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

Insulin action is highly likely to be primarily genetically determined (given a permissive or facilitative environment, for example sufficient calorie availability), as shown by variations in ethnic distribution, evidence for familial transmission and genotypic responses to experimentally induced metabolic stresses. Further, it is likely that the genetic predisposition to insulin resistance is closely linked to (or perhaps synonymous with) the predisposition to develop overt NIDDM. Alternatively, in the development of diabetes, the genetic basis for insulin resistance may be necessary, but not sufficient, requiring a second major gene for beta-cell vulnerability (e.g. exhaustion, deterioration of function, amyloid deposition). The future examination of the genetics of insulin action depends in large measure on the method of assessment of insulin action that is selected and its consistent application to individuals, families and populations. The phenomenological approaches currently being used to describe and define insulin resistance could be identifying many different disorders, all leading to an apparent decrease or impairment of insulin action compared with that in 'normals'. Selection of any method for determining the presence of insulin resistance, together with selection of the threshold for 'present versus absent' is, at best, difficult. It is further complicated by the frequent association of insulin resistance with a wide range of disturbances, including hypertension, dyslipidaemia and glucose intolerance--the insulin resistance 'syndrome'. A number of possible loci and candidate genes controlling insulin action have been studied, and most have been ruled out as the probable underlying cause of the majority of cases of defective insulin action. Among those genes that are unlikely to be determinants of insulin resistance (except in a few rare cases of mutations) are those for insulin, the insulin receptor, glucose transporters and the genes for many specific enzymes. While these are unlikely to be responsible for insulin resistance, such potential genetic defects cannot be fully excluded using present methods. Direct gene sequencing of polymerase-chain-reaction amplified DNA may be the ultimate approach to identifying the critical defects underlying insulin resistance. Other candidate genes regulating insulin action are likely soon to come forth, such as those controlling the generation and function of the intracellular mediators of insulin action.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetics of insulin action. 830 12

The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
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PMID:On the pathogenesis of germinal layer hemorrhage in the neonate. 831 97

Vascular endothelial cells are thought to play an important role in human aging as their senescence and/or detachment from vascular wall contribute to arteriosclerosis and high blood pressure in elderly persons. Since fibronectin is necessary for cell attachment and spreading and its increased expression has been reported in aging fibroblasts, we checked its expression in aortic endothelial cells aged in vivo. We found that the steady-state level of fibronectin expression increases with increasing donor age, while the labeling index of cultured cells decreases with age. The increased level of fibronectin expression correlated well with an increase in cell area. To explore whether these changes were a reflection of exhaustion of proliferation potential in vivo, we examined fibronectin expression in human umbilical vein endothelial cells aging in vitro. Very similar results were obtained, supporting the idea that vascular endothelial cells age in vivo by using up division potential. When we examined the expression of fibronectin in human skin fibroblasts aged in vivo and fetal lung fibroblasts aged in vitro, we obtained similar results. In conclusion, the level of expression of fibronectin and cell size increase during in vivo and in vitro aging of both endothelial cells and fibroblasts in a coordinate manner.
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PMID:Enhanced expression of fibronectin during in vivo cellular aging of human vascular endothelial cells and skin fibroblasts. 848 45

The purpose of this investigation was to study exercise-induced hypertension after surgical repair of coarctation of the aorta (CoA). Groups of 27 patients with CoA and 27 healthy control subjects, 6-21 years old, were exercised to exhaustion using the Bruce protocol. Fourteen patients had undergone surgery during the first year of life (group A), and 13 patients had been operated on later (group B). The pulse rate and systolic blood pressures (BP) in the arm and leg were measured before, during, and after exercise to evaluate changes in the BP and the arm/leg BP gradient with exercise. The systolic BP was significantly higher in the patients than in the controls at all stages of the exercise test (p < 0.01), as was the arm/leg BP gradient both before and after exercise (p < 0.01); the latter increased significantly with exercise in the patient group (p < 0.05). We found hypertension to be a more common and severe problem in group B patients, who had higher blood pressures than their controls at rest and during exercise (p < 0.05). Exercise-induced hypertension was also more common in group B (23%) than in group A (7%). We conclude that exercise-induced hypertension and recoarctation are problems in postoperative CoA patients. Moreover, exercise-induced hypertension is more common in patients with CoA operated on after the first year of life.
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PMID:Exercise-induced hypertension after corrective surgery for coarctation of the aorta. 866 Apr 44

