UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated left ventricular (LV) function in 40 patients (pts) with hypertension (HT), 16 pts with hypertrophic cardiomyopathy (HCM), 3 pts with ASH and HT and in 27 control subjects by M-mode echocardiography using supine exercise (50 watts, 3 minutes). The hypertensive subjects were echocardiographically divided into three subsets; the normal LV (17 cases), the hypertrophied LV (17 cases) and the dilated LV (6 cases). Similarly, pts with HCM were echocardiographically and cineangiographically divided into three subsets; ASH (asymmetric septal hypertrophy, 6 cases), APH (predominant apical hypertrophy, 6 cases) and DFH (diffuse left ventricular hypertrophy, 4 cases). Changes of left ventricular dimension Controls and HT: Stroke volume was increased during exercise in the controls, normal LV and hypertrophied LV groups by decreasing LV end-systolic dimension ( LVDs ), but it was increased in dilated LV group by increasing LV end-diastolic dimension ( LVDd ) (Frank-Starling mechanism). LVDd was increased transiently in the controls and normal LV group during recovery, but its grade and duration were more pronounced in the latter. LVDd did not change significantly in hypertrophied and the dilated LV groups. HCM: LVDd and LVDs did not change significantly during exercise in all 3 groups. LVDd was increased transiently during recovery in ASH group, but not in the other groups. Changes of peak velocity of circumferential fiber shortening (VCF) and the ratio of peak systolic blood pressure to LV end-systolic volume (PSP/ LVVs ). Controls and HT: Peak VCF was increased during exercise most markedly in the normal LV group, but it was not increased in the dilated LV group. PSP/ LVVs was increased significantly during exercise in the controls, the normal and hypertrophied LV groups, but not in the dilated LV group. HCM: Peak VCF showed a significant increase during exercise in ASH group, but not in the other two groups. Changes of the D/S ratio. The ratio of systolic to diastolic velocity of the LV posterior wall was expressed as a D/S. This ratio did not change significantly in the controls, HT and APH groups, but it was decreased significantly in ASH and DFH groups. LV end-systolic wall stress and LVDs relationship ( ESWst - LVDs ).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Exercise echocardiography in different types of hypertension classified by left ventricular geometry; comparison with hypertrophic cardiomyopathy]. 668 25

Intense physical training through isotonic exercises has controversial effects in individuals with moderate to severe hypertension. In this study, normotensive Wistar rats and rats with renovascular hypertension (Goldblatt II) were subjected to intense physical exercise involving two 50-min swimming sessions per day for a period of 12 weeks. At the end of the study, we evaluated the effect of training on arterial pressure, the capacity for aerobic work and cardiac function. Our results demonstrate that intense physical training has no effect on the arterial blood pressure of normotensive rats or of animals with moderate renovascular hypertension. Hypertensive animals with cardiac hypertrophy require a greater period of training in order to attain the same capacity for aerobic work as normotensive rats. This difference may result from an inability of the former animals to increase cardiac compliance, thereby impeding more extensive usage of the Frank-Starling mechanism to subsequently increase the systolic cardiac performance. Cardiac hypertrophy induced by exercise did not summate with that induced by arterial hypertension. Physical exercise normalized the end-diastolic left ventricular pressure in hypertensive animals without any corresponding increase in the compliance of the chamber. The first derivative of left ventricular pulse pressure (+/- dP/dt) was greater in the hypertensive trained group than in the hypertensive sedentary rats. These observations suggest that a systolic dysfunction of the left ventricle involving an elevated residual volume secondary to arterial hypertension may be corrected by physical exercise such as swimming.
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PMID:The influence of isotonic exercise on cardiac hypertrophy in arterial hypertension: impact on cardiac function and on the capacity for aerobic work. 758 22

