pituitrin and Cardiomegaly

pituitrin has been researched along with Cardiomegaly* in 14 studies

Reviews

4 review(s) available for pituitrin and Cardiomegaly

ArticleYear
Cardiac effects of vasopressin.
    Journal of cardiovascular pharmacology, 2014, Volume: 64, Issue:1

    Vasopressin is an essential hormone involved in the maintenance of cardiovascular homeostasis. It has been in use therapeutically for many decades, with an emphasis on its vasoconstrictive and antidiuretic properties. However, this hormone has a ubiquitous influence and has specific effects on the heart. Although difficult to separate from its powerful vascular effects in the clinical setting, a better understanding of vasopressin's direct cardiac effects could lead to its more effective clinical use for a variety of shock states by maximizing its therapeutic benefit. The cardiac-specific effects of vasopressin are complex and require further elucidation. Complicating our understanding include the various receptors and secondary messengers involved in vasopressin's effects, which may lead to various results based on differing doses and varying environmental conditions. Thus, there have been contradictory reports on vasopressin's action on the coronary vasculature and on its effect on inotropy. However, beneficial results have been found and warrant further study to expand the potential therapeutic role of vasopressin. This review outlines the effect of vasopressin on the coronary vasculature, cardiac contractility, and on hypertrophy and cardioprotection. These cardiac-specific effects of vasopressin represent an interesting area for further study for potentially important therapeutic benefits.

    Topics: Animals; Antidiuretic Agents; Cardiomegaly; Cardiovascular Physiological Phenomena; Coronary Vessels; Homeostasis; Humans; Myocardial Contraction; Vasoconstrictor Agents; Vasopressins

2014
[Hypertension associated with hyperthyroidism and hypothyroidism].
    Nihon rinsho. Japanese journal of clinical medicine, 2004, Volume: 62 Suppl 3

    Topics: Animals; Atrial Natriuretic Factor; Blood Volume; Cardiomegaly; Catecholamines; Humans; Hypertension; Hyperthyroidism; Hypothyroidism; Myocardial Contraction; Receptors, Thyroid Hormone; Renin-Angiotensin System; Thyroxine; Triiodothyronine; Vascular Resistance; Vasopressins

2004
[Molecular pathobiology in heart failure].
    Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology, 1994, Volume: 13, Issue:11

    Heart failure is a pathophysiological state resulting from disturbed cardiac function. It is based on complex molecular processes, many of which are not fully understood. During heart failure adaptive mechanisms, that reinstall altered cardiac function, are activated. The main mechanisms are: a) Alteration of the structure and composition of myocytes by myocardial hypertrophy, reexpression of fetal and neo-natal proteins and the expression of certain proto-oncogenes; b) Activation of the neuroendocrinal system, specifically the sympathetic nervous system, renin-angiotensin-aldosterone system and vasopressin release; c) Activation of autocrine and paracrine systems. However, when these systems are activated beyond a certain limit they contribute to heart failure aggravation. This can also be promoted by alteration of the calcium metabolism inherent in heart failure. The synthesis of the counterregulator atrial natriuretic factor is also increased.

    Topics: Atrial Natriuretic Factor; Calcium; Cardiomegaly; Heart Failure; Humans; Neurosecretory Systems; Protein Biosynthesis; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins

1994
[Atrial natriuretic factor].
    Annales francaises d'anesthesie et de reanimation, 1990, Volume: 9, Issue:2

    Although ANF research started 30 years ago, the atrial natriuretic factor (ANF) was only discovered recently (1981). The presence of such a factor has been suspected for many years because of histological and physiological arguments. In 1956, Kish found "dense granules" in the atrial walls of guinea pigs. Gauer and Henry could explain some of their experimental results on diuresis and natriuresis only by suggesting the presence of a third hormonal factor, but neither by the renin-angiotensin system, nor the anti-diuretic hormone. Hall et al. were the first to recognize a link between the granules and water and sodium metabolism. But it was De Bold who published the crucial experiment in 1981: injecting right atrial extracts to anaesthetized rats rapidly induced intense and transitory diuresis and natriuresis. ANF was born, and, at the same time, the concept of the heart as an endocrine gland. Indeed, ANF corresponds to the strict definition of a hormone. It has the following properties: natriuresis and diuresis via an increase in glomerular filtration fraction without any major changes in renal plasma flow; direct vasodilation of the large arteries with only few effects on small arterioles and veins. The stimuli for ANF secretion are mechanical and pharmacological, especially drugs currently used by anaesthetists. Atrial distension is the main mechanical stimulus. An increase in atrial transmural pressure is always followed by a release in ANF, but this effect is not constant for increases in intra-luminal pressure. It is the former pressure gradient alone that reflects the volume of the right atrium, the mechanical stimulus for ANF secretion. Tachycardia, or, more precisely, an increase in the atrial contraction rate, also leads to an important release of ANF. Cardiac nerves are not necessary for this, as demonstrated by studies in heart transplant patients. Only few pharmacological agents have been shown to really stimulate ANF secretion. In rats, morphine has a direct secretory effect, whereas ketamine hydrochloride, diethylether and chloral hydrate do so by increasing the release of catecholamines. The effects of alpha, beta adrenergic agonists and calcium agonists remain controversial. ANF, which has diuretic and vasodilator effects, plays a part, together with the renin-angiotensin system and the anti-diuretic hormone, in blood volume control in mammals. However, it has a special role to play, because it is a rapid release hormone: rapid vascular fi

    Topics: Anesthetics; Animals; Atrial Natriuretic Factor; Calcium Channel Agonists; Cardiomegaly; Diuresis; Fentanyl; Glomerular Filtration Rate; Humans; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Sympathomimetics; Tachycardia; Vasodilation; Vasopressins

1990

Trials

1 trial(s) available for pituitrin and Cardiomegaly

ArticleYear
[Increase by ANP and ADH of the duration of activation and deactivation of the cardiopulmonary baroreceptor reflex: modification in the presence of left ventricular hypertrophy].
    Cardiologia (Rome, Italy), 1990, Volume: 35, Issue:5

    The involvement of cardiopulmonary and arterial sinoaortic receptors in the control of antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) release is still controversial in humans. Moreover, it is not clear if this control may be impaired in hypertensive patients with left ventricular hypertrophy (LVH). We studied 17 male subjects, age 18-58 (6 normotensives and 9 mild hypertensives, 5 without and 4 with LVH). Each subject underwent selective loading and unloading of cardiopulmonary receptors, in a randomized sequence, by application of a positive (LBPP) or negative (LENP) pressure to the lower body (steps: +10, +20, +40, -10, -40 mmHg, each for about 30 min), through a plexyglass-constructed tubular apparatus with a rubber adhesion round the patients' waist. Blood samples were taken at the end of every step for measurement of ADH, ANP, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. Cuff arterial pressure was measured every 5 min, while heart rate was evaluated by continuous ECG recording. Hypertensive subjects underwent right atrial pressure measurement by an iv catheter and forearm blood flow evaluation at rest and during the different steps (venous occlusion plethysmography). During LBNP, ADH plasma levels increased progressively, but the increase became statistically significant only at the step of -40 mmHg. ANP increased significantly during LBPP. Taking into account only hypertensive patients, a consistent reduction in the changes of ADH and ANP plasma levels, respectively during LBNP and LBPP in patients with LVH in respect to those without LVH was found.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adolescent; Adult; Atrial Natriuretic Factor; Blood Pressure; Cardiomegaly; Electrocardiography; Heart; Heart Ventricles; Humans; Lung; Male; Middle Aged; Pressoreceptors; Pressure; Reflex; Vasopressins

1990

Other Studies

9 other study(ies) available for pituitrin and Cardiomegaly

ArticleYear
Protein kinase C regulates internal initiation of translation of the GATA-4 mRNA following vasopressin-induced hypertrophy of cardiac myocytes.
    The Journal of biological chemistry, 2007, Mar-30, Volume: 282, Issue:13

    GATA-4 is a key member of the GATA family of transcription factors involved in cardiac development and growth as well as in cardiac hypertrophy and heart failure. Our previous studies suggest that GATA-4 protein synthesis may be translationally regulated. We report here that the 518-nt long 5'-untranslated region (5'-UTR) of the GATA-4 mRNA, which is predicted to form stable secondary structures (-65 kcal/mol) such as to be inhibitory to cap-dependent initiation, confers efficient translation to monocistronic reporter mRNAs in cell-free extracts. Moreover, uncapped GATA-4 5'-UTR containing monocistronic reporter mRNAs continue to be well translated while capped reporters are insensitive to the inhibition of initiation by cap-analog, suggesting a cap-independent mechanism of initiation. Utilizing a dicistronic luciferase mRNA reporter containing the GATA-4 5'-UTR within the intercistronic region, we demonstrate that this leader sequence confers functional internal ribosome entry site (IRES) activity. The activity of the GATA-4 IRES is unaffected in trans-differentiating P19CL6 cells, however, is strongly stimulated immediately following arginine-vasopressin exposure of H9c2 ventricular myocytes. IRES activity is then maintained at submaximal levels during hypertrophic growth of these cells. Supraphysiological Ca(2+) levels diminished stimulation of IRES activity immediately following exposure to vasopressin and inhibition of protein kinase C activity utilizing a pseudosubstrate peptide sequence blocked IRES activity during hypertrophy. Thus, our data suggest a mechanism for GATA-4 protein synthesis under conditions of reduced global cap-dependent translation, which is maintained at a submaximal level during hypertrophic growth and point to the regulation of GATA-4 IRES activity by sarco(ER)-reticular Ca(2+) stores and PKC.

    Topics: Cardiomegaly; Cell Line, Tumor; GATA4 Transcription Factor; HeLa Cells; Humans; Myocytes, Cardiac; Protein Biosynthesis; Protein Kinase C; RNA, Messenger; Vasopressins

2007
Increased preload directly induces the activation of heat shock transcription factor 1 in the left ventricular overloaded heart.
    Cardiovascular research, 2002, Aug-01, Volume: 55, Issue:2

    The rapid induction of heat shock proteins (HSPs) by cardiac overload has been shown using in vivo models and it is assumed that HSPs are involved in myocardial protection against cardiac overload. However, the mechanisms for the induction of heat shock response by cardiac overload remain unclear. We examined whether increased preload as mechanical stress directly induces heat shock gene expression.. Rat hearts were isolated and perfused with Krebs-Henseleit buffer by the Langendorff method. Whole-cell extracts were prepared for gel mobility shift assay using oligonucleotides containing the heat shock element. We examined the induction of the DNA-binding activity of heat shock transcription factor (HSF), by which the transcription of heat shock genes is mainly regulated, during increased preload of left ventricle (LV) or perfusion with the buffer containing epinephrine, norepinephrine, angiotensin II, or vasopressin.. In preloaded hearts, with LVEDP of both 30 and 50 mmHg, the DNA-binding activity of HSF1 was detected at 10 min, and increased at 20 and 60 min. At any time point, the activity with LVEDP of 50 mmHg was stronger than that with LVEDP of 30 mmHg. However, none of these hypertensive agents activated the DNA-binding activities of HSF. In afterloaded hearts, with the perfusion of norepinephrine, the activation of HSF was not induced.. Our findings demonstrate that increased preload as mechanical stress directly induces the activation of HSF1 in the LV-overloaded heart.

    Topics: Angiotensin II; Animals; Cardiomegaly; DNA-Binding Proteins; Epinephrine; Gene Expression Regulation; Heat Shock Transcription Factors; Heat-Shock Proteins; Hemodynamics; Male; Norepinephrine; Organ Culture Techniques; Rats; Rats, Sprague-Dawley; Stress, Mechanical; Transcription Factors; Vasopressins; Ventricular Dysfunction, Left

2002
Hypertrophic growth of cultured neonatal rat heart cells mediated by vasopressin V(1A) receptor.
    European journal of pharmacology, 2000, Mar-10, Volume: 391, Issue:1-2

    Primary cultures of neonatal cardiac myocytes were used to determine both the identity of second messengers that are involved in vasopressin receptor-mediated effects on cardiac hypertrophy and the type of vasopressin receptor that is involved in vasopressin-induced cell growth. Neonatal rat myocytes were plated at a density of 1x10(6) cells per 60 mm dish and were incubated with serum-free medium for 7 days. Treatment of myocytes with vasopressin significantly increased the RNA-to-DNA ratio, by 18-25%, at culture days 4-6 and the protein-to-DNA ratio by 18-20% at culture days 5-7. Rates of protein synthesis were determined to assess their contribution to protein contents during myocyte growth. Vasopressin significantly accelerated rates of protein synthesis by 25% at culture day 6. Intracellular free Ca(2+) ([Ca(2+)](i)) was transiently increased after vasopressin exposure. After the peak increase in [Ca(2+)](i) at less than 30 s, there was a sustained increase for at least 5 min. The specific activity of protein kinase C in the particulate fraction was increased rapidly after exposure to vasopressin, and its activity remained higher for 30 min, returning to its control level within 60 min. The activity of protein kinase C in the cytosol was significantly decreased at all times after exposure to vasopressin. After vasopressin treatment, the content of c-fos mRNA was increased. The stimulatory effects of vasopressin on these parameters were significantly inhibited by vasopressin V(1A) receptor antagonist, OPC-21268, but not by vasopressin V(2) receptor antagonist, OPC-31260. These results suggest that vasopressin directly induces myocyte hypertrophic growth via the V(1A) receptor in neonatal rat heart cells.

    Topics: Animals; Animals, Newborn; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Blotting, Northern; Calcium; Cardiomegaly; Cells, Cultured; Culture Media; DNA; Kinetics; Myocardium; Piperidines; Protein Biosynthesis; Protein Kinase C; Proteins; Proto-Oncogene Proteins c-fos; Quinolones; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; RNA, Messenger; Second Messenger Systems; Vasopressins

2000
Antidiuretic hormone and atrial natriuretic peptide during lower body negative or positive pressure in hypertensive patients with and without left ventricular hypertrophy.
    Clinical and experimental hypertension. Part A, Theory and practice, 1992, Volume: 14, Issue:4

    Aim of the study was to evaluate the effect of cardiopulmonary receptors activation and deactivation on antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) incretion in hypertensive and normotensive subjects. Twenty-one male subjects, 7 normotensives and 14 mild hypertensives, 7 without and 7 with left ventricular hypertrophy (LVH) were admitted to the study. Each subject underwent selective loading and unloading of cardiopulmonary receptors, by application of a positive (LBPP) or negative (LBNP) pressure to the lower body. Blood samples were taken for measurement of ANP, ADH, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. ADH plasma concentration increased during cardiopulmonary receptors inhibition, but this increase became statistically significant (p less than 0.05) at a step of LBNP (-40 mm Hg), in which an involvement of the sinoaortic receptors cannot be excluded. ANP plasma levels increased progressively during LBPP (p less than 0.05 at least). These changes were significantly reduced in hypertensive patients with LVH.

    Topics: Adolescent; Adult; Atrial Natriuretic Factor; Cardiomegaly; Hemodynamics; Hormones; Humans; Hypertension; Lower Body Negative Pressure; Male; Middle Aged; Pressoreceptors; Pressure; Vasopressins

1992
Cardiac function and cardiovascular hormone balance during hemodialysis with special reference to atrial natriuretic peptide.
    Clinical nephrology, 1988, Volume: 30, Issue:6

    Echocardiographically determined left ventricular function and cardiovascular hormone balance were assessed before and after hemodialysis in 10 patients who had been on hemodialysis for 4 months to 15 years. Plasma levels of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), renin activity and aldosterone were determined. All patients had vector- and echocardiographic evidences of slight to moderate left ventricular hypertrophy. The body weight decreased 2.0 kg (3.3 +/- 0.5%) with dialysis. Nine out of ten patients showed a slightly reduced ejection fraction that normalized after dialysis (p less than 0.05). Left atrial and ventricular systolic dimensions were around the upper reference limit before dialysis with a decrease after dialysis (p less than 0.05 and p less than 0.02, respectively). The levels of ANP decreased with dialysis from 2-17 times to 1 to 15 times the upper reference value in nine out of the ten patients. In the whole group the decrease was 117 +/- 35% (p less than 0.005). A significant regression was obtained between percentage decrease of body weight and percentage change of ANP (r = 0.67; p less than 0.05). The plasma concentration of ADH did not change following dialysis but the mean value was significantly higher than the mean value of the reference group of the laboratory (p less than 0.05 before and p less than 0.005 after dialysis). Renin activity and aldosterone levels were low and did not change during dialysis. In conclusion, the slight left ventricular hypertrophy may partly be a response to volume overload with hyperdynamic circulation and partly to metabolically depressed myocardial function.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Cardiomegaly; Echocardiography; Female; Heart; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Renin; Vasopressins

1988
Relation between left atrial diameter and plasma atrial natriuretic peptide, renin and vasopressin.
    The American journal of cardiology, 1986, Nov-15, Volume: 58, Issue:11

    Topics: Adult; Aged; Atrial Natriuretic Factor; Cardiomegaly; Female; Heart Atria; Humans; Male; Middle Aged; Renin; Vasopressins

1986
Rate and extent of adaptive cardiovascular changes in rats during experimental renal hypertension.
    Acta physiologica Scandinavica, 1974, Volume: 91, Issue:1

    Topics: Age Factors; Animals; Aorta, Thoracic; Barium Sulfate; Blood Pressure; Body Water; Body Weight; Cardiomegaly; Constriction; Dose-Response Relationship, Drug; Heart Ventricles; Hypertension, Renal; Kidney; Male; Muscle, Smooth; Norepinephrine; Organ Size; Renal Artery; Time Factors; Vasopressins

1974
[Diuresis caused by left atrial distension or negative pressure respiration. New arguments in favour of a neuropituitary participation].
    Pathologie et biologie, 1968, Volume: 16, Issue:19

    Topics: Anesthesia; Animals; Cardiac Catheterization; Cardiomegaly; Diabetes Insipidus; Diuresis; Dogs; Heart Atria; Hypothalamo-Hypophyseal System; Methods; Polyuria; Pressoreceptors; Pressure; Respiration; Vagotomy; Vasopressins

1968
[ON THE EFFECT OF DILATATION OF THE LEFT ATRIUM ON RENAL WATER AND SODIUM EXCRETION IN THE NONANESTHETIZED AND ANESTHETIZED DOG].
    Verhandlungen der Deutschen Gesellschaft fur Kreislaufforschung, 1964, Volume: 30

    Topics: Anesthetics; Anesthetics, Local; Arginine Vasopressin; Cardiomegaly; Dilatation; Dogs; Heart Atria; Kidney; Physiology; Research; Sodium; Vasopressins; Water; Water-Electrolyte Balance

1964
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