A study was undertaken to provide further information on the ruminal, cardiorespiratory and hypothalamo-pituitary-adrenocortical (HPAC) physiological sequelae of hypocalcaemia in dairy calves. The functional picture observed in standing calves experiencing Na2EDTA-induced progressive hypocalcaemia showed a biphasic pattern. During the first phase (Ca2+ varying between 1.20 +/- 0.09 and 0.64 +/- 0.15 mmol/L, mean +/- SD), the animals became dull and lethargic, shifting their weight from one hind limb to the other, with cool extremities and hypersalivation. Their ventilation was slightly increased but their heart rate, thoracoabdominal pressure, pulmonary mechanics, haemoglobin and temperature remained constant. Conversely, their systemic arterial pressure (SAP) and the amplitude of their ruminal contractions (RCA) were severely decreased. During the second phase (Ca2+ < 0.64 +/- 0.15 mmol/L), there was restlessness, tachycardia, hypertension, polycythaemia and, finally, inability to stay upright. It is suggested that the diminished Ca2+ availability caused smooth-muscle and myocardial dysfunctions which could explain the RCA and SAP changes recorded during the first phase, whereas neural and/or humoral sympathetic discharge probably accounted for the reversal in SAP and heart rate when Ca2+ was decreased further. Serum cortisol increased regularly and remained significantly correlated with Ca2+ in each animal. Moreover, regression of delta cortisol/delta Ca2+ on delta Ca2+/delta Na2EDTA was significant (p < or = 0.001). It was concluded that mild asymptomatic hypocalcaemia severely impairs ruminal function, which will progressively worsen the Ca2+ deficit; that the inability to maintain posture in hypocalcaemia is not due to hypotension; and that the higher the HPAC response to hypocalcaemia, the higher the resistance to its effects. An asymptomatic periparturient cow with barely detectable ruminal activity may merit preventive calcium borogluconate therapy. Also, the physiological role of hypotension in explaining the clinical picture may be less important than other processes, such as neuromuscular failure. Finally, the present results imply a possible HPAC exhaustion in cows with periparturient paretic hypocalcaemia.
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PMID:Ruminal, cardiorespiratory and adrenocortical sequelae of Na2EDTA-induced hypocalcaemia in calves. 869 1

The aim of this study was to investigate the prognostic value of cardiopulmonary fitness in hypertension. From 1972 to 1982 oxygen uptake and heart rate were recorded during an exercise test to exhaustion in 216 patients (143 men). Their outcome was ascertained in 1994. During 3,411 patient years of follow-up, 53 patients suffered at least one fatal or nonfatal cardiovascular event and 25 patients died. After adjustment for age, gender, and weight, the relative hazard rates (RHR; Cox regression) of peak oxygen uptake (l.min-1) amounted to 0.44 (P = 0.01) for the first occurring cardiovascular events and 0.35 (P = 0.05) for all-cause mortality. These RHR remained significant after additional adjustment for traditional cardiovascular risk factors (RHR = 0.45 and 0.28, respectively; P < 0.05). Heart rate at 50 W did not predict outcome after adjustment for age and gender (P = 0.94 and 0.14, respectively), nor after additional adjustment for heart rate at rest (P = 0.86 and 0.61, respectively). In conclusion, a lower peak oxygen uptake, but not a higher submaximal heart rate, is significantly and independently associated with a higher incidence of cardiovascular events and a higher total mortality in hypertensive patients.
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PMID:Prognostic significance of peak oxygen uptake in hypertension. 883 31

Low heart rate variability (HRV) has been reported to be an independent risk factor for the development of coronary heart disease in women and has recently been identified as a risk factor for cardiac sudden death and all-cause mortality. We have recently demonstrated that endurance-trained post-menopausal women demonstrate higher levels of HRV than sedentary control subjects. The purpose of the present study was to test the hypothesis that 12 weeks of regular aerobic exercise would increase HRV in sedentary post-menopausal women with elevated arterial blood pressure (BP) (i.e. either high normal BP or stage I hypertension). A secondary aim was to test the hypothesis that the increase in HRV with exercise training, if observed, would be associated with an increase in spontaneous cardiac baroreflex sensitivity (SBRS), an important physiological determinant of HRV. To accomplish these aims, we studied eight sedentary post-menopausal women (age = 54.5 +/- 1.3 years) before and after 12 weeks of aerobic exercise training (3.3 +/- 0.3 days per week at 70% +/- 2% of maximal heart rate for 43 +/- 3 min per day). Maximal oxygen uptake and body weight did not change (P > 0.05) with training, but percentage fat (35.5 +/- 2.6% vs. 34.5 +/- 2.3%, P < 0.05) decreased and treadmill time to exhaustion increased (9.8 +/- 0.5 vs. 11.3 +/- 0.5 min, P < 0.05). Supine resting levels of heart rate, RR interval and the standard deviation of the RR interval (time domain measure of HRV) were unchanged (all P > 0.05) from baseline levels after 12 weeks of aerobic training. Similarly, the high-frequency, low-frequency and total power of HRV (frequency domain measures) were also unchanged from baseline (all P > 0.05). SBRS was also not different before and after aerobic exercise training (10 +/- 2 vs. 13 +/- 3 ms mmHg-1 respectively, P > 0.05). In contrast, systolic and diastolic BP were reduced approximately 8 and approximately 5 mmHg with training (both P < 0.05) respectively. These results indicate that 12 weeks of moderate-intensity aerobic exercise training does not increase HRV or SBRS, despite producing a clinically significant reduction in BP at rest in post-menopausal women with elevated BP. Considered together with our previous findings in female master endurance athletes, these findings suggest that more intense and prolonged exercise training may be required to produce increases in HRV and SBRS in sedentary post-menopausal women.
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PMID:Influence of exercise training on heart rate variability in post-menopausal women with elevated arterial blood pressure. 901 56