The Framingham heart study has shown that arterial hypertension is the major aetiological factor for the development of heart failure. In the presence of heart failure, various regulatory systems may be operative. These include the Frank-Starling mechanism, the neurohormonal system, regulation of cardiac growth and peripheral oxygen delivery. Recently, the interrelationship of the neuroendocrine system and cardiac growth has been examined. In the pressure or volume overloaded heart, growth of the myocardium involves the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Non-myocyte cell growth, including cardiac fibroblasts, may also occur. However, the haemodynamic load does not appear to be its major physiological stimulus. Cardiac fibroblast activation is responsible for the accumulation of type I and III collagens, the major fibrillar proteins of the myocardial collagen matrix, while vascular smooth muscle cell growth accounts for medial thickening of coronary resistance vessels. This structural remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy: it accounts for abnormal myocardial stiffness and impaired coronary reserve, thereby leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems are involved in the structural remodelling of the non-myocyte compartment, including the 'cardioprotective' effects of angiotensin converting enzyme (ACE) inhibition or the beneficial effects of anti-aldosterone treatment that were found to prevent myocardial fibrosis in renovascular hypertension due to unilateral renal ischaemia under experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of the structural remodelling of the myocardium: from hypertrophy to heart failure. 771 13

Adenosine triphosphate (ATP), a co-transmitter in sympathetic nerves and released from platelets, has recently been shown to stimulate growth of vascular smooth muscle cells. It might therefore contribute to the development of vascular hypertrophy seen in hypertension and atherosclerosis. We aimed at characterising the receptor mediating this mitogenic effect in rat aorta smooth muscle cells. The potency of agonists indicates a P2 purinoceptor since ATP > or = ADP >> AMP, adenosine. The P2x-receptor subtype, which is responsible for ATP induced vasoconstriction in rat aorta, does not mediate the mitogenic effect since alpha, beta-methyleneATP had no effect and beta, gamma-methyleneATP had lower potency than ATP. The P2Y-receptor subtype was excluded since the selective agonist 2-methylthioATP had weak effect with lower potency than ATP. When we studied the involvement of other nucleotides similar effects were seen of the purines ATP, GTP and ITP; also the pyrimidine UTP had powerful mitogenic effects (Emax = 52% of ATP) with similar potency. Nucleotides with fewer phosphate groups showed a stepwise fall in mitogenic effect. This indicates involvement of a nucleotide-receptor (P2U). Ap4A were of equal potency and effect as ATP. There was strong correlation between the mitogenic effects of the nucleotides and analogues with both 45Ca(2+)-influx and inositol phosphate (IP) production, indicating that they may participate in mediating the mitogenic response. This is the first study describing the potencies for the mitogenic effects of the selective ATP-analogues and other nucleotides in vascular smooth muscle cells. The receptor characterisation indicates a nucleotide-receptor similar to the receptor which stimulates 45Ca(2+)-influx and inositol phosphate-formation in rat aorta smooth muscle cells. Substances related to ATP such as GTP, ITP, UTP and Ap4A which also can be released extracellularly in vivo stimulate mitogenesis of rat aorta smooth muscle cells through the same receptor.
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PMID:Characterisation of an ATP receptor mediating mitogenesis in vascular smooth muscle cells. 778 5

According to the Framingham Study, arterial hypertension and coronary artery disease are the major etiologic factors in the development of heart failure. Regulatory systems that may affect heart failure include the Frank-Starling mechanism, neurohormonal responses, cardiac growth and peripheral oxygen delivery. Recently, the interrelationship between the neuroendocrine system and cardiac growth has aroused much interest. In the pressure- or volume-overloaded heart, hypertrophic growth of the myocardium includes the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Nonmyocyte cell growth involving cardiac fibroblasts may also occur but is not primarily regulated by the hemodynamic load. Cardiac fibroblast activation is responsible for the accumulation of fibrillar type I and type III collagens within the interstitium and adventitia of intramyocardial coronary arteries, while vascular smooth muscle cell growth accounts for the medial thickening of these vessels. This remodeling of the cardiac interstitium is a major determinant of pathological hypertrophy in that it accounts for abnormal myocardial stiffness and impaired coronary vasodilator reserve, leading to ventricular diastolic and systolic dysfunction and, ultimately, symptomatic heart failure. Several lines of evidence suggest that the renin-angiotensin-aldosterone system is involved in regulating the structural remodeling of the nonmyocyte compartment; this accounts for the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition, which prevents myocardial fibrosis in rats with renovascular hypertension. In rats with genetic hypertension, established left ventricular hypertrophy, abnormal diastolic stiffness due to interstitial fibrosis and reduced coronary vasodilator reserve associated with medial wall thickening of intramyocardial resistance vessels, the ACE inhibitor lisinopril restored myocardial structure and function towards normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cardiac structure-function relationship and the renin-angiotensin-aldosterone system in hypertension and heart failure. 782 69

The causes of left ventricular hypertrophy (LVH) in chronic renal failure are multifactorial. The tail arterial pressure, heart weight, maximum developed pressure and pressure-volume relationship in animals with 5/6 nephrectomy (CRF, n = 16) and CRF animals who received furosemide by oral gavage (CRF-F, n = 17) were studied. All CRF animals increased their blood pressure (Basal: 117.2 +/- 0.8; 6th week: 184.8 +/- 2.9, p < 0.001) but in those treated with furosemide the blood pressure stayed within normal levels (Basal: 118.23 +/- 1.3; 6th week = 118.8 +/- 1.6, p = 0.5734). SHAM animals served as control (SHAM, n = 15). All CRF and CRF-F animals increased their levels of serum creatinine (CRF = 1.81 +/- 0.05; CRF-F = 1.75 +/- 0.05; SHAM = 0.72 +/- 0.09 mg/dL p < 0.001). Cardiac weight was elevated in CRF and CRF-F when compared with SHAM rats. The operational maximum developed pressure was similar in the three groups (CRF = 221.2 +/- 7.04; CRF-F = 255.7 +/- 10.1; SHAM = 239.9 +/- 5.5 mmHg, n.s.). However, the end-diastolic volume was significantly increased in both CRF and CRF-F when compared with SHAM rats (CRF = 91.4 +/- 9.44; CRF-F = 70.9 +/- 6.22; SHAM = 28.75 +/- 3.12 microL. p < 0.001). These data demonstrate that LVH in chronic renal failure is not dependent of the arterial hypertension, that accompanies this condition. Moreover, the systolic work of LVH animals is similar to that of normal animals, but a greater utilization of Frank-Starling mechanism to maintain normal ventricular function is needed.
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PMID:[Ventricular function in animals undergoing renal mass ablation. Effect of blood pressure control]. 824 6

The aim of this investigation was to study the coronary pressure-flow relationship in 60 patients with chronic arterial hypertension of diverse aetiologies and in 14 normotensive subjects (control group). The hypertensive cohort included 6 patients with isolated systolic hypertension (ISH), 7 renovascular hypertensive patients with abnormally elevated angiotensin II plasma levels but without electrocardiographic and/or echocardiographic evidence of left ventricular hypertrophy (LVH) and 47 subjects with essential hypertension (EH), 21 of whom had LVH by electrocardiogram and/or echocardiogram. In the hypertensive cohort a Frank-Starling-like curve was found to describe the coronary pressure-flow relationship when the baseline values for coronary sinus blood flow (CBF, intravascular Doppler technique) were plotted against mean aortic pressure (intra-arterial blood pressure). In particular, the descending limb of such a curve represented a critical region where CBF was "inappropriately" low with respect to perfusion pressure. It was thus concluded that this inability of the heart to adapt CBF to its needs might account for the higher propensity to develop myocardial ischaemia encountered in severe essential hypertensive subjects with concomitant LVH and renovascular hypertensive patients.
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PMID:Coronary blood flow and myocardial ischaemia in hypertension. 853 20

We treated 10 patients who had chronic refractory idiopathic thrombocytopenic purpura (ITP) with high-dose dexamethasone (DXM, 40 mg/d for 4 sequential days every month). The interval from diagnosis ranged from 49 to 300 months, and patients had previously received a median of 5.5 treatments (including splenectomy in nine cases). Median platelet count was 14 x 10(9)l (range 6-26 x 10(9)/l) at the onset of DXM and eight patients had bleeding symptoms. Eight patients received at least three cycles of DXM. Five patients had a response (i.e. platelet count at least doubled and increased by > 20 x 10(9)/l), including one almost complete remission and four minor responses (MR). Of the MR, one was probably due to concurrent IVIg administration, and all four MR were transient, in spite of further cycles of DXM. In three patients DXM was a failure after three or four cycles. In two patients DXM had to be stopped after one course because of major side-effects (systemic hypertension with stroke and insulin-dependent diabetes, respectively). In our experience, high-dose DXM had a relatively limited effect in chronic refractory ITP and was associated with severe side-effects in some cases.
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PMID:Pulsed high-dose dexamethasone in refractory chronic idiopathic thrombocytopenic purpura: a report on 10 cases. 854 98

ETIOLOGY AND ANATOMY: Up to the Middle Ages, nosebleeds were considered a natural means of purification in internal diseases. In addition injuries, extreme physical exertion, and influences from the sexual sphere were recognized causes. In the 19th century, low atmospheric pressure on mountains and in balloons was also assumed to be an etiological factor. It was only at the end of the 19th century that the importance of high blood pressure and defective coagulation were diagnosed in context with nosebleeds. In ancient times, it was known that compressing the nasal alae can often stop the bleeding, but that blood may as well run down the throat and mimick a hemorrhage coming from the trachea. Between 1874 and 1884, several authors, among them J. L. Little in USA and W. Kiesselbach in Germany, recognized the anterior part of the nasal septum as a frequent location of bleeding. GENERAL THERAPY AND ANTERIOR NASAL PLUGGING: General measures of hemostasis recommended already in ancient times were the application of cold and diverting the blood to other regions of the body by applying tourniquets to legs and arms, or by cupping. Anterior nasal plugging was already known to the ancient Assyrians and Hippocrates. Scribonus Largus (1st century) was the first to describe a nasal plugging around a tube, thus preserving a patient respiratory passage. During the Middle Ages local application of assumedly hemostatic substances of the apothecary of that time played an important part, among them "cranial moss", the lichen that grew on the skulls of hanged corpses exposed to the weather for a long time, and "mumia", a black unctuous substance made of Egyptian mummies. Plugging the nares with an inflated balloon, fabricated from animal intestines, was described first by J. P. Frank in 1807. During the second half of the 19th century, numerous varieties of rubber balloons, rubber caps, and condoms came in use for this technique. The first nasal balloon combined with a respiratory tube was presented by Dionisio in 1890. POSTERIOR NASAL PLUGGING: Plugging of the posterior nares was anticipated by Hippocrates technique of removing a pendulous polyp by pulling a sponge tied to four strings backwards through the nasal cavity. Le Dran, surgeon in Paris in 1731, was the first to adopt this technique for stopping a nasal hemorrhage. The instrument named after Belloc (or Belloq) for placing a posterior nasal plug consists of a metal tube in which a curved spring can be pushed forwards and backwards. The first description of this instrument remains a mystery. There were at least two French surgeons named Belloc and Belloq, and this has been the source of some confusion. A paper of a certain Belloq of 1757, which is generally regarded as the source, deals with means of stopping certain hemorrhages. It exists in two different printed versions with identical wording and describes the application of candle wax for stopping severe hemorrhages after tooth extraction and abdominal puncture; however, it makes no mention of nosebleeds. Bellocq's tube was made known by Deschamps' book on diseases of the nose in 1804. For about 150 years, it was one of the instruments most frequently illustrated in textbooks and most rarely used in practice because surgeons generally preferred a simple catheter for placing a posterior nasal plug. The article concludes with a short survey of the history of chemical and thermal cauterisation and ligation of blood vessels for stopping nosebleeds.
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PMID:[Nosebleed in the history of rhinology. Images of the history of otorhinolaryngology presented by instruments from the collection of the Ingolstadt Medical History Museum]. 886 51

1. Extracellular adenosine triphosphate (ATP) is mitogenic for vascular smooth muscle cells (VSMC) and stimulates several events that are important for cell proliferation: DNA synthesis, protein synthesis, increase of cell number, immediate early genes, cell-cycle progression, and tyrosine phosphorylation. 2. Receptor characterization indicates mitogenic effects of both P2U and P2Y receptors. The P2X receptor is lost in cultured VSMC and is not involved. Several related biological substances such as UTP, ITP, GTP, AP4A, ADP, and UDP are also mitogenic. 3. Signal transduction is mediated via Gq-proteins, phospholipase C beta, phospholipase D, diacyl glycerol, protein kinase C alpha, delta, Raf-1, MEK, and MAPK. 4. ATP acts synergistically with polypeptide growth factors (PDGF, bFGF, IGF-1, EGF, insulin) and growth factors acting via G-protein-coupled receptors (noradrenaline, neuropeptide Y, 5-hydroxytryptamine, angiotensin II, endothelin-1). 5. The mitogenic effects have been demonstrated in rat, porcine, and bovine VSMC and cells from human coronary arteries, aorta, and subcutaneous arteries and veins. 6. The trophic effects on VSMC and the abundant sources for extracellular ATP in the vessel wall make a pathophysiological role probable in the development of atherosclerosis, neointima-formation after angioplasty, and possibly hypertension.
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PMID:Extracellular ATP: a growth factor for vascular smooth muscle cells. 959 70

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