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

The literature concerned with studies of the occurrence and function of the cyclic nucleotides in blood vessels is reviewed. Emphasis is placed on the critical evaluation of the evidence which relates to the hypothesis that cyclic nucleotides meditate the effects of drugs and neurotransmitters on vascular contractility. The hypothesis that cyclic AMP mediates vasodilation, especially that induced by beta-adrenergic relaxation, is supported by many experimental approaches, but it is concluded that the evidence remains unconvincing based on the criteria established for such a mediator role. Possible sites of action of cyclic AMP are discussed. The demonstrated action of cyclic AMP on vascular membrane electrophysiology and calcium ion pumps are reviewed as possible causes of relaxation. The role of both nucleotides in vascular disease, especially hypertension is discussed. Finally the needs for further research in this area are suggested.
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PMID:Occurrence and function of cyclic nucleotides in blood vessels. 17 65

Lipids and lipoproteins were analysed in forty-one survivors of stroke, aged less than 65 years, and the same number of age and sex matched controls without vascular disease. The stroke subjects had no evidence of coronary artery or peripheral vascular disease. High density lipoprotein cholesterol was significantly lower (1.19 +/- 0.06 mmol/l) in the stroke subjects than the controls (1.47 +/- 0.07 mmol/l). Triglyceride was also elevated in the stroke subjects, but this was confined to those who were taking antihypertensive treatment which included beta-blockers and/or thiazides. The low levels of high density lipoprotein in stroke were independent of hypertension or its treatment. Thus low levels of high density lipoprotein appear to be associated with cerebrovascular disease, while elevated triglyceride is a complication of anti-hypertensive therapy.
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PMID:Reduced high density lipoprotein in stroke: relationship with elevated triglyceride and hypertension. 22 76

The effects of mechanical ventilation with and without positive end-expiratory pressure (PEEP) on hemodynamic performance and blood-gas exchange were studied in ten patients following open-heart surgery. Ventilation at constant tidal volume (15 ml/kg body weight) with 10 cm H2O PEEP following aortic valve replacement (AVR) IN FIVE PATIENTs without pulmonary vascular disease was associated with the following significant changes: a rise in arterial Po2, a fall in the alveolar-arterial Po2 gradient when Fio2 = 1.0, decreases in calculated Qs/Qt and cardiac index. Using a similar pattern of ventilation following mitral valve replacement (MVR) in patients with elevated pulmonary vascular resistance, we found a significant decrease in cardiac index (but less than in the AVR group), a significant elevation of calculated physiologic deadspace (Vd/Vt) and no change in Qs/Qt. An hour after removal of PEEP, intravascular pressures, blood flow and blood-gas exchange values of all patients with AVR had returned to control levels; patients with MVR had persistently significantly low cardiac indices, while Vd/Vt returned to pre-PEEP values. These findings suggest that evaluation of responses to different ventilation patterns must take into account pre-existing V/Q abnormalities secondary to pulmonary vascular disease, particularly when these are secondary to chronic congestive heart failure. Following AVR, Qs/Qt changed in the same direction as cardiac index (CI) irrespective of ventilatory pattern: CI decreased and rose as CI increased. The authors conclude that with increasing severity of pulmonary vascular disease, changes in airway pressure will have an unpredictable effect on cardiac index unless the level of myocardial competence is taken into account. In the presence of ventricular failure, changes in pleural (and therefore transmural) pressures will be minimal compared with the high filling pressures and exert no influence on stroke volume. Although pulmonary venous hypertension was more pronounded in the MVR than in the AVR group, there was no significant difference between the postoperative values for Qs/Qt (Fio2 = 1.0), a condition probably fostered by marked differences in pre-existing V/Q.
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PMID:The effect of pre-existing pulmonary vascular disease on the response to mechanical ventilation with PEEP following open-heart surgery. 23 11

1. Diabetics have a greater risk of experiencing and of dying from a CHD event than age matched non-diabetics. 2. The excess risk is particularly notable in insulin dependent female diabetics who seem to lose the usual 'protection' accorded to women. 3. The cause or causes of the excess risk are not known. There are a variety of 'risk factors' observed in diabetics which, in sum, may contribute. 4. At least in insulin-dependent diabetics some cardiac morbidity and mortality may also be due, not to coronary heart disease, but to a cardiomyopathy secondary to intramural obstructive vascular disease and/or disordered myocardial metabolism. 5. No therapy has yet been convincingly proved to reduce (or to increase) the risk of cardiac morbidity or mortality. Nevertheless, in treating diabetics there is an a priori case for using diets designed to lower plasma lipid levels as well as the blood sugar, for early treatment of hypertension and for discouraging cigarette smoking.
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PMID:Diabetes and the heart: coronary heart disease. 33 40

Progress in our understanding diabetic angiopathy has been slow, but we are now learning a number of lessons of interest to the cardiologist. Diabetic angiopathy is a collective term for conditions specific to the diabetic state and related to its duration more than to patient age. The angiopathy produces calcification of the media of larger arteries, but its major effects are in the microcirculation. Intense interest in one feature, skeletal muscle capillary basement membrane thickening, has dominated the last decade. Capillary basement membrane thickening, while characteristic of diabetes, is associated with little direct impairment of the microcirculatin. It appears to play no role in the pathogenesis of diabetes itself. The pathology of diabetic retinopathy and diabetic nephropathy suggests that arteriolar changes may be the major mediator of diabetic angiopathy. This concept is supported by the interactions between hypertension and diabetes in the eye and kidney. The course of diabetes of youthful onset differs from that of maturity onset. The relative frequency of diabetic angiopathy is higher, and of atherosclerotic complications is lower. This has made it difficult to demonstrate the potential value of preventive measures. Benefit to one type of problem may become hidden by worsening of the other. If the diabetic benefits from what is learned about how ischemic heart disease risk can be reduced, he will require even more effective management to prevent or control diabetic angiopathy.
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PMID:Diabetic angiopathy--its lessons in vascular physiology. 35 70

To characterize the renin-angiotensin system in the Aoki-Okamoto spontaneously hypertensive rat (SHR) more fully, serial measurements of plasma renin activity (PRA), plasma renin concentration (PRC), renin reactivity (as relative index of circulating modifiers of the renin reaction) and renin substrate concentration were made in 6- to 64-week-old SHR and in age-matched Wistar-Kyoto normotensive rats (WKY). In the evolving phase of SHR hypertension (6 and 13 weeks of age), PRA was comparable to WKY control values, whereas mature SHR with established hypertension developed, between 13 and 35 weeks of age, a high-PRA state persisting through 64 weeks of age. In 64-week-old SHR, increased plasma volume (3.54 +/- 0.91 in SHR vs. 3.18 +/- 0.90 ml/100 g body weight in WKY, p less than 0.025), together with increased PRA (24.9 +/- 3.8 in SHR vs. 13.1 2.2 ng AI/ml plasma/hr in WKY, p less than 0.025), suggest that volume decrease cannot explain increased PRA. In 42-week-old SHR, PRA was incompletely suppressed by deoxycorticosterone acetate plus 1% saline orally for 4 days: 4.9 +/- 1.2 in SHR vs. 0.6 +/- 0.8 ng angiotensin I/ml plasma/hr in WKY, p less than 0.001. Modestly increased renin reactivity of plasma was observed in SHR at all ages studied, supporting the ubiquity of increased circulating accelerators (or decreased inhibitors) of the renin reaction in hypertensive states. However, elevated renin reactivity did not account for the transition from normal to high PRA observed in mature SHR, nor did renin substrate concentration, which was consistently lower in SHR than in age-matched WKY. Temporal patterns of, and strain differences in PRA were closely paralleled by variations in PRC but not by other reaction components. Significant elevation of serum creatinine in old SHR support the presence of renal injury. We conclude that PRA and PRC are normal in evolving SHR hypertension and progress to abnormally elevated levels after hypertension is established. We postulate that "high-renin" hypertension may develop as a consequence of the hypertensive state per se, perhaps due to nephrosclerotic vascular disease.
Hypertension
PMID:Serial renin-angiotensin studies in spontaneously hypertensive and Wistar-Kyoto normotensive rats. Transition from normal- to high-renin status during the established phase of spontaneous hypertension. 39 38

Simultaneous determinations of unconjugated estriol and 15alpha-hydroxyestriol (E4) levels in maternal serum were studied serially to ascertain the relative usefulness of these estrogens as indicators of fetal welfare. Complicated pregnancies included 16 patients with pre-eclampsia and/or hypertension, six patients with severe Rh-isoimmunization, 12 patients with diabetes mellitus, of which four had vascular disease, three patients with fetal death in utero, and three twin pregnancies. Retrospective analysis failed to indicate a clinically useful role for serum E4 determinations in the evaluation of fetal welfare during high-risk pregnancies.
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PMID:Unconjugated estriol and 15alpha-hydroxyestriol in complicated pregnancies. 40 91

Tubular uptake of ferritin given intravenously was studied in the right and left kidneys of 74 Goldblatt-hypertensive rats. Previous observations pointed out the pathologically enhanced permeability of glomerular barrier as the cause of the phenomenon. It was assumed, that the extent of tubular areas taking up ferritin, refers to the number of damaged glomeruli. The process was characterized semiquantitatively by planimetric measurements and determination of the non-hemin iron concentration in the renal cortical tissue. A more frequent and extensive tubular ferritin-uptake (and glomerular damage) was bilaterally recorded in the kidneys of malignant hypertensive rats in comparison to the benign ones. The development of the phenomenon in the clamped kidneys, being defended from high blood pressure, suggests a humoral factor behind the enhanced glomerular permeability. Saline intake has a beneficial effect on the glomerular damage similar to the hypertensive angiopathy.
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PMID:Renal tubular ferritin-uptake, a consequence of the increased glomerular permeability, during the benign and malignant course of renal hypertension in rats. 42 54

Systemic hemodynamics (cardiac output, intraarterial pressure, total peripheral resistance) and intravascular volume (plasma volume and red cell mass) were measured in a population of 126 black and white patients, 51 with borderline hypertension and 75 with established essential hypertension. The findings were compared with those in 29 age-matched normotensive control subjects of both races. The white patients with established hypertension demonstrated a faster heart rate than the black patients (less than 0.05); this difference was more pronounced during upright tilt (p less than 0.02). No significant difference in cardiac index, total peripheral resistance, plasma volume or total blood volume was found between the two racial populations. Cardiac index correlated directly with plasma and total blood volume in black patients (r = 0.32, p less than 0.05) and white patients (r = 0.35, p less than 0.001) as well as in the whole study population (r = 0.36, p less than 0.001). The regression lines were similar in the two races. Further, a negative correlation was observed between the total peripheral resistance and plasma volume (r = -0.31, p less than 0.001) or total blood volume (r = -0.34, p less than 0.001), and it was similar in both races (blacks r = -0.48, p less than 0.01; whites r = -0.25, p less than 0.05). Age correlated significantly with total peripheral resistance in the white patients (r = 0.35, p less than 0.001) and in the total study population (r = 0.28, p less than 0.001). We conclude that, for every given age or level of arterial pressure, systemic hemodynamics are similar for the black and white patients with essential hypertension. These data, therefore, do not support the clinical impression that basic pathophysiology and hypertensive vascular disease are different in the black patient with essential hypertension.
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PMID:Essential hypertension in black and white subjects. Hemodynamic findings and fluid volume state. 46 13

Atherosclerotic vascular disease is very common in diabetic patients. It often occurs at an earlier age and is more severe than in nondiabetic individuals. The medical management of cardiac disease in diabetics is much the same as in nondiabetics. Risk factors such as obesity, hypertension, and hyperlipidemia must be vigorously treated, and smoking should be restricted.
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PMID:Office management of cardiac disease in the diabetic. 46 80


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