1. To determine whether coronary flow regulation by nitric oxide (NO) is impaired in the hypertensive heart (HTH), coronary perfusion was measured in isolated rat hearts using NO synthesis inhibitor L-NG-monomethyl arginine (L-NMMA) in Wistar-Kyoto (WKY) rat and spontaneously hypertensive rat (SHR) with and without chronic Nomega-nitro-L-arginine-methylester (L-NAME) treatment. Moreover, the effect of angiotensin II receptor antagonist (AT1 receptor antagonist) (TCV-116) on the impaired coronary circulation in HTH was examined. 2. Coronary flow (CF) was decreased in HTH accompanied with cardiac hypertrophy. The decreased response of CF to L-NMMA infusion was diminished in HTH. It is suggested that NO production was reduced in coronary vasculature in HTH. 3. In chronic L-NAME treated SHR, blood pressure and cardiac hypertrophy were accelerated. Although coronary flow resistance (CFR) was increased, the increased response of CFR to L-NMMA infusion was not altered. 4. The AT1 antagonist improved total minimal coronary flow resistance (MCFR) restoring CFR response in SHR, although it did not recover CFR response in chronic L-NAME treated SHR. 5. Taken together the findings suggest that NO production was exhausted in the coronary artery even in the developing stage of hypertension and this exhaustion could contribute to the impairment of coronary circulation of HTH.
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PMID:Role of nitric oxide in impaired coronary circulation and improvement by angiotensin II receptor antagonist in spontaneously hypertensive rats. 907 32

Sodium is the major cation of the extracellular fluid and has a potent influence on fluid movement. Sodium has been likened to a sponge that draws fluids into the extracellular space, including the plasma volume, to equalize gradients in concentration. Conventional wisdom suggests limiting dietary intake of Na+ to decrease risk of hypertension. However, there are some extreme occupational or exercise-related conditions where sweat losses are great and Na+ losses may exceed normal dietary intake. This can occur acutely such as in an ultra-endurance event or chronically as in hard manual work in the hear. In such cases, additional Na+ in the form of a higher Na+ diet or adding Na+ to beverages used for fluid replacement may be warranted. A higher Na+ diet also appears to accelerate the cardiovascular and thermoregulatory adaptations that accompany heat acclimation or short term exercise training. Saline ingestion before exercise causes an expansion of plasma volume at rest and throughout the subsequent exercise bout. This expansion of plasma volume alters cardiovascular and thermoregulatory responses to exercise in ways that may lead to beneficial changes in endurance exercise performance. Plasma volume expansion also occurs with saline infusion during exercise, but exercise performance advantages have yet to be reported. The purpose of this article is to review the literature concerning dietary sodium and its influence on fluid balance, plasma volume and thermoregulation during exercise. It contains 2 major sections. First, we will discuss manipulations in daily Na+ intake initiated before or throughout an exercise regime. Second, we will examine studies where an acute Na+ load was administered immediately before or during an exercise trial. The dependent variables that we will discuss pertain to: (i) body water compartments, i.e. plasma volume; (ii) thermoregulatory variables, i.e. core temperature and sweat rate; (iii) cardiovascular variables, i.e. heart rate and stroke volume; and (iv) performance, i.e. time trial performance and time to exhaustion. Particular attention will be given to the route by which Na+ was administered, the environmental conditions, the level of acclimation of the participants and specifics relating to Na+ administration such as the osmolality of the Na(+)-containing beverage.
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PMID:Dietary sodium and plasma volume levels with exercise. 918 66

Cigarette smoking is a major risk factor for coronary heart disease. To further investigate the relationship of nicotine with other cardiac risk factors, we studied the impact of nicotine on blood pressure and glucose tolerance. Adult male Sprague-Dawley rats were randomly assigned to receive nicotine or placebo pellets implanted subcutaneously. Weight gain was controlled by pair-feeding, and was not significantly different between nicotine- and placebo-treated animals. Blood pressure (in mm Hg) increased throughout a 3-week treatment period in nicotine-treated animals and was significantly higher [P < .05 by two-way ANOVA] than in placebo-treated rats. Blood pressure returned to normal within 1 week following exhaustion of the pellets. Oral glucose tolerance tests performed 2.5 weeks after pellet placement showed similar glucose, insulin, and free fatty acid (FFA) profiles by two-way ANOVA. In summary, smokeless nicotine exposure leads to sustained but reversible hypertension without deterioration in glucose tolerance or insulin action when weight gain is controlled. We conclude that in rats smokeless nicotine adversely affects the coronary risk profