage us to perform new studies that take advantage of a dialogue between basic scientists and clinician scientists to ensure appropriate design, incorporation of current knowledge, and proper interpretation of results. Only then will we have a better understanding of what hormonal compounds should be used in which populations of women and at what stages of menopausal/postmenopausal life.

Adipose Tissue↗
PubMedDate not supplied

Nitric oxide and its role in the cardiovascular system.

Nitric oxide (NO) is a ubiquitous, naturally occurring molecule found in a variety of cell types and organ systems. In the cardiovascular system, NO is an important determinant of basal vascular tone, prevents platelet activation, limits leukocyte adhesion to the endothelium, and regulates myocardial contractility. NO may also play a role in the pathogenesis of common cardiovascular disorders, including hypotension accompanying shock states, essential hypertension, and atherosclerosis. In this review, we discuss the biochemistry of NO and focus on its biology and pathophysiology in the cardiovascular system.

Animals↗
PubMed2003

Gene-engineered models for genetic manipulation and functional analysis of the cardiovascular system in mice.

Cardiovascular disease remains a key issue in healthcare. During the last decade, transgenic and gene-targeted mouse technology has provided invaluable insights into cardiovascular molecular biology. Given the similarities between the mouse and human genomes, this study proposes that information experimentally derived using genetically manipulated mice can contribute significantly to the understanding of human cardiovascular pathophysiology. We first introduced the basic principles and methods of genetic manipulation, such as the breeding background in mice and the factors of construct design. Secondly, we reviewed the analyses related to genetic manipulation of the cardiovascular system from embryonic to adult mice. In conclusion, the gene-engineered mouse model is one of the most important tools developed in recent basic and clinical research.

Animals↗
PubMed2006

5-hydroxytryptamine receptors in the human cardiovascular system.

The human cardiovascular system is exposed to plasma 5-hydroxytryptamine (5-HT, serotonin), usually released from platelets. 5-HT can produce harmful acute and chronic effects. The acute cardiac effects of 5-HT consist of tachycardia (preceded on occasion by a brief reflex bradycardia), increased atrial contractility and production of atrial arrhythmias. Acute inotropic, lusitropic and arrhythmic effects of 5-HT on human ventricle become conspicuous after inhibition of phosphodiesterase (PDE) activity. Human cardiostimulation is mediated through 5-HT4 receptors. Atrial and ventricular PDE3 activity exerts a protective role against potentially harmful cardiostimulation. Chronic exposure to high levels of 5-HT (from metastatic carcinoid tumours), the anorectic drug fenfluramine and its metabolites, as well as the ecstasy drug 3,4-methylenedioxymethamphetamine (MDMA) and its metabolite 3,4-methylenedioxyamphetamine (MDA) are associated with proliferative disease and thickening of cardiac valves, mediated through 5-HT2B receptors. 5-HT2B receptors have an obligatory physiological role in murine cardiac embryology but whether this happens in humans requires research. Congenital heart block (CHB) is, on occasion, associated with autoantibodies against 5-HT4 receptors. Acute vascular constriction by 5-HT is usually shared by 5-HT1B and 5-HT2A receptors, except in intracranial arteries which constrict only through 5-HT1B receptors. Both 5-HT1B and 5-HT2A receptors can mediate coronary artery spasm but only 5-HT1B receptors appear involved in coronary spasm of patients treated with triptans or with Prinzmetal angina. 5-HT2A receptors constrict the portal venous system including oesophageal collaterals in cirrhosis. Chronic exposure to 5-HT can contribute to pulmonary hypertension through activation of constrictor 5-HT1B receptors and proliferative 5-HT2B receptors, and possibly through direct intracellular effects.

Animals↗
PubMed2000

Cell cycle molecules and diseases of the cardiovascular system.

Injury to the cardiovascular system causes an elevated expression of endothelin-1 (ET-1) and activation of several important signaling pathways including the mitogen-activated kinase (MAPK) cascade. The activation of these pathways has been implicated in the pathogenesis of cardiovascular disease caused by hypoxia, infections, and ischemia /reperfusion injury, cardiomyopathy and restenosis after balloon angioplasty. Important downstream targets of the MAPK and ET-1 pathways are the cell cycle regulatory molecules (cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors). Regulation of these molecules contributes to remodeling throughout the cardiovascular system. In addition, cell cycle molecules are important in the regulation of angiogenesis. These new data have led to the development of potential therapeutic modalities targeting these regulatory molecules in order to ameliorate various cardiovascular disease states.

Cardiovascular Diseases↗
PubMed1998

Molecular mechanisms underlying the role of nitric oxide in the cardiovascular system.

In the cardiovascular system, nitric oxide (NO) is involved in the short and long-term regulation of haemodynamics, and in a number of their pathological alterations. Investigation into the biochemistry of NO-synthase isoforms has confirmed that they also all produce superoxide anion (O(*)). The free radical NO can interact with many targets on which novel information has been recently obtained. The major results of these interactions are not only the well known activation of guanylyl cyclase, but also the formation of potentially cytotoxic peroxynitrite (ONOO(-)), and the formation of S-nitrosothiols and non-haem iron-dinitrosyl dithiolate complexes. Tissue O(2), O(*), low molecular weight thiols and transition metals (especially FeII) play a pivotal role in directing NO towards targets responsible for biological effects, or storage or release from these stores. In addition, circulating forms of NO have been proposed with S-nitrosation of blood proteins. All these mechanisms provide potential pharmacological targets for future therapeutic strategies.

Journal Article↗
PubMed2000

Skeletal muscle: master or slave of the cardiovascular system?

Skeletal muscle and cardiovascular system responses to exercise are so closely entwined that it is often difficult to determine the effector from the affector. The purpose of this manuscript and its companion papers is to highlight (and perhaps assist in unraveling) the interdependency between skeletal muscle and the cardiovascular system in both chronic and acute exercise. Specifically, we elucidate four main areas: 1) how a finite cardiac output is allocated to a large and demanding mass of skeletal muscle, 2) whether maximal muscle oxygen uptake is determined peripherally or centrally, 3) whether blood flow or muscle metabolism set the kinetic response to the start of exercise, and 4) the matching of structural adaptations in muscle and the microcirculation in response to exercise. This manuscript, the product of an American College of Sports Medicine Symposium, unites the thoughts and findings of four researchers, each with different interests and perspectives, but with the common intent to better understand the interaction between oxygen supply and metabolic demand during exercise.

Adaptation, Physiological↗
PubMed2000

[Circadian alterations of the cardiovascular system].

Circadian variations have been known for a long time for the influence they have on the physiological systems, including the cardiovascular system. The study of the mechanisms with circadian variation that change the function of the cardiovascular system and its diseases has increased greatly in recent years due to its clinical prominence. Through these studies, physiopathology, epidemiology and factors involved in cardiovascular diseases are more understandable. Thus, the incidence of cardiac events has been clearly associated with the morning hours, as well as the possible mechanisms involved in this variation during the daytime hours. The arterial blood pressure, plasma catecholamine levels and cortisol, platelet aggregation, and fibrinolytic system action are the most implicated mechanisms. From this knowledge, it is possible to design new therapeutic strategies that should consider the time of the day of higher risk for the onset of cardiovascular events.

Cardiovascular Diseases↗