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

Serotonin is a naturally occurring vasoactive substance that has diverse cardiophysiological effects. These effects can be explained by the existence of serotonin receptor subtypes which mediate different biological actions. The vasoconstrictive actions of serotonin are mediated by 5-HT2 serotonergic receptors, and serotonin also amplifies the release and activities of other vasoconstrictors, such as angiotensin and norepinephrine. Abnormalities in the serotonergic system may play an important role in the pathophysiology of multiple cardiovascular disease states such as systemic hypertension, primary pulmonary hypertension and peripheral vascular disease. Selective 5-HT2 serotonergic receptor blockers have been developed which appear to be potent vasodilators with therapeutic potential in various cardiovascular disease states. The largest clinical experience has been collected with ketanserin, and other agents in this class are being investigated. Prolongation of the ECG QT interval with 5-HT2 serotonergic receptor blockers may pose a potential risk with these treatments in some patients.
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PMID:Serotonin and the heart. 1082 27

37 patients with obvious pregnancy-induced hypertension, 56 normal pregnant women and 40 nonpregnant women in the same age groups were tested on their serum calcium(Ca), phosphorus(P) alkaline phosphatase(AKP), parathyroid hormone(PHT) and calcitonin(CT). Results indicated that the respective means of serum Ca and CT were statistically lower (P < 0.05), while AKP and PTH were higher (P < 0.01) than that of normal pregnant women. It was also confirmed that Ca metabolism of patients with pregnancy-induced hypertension was obviously abnormal. In addition, pathogenesis of pregnancy-induced hypertension was also discussed.
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PMID:[Observation and analysis on metabolism of serum calcium and phosphorus in patients with pregnancy-induced hypertension]. 1092 Nov 21

Pulmonary arterial hypertension in children can occur secondary to shunt lesion like ventricular septal defect, patent ductus arteriosus or it may be idiopathic, the so-called primary pulmonary hypertension (PPH). The progression of PPH is usually rapid in children as compared to adults and the mean survival is 2-3 years after the diagnosis is made. Histological changes in the form of medical muscular hypertrophy, intinal hyperplasia and later angiornatous, plexiform lesions occur in pulmonary vasculature. The pulmonary vasculature normally is a high flow, low resistance circuit and allows large blood flow without marked increase in pulmonary arterial pressure. However, with prolonged increased flow or any other vasoconstrictor stimulus, histological changes start occurring in the pulmonary bed resulting in increasing pressure in pulmonary artery. Right ventricular hypertension follows resulting in right ventricular hypertrophy and later dysfunction. Life threatening arrhythmias may result in sudden death in some of these patients. Clinical presentation is in the form of exertional dyspnoea with syncope at times. Over 50% of children with PPH are helped by vasodilators. They may be treated with calcium channel blockers (e.g. nifedipine, dose titrated to blood pressure) orally. Those not responding to oral vasodilators can be put on chronic inhaled nitric oxide or continuous intravenous prostacyclin infusion. Chronic anticoagulation therapy may also increase survival. In symptomatic cases, blade/balloon atrial septostomy may increase survival in patients of PPH with intact atrial sptum. For children not responding to medical therapy, lung transplantation may be the answer in near future.
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PMID:Diagnosis and management of primary pulmonary hypertension. 1095 38

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
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PMID:Cardiac abnormalities in birth asphyxia. 1095 39

Biochemical and molecular biological evidence indicates that endothelin (ET)-1 and its receptors are selectively upregulated in the lung during exposure to hypoxia, while functional evidence indicates that ET-1 is a major mediator of hypoxia-induced pulmonary vasoconstriction and vascular remodeling. Hypoxia stimulates ET-1 gene transcription and peptide synthesis in cultured endothelial cells, and plasma ET-1 levels are increased in patients with primary pulmonary hypertension, and in humans exposed to high altitude, while immunoreactive ET-1 and ET-1 mRNA levels are increased in pulmonary artery endothelial cells of patients with primary pulmonary hypertension. Rats exposed to normobaric hypoxia exhibit increased pulmonary artery pressure, increased ET-1 peptide levels in plasma and lung, and selective increases in steady-state ET-1 and ET(A) and ET(B) receptor mRNA levels in lung but not in organs perfused by the systemic vasculature. The observations that both ET-1 and its major vascular smooth-muscle cell receptor are upregulated in response to hypoxia suggest that ET-1 may be a mediator of hypoxia-induced pulmonary hypertension. Moreover, hypoxic pulmonary vasoconstriction and vascular remodeling can be prevented and reversed by administration of either an ET(A)-selective or a combined ET(A) and ET(B) receptor antagonist. These findings support the hypothesis that endogenous ET-1 plays a major role in hypoxic pulmonary vasoconstriction/hypertension, right heart hypertrophy, and pulmonary vascular remodeling and suggest that ET-receptor blockers may be useful in the treatment and prevention of hypoxic pulmonary hypertension in humans.
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PMID:Endothelin and pulmonary hypertension. 1097 82

Pulmonary hypertension is a pathologic condition characterized by elevated pulmonary artery pressures and an associated vasculopathy. Primary pulmonary hypertension (PPH) is a rare condition with a sporadic occurrence and a familial form of the disorder. Abnormal vasomotor tone in the pulmonary vasculature results from an imbalance of the action of various vasoconstrictors/ vascular proliferative agents (endothelin and thromboxane) versus vasodilators /anti-proliferative agents (prostacyclin and nitric oxide). The mainstay of outpatient therapy has been the use of digitalis, diuretics, oxygen, and coumadin and the judicious use of vasodilator therapy. Calcium channel blockers in a select group and intravenous prostacyclin have dramatically improved survival for those with primary pulmonary hypertension. Use of prostaglandin I2 (PGI2) in other forms of chronic pulmonary arterial hypertension is not as clear, although evidence of initial beneficial response is promising. Importantly, over the next few years both pharmacologic and nonpharmacologic treatment modalities for pulmonary hypertension may rapidly change as we focus more on the abnormal pulmonary vascular biology and concomitant hemodynamic and neurohormonal milieu.
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PMID:Current management of patients with pulmonary hypertension and right ventricular insufficiency. 1098 Aug 99

Endogenous peptidases participate in a major way in the formation of peptide pressor substances such as angiotensin II (A II) and endothelin (ET) as well as in the degradation of depressor substances, e.g. atrial natriuretic peptide (ANP) or bradykinin. They include on the one hand the angiotensin converting enzyme (ACE) and endothelin converting enzyme (ECE), on the other hand kinase II for bradykinin and neutral endopeptidase 24.11 (NEP) for ANP. Inhibition of these enzymatic reactions leads to a decline of vasopressors A II and ET and conversely delays the break-down of vasodilatating bradykinin and ANP. The main haemodynamic consequence of this double inhibition is a reduced peripheral vascular resistance and decline of the blood pressure. The concurrent block of both systems (dual inhibition) is more effective than the isolated block of one substance. The first dual endopeptidase inhibitors were ACE inhibitors blocking the conversion of angiotensin I to A II and inhibiting at the same time the degradation of bradykinin by kininase II which is identical with ACE. At present further substances were synthetized with a dual inhibitory effect e.g. on ECE and on NEP (phosphoramidone, thiorphan, ecadatril etc.). Under experimental conditions they have a long-term antihypertensive effect on the vascular wall and heart muscle. The development of another dual ACE and NEP inhibitor has reached already the stage of clinical tests and the first clinical studies. The preparation omapatrilate in amounts of 2.5-80 mg significantly reduced the BP in a dose-dependent way in mild and medium advanced essential hypertension. Normalization of the blood pressure, i.e. a drop below 140/90 mm Hg, was achieved with omapatrilate monotherapy in as many as 83% of patients with hypertension stage I and in 53% patients with essential hypertension stage II. The drop of blood pressure after 20-80 mg/day depended on the degree of hypertension and was comparable or better than monotherapy with lisonopril 20 mg/day or amlodipine 10 mg/day. Treatment with omapatrilate was well tolerated. Dual peptidase inhibitors interfering with the formation of pressor substances and with the degradation of depressor substances seem to be a perspective class of antihypertensives also useful in the treatment of other cardiovascular diseases (heart failure, primary pulmonary hypertension). Before its final inclusion in the therapeutic pattern, further comparative and clinical mortality studies must be implemented.
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PMID:[Dual endopeptidase inhibitors--a new direction in the development of hypertensive agents]. 1104 16

Lung transplantation has become an accepted therapy for patients with end-stage lung disease. The survival rate after this operation is not, however, satisfactory, being 40-50% at 5 yrs after lung transplantation; infections and pulmonary rejection (acute and chronic) are the cause of this brief survival. Recently, it has been shown that lung transplantation is an advantageous solution only for selected pathologies. The introduction of alternatives to lung transplantation (lung volume reduction surgery in emphysema, prostacyclin therapy in primary pulmonary hypertension and pulmonary thromboendarterectomy in chronic thromboembolic hypertension) has modified the number of patients admitted to the lung transplantation waiting list. In this study, admission to the lung transplantation waiting list in the first 50 and in the following 50 months of activity of the Pulmonary Division Medical Centre of Montescano were retrospectively compared in order to verify whether experience gained has influenced admission to the lung transplantation waiting list. The mortality rate of patients with idiopathic pulmonary fibrosis (44%), chronic thromboembolic pulmonary hypertension (50%) and primary pulmonary hypertension (52%) before lung transplantation was high; the mortality after lung transplantation was low in idiopathic pulmonary fibrosis (16%), but rather high in primary pulmonary hypertension (55%) and chronic thromboembolic pulmonary hypertension (50%). In contrast, the mortality rate of patients with Eisenmenger's syndrome and emphysema was fairly low while on the lung transplantation waiting list, but rather high after lung transplantation. The trend in admission to the lung transplantation waiting list changed during the two observation periods, with a reduction in the number of patients with Eisenmenger's syndrome and emphysema, but not of those with idiopathic pulmonary fibrosis, chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension. The experience gained modified the authors' approach to lung transplantation, but the "world" of lung transplantation still needs a lot more experience.
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PMID:Lung transplantation: the new point of view of an Italian centre. 1105 79

Systemic hypertension is a pathophysiological state that is manifested as high blood pressure and is a major risk factor for stroke, ischemic heart disease, peripheral vascular disease, and progressive renal damage. Pulmonary hypertension occurs in 3 distinct forms: primary pulmonary hypertension, pulmonary hypertension of the newborn, or secondary pulmonary hypertension attributable to a variety of lung and cardiovascular diseases. This review discusses the use of gene therapy in the control of systemic and pulmonary hypertension. Overexpression of vasodilator genes as well as antisense knockdown of vasoconstrictor genes has been successfully used in animal models of both forms of hypertension. Furthermore, the use of viral vectors to deliver these constructs has achieved long-term control of hypertension. The successful establishment of gene therapy techniques in the animal models of hypertension coupled with the anticipated advances in the genetic aspects of this disease would make it highly feasible to attempt gene delivery in the control of human hypertension.
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PMID:Current perspectives on the use of gene therapy for hypertension. 1111 Jul 68

Cardiac abnormalities in birth asphyxia were first recognised in 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the new born (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and therefore, requires treatment in the form of inotropic and ventilatory support, (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required, (v) persistent pulmonary hypertension of the new born (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory distress and cyanosis (sometimes differential). Clinical examination also reveals evidence of pulmonary arterial hypertension and right ventricular failure with systolic murmur of tricuspid and, at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
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PMID:Cardiac abnormalities in birth asphyxia. 1112 17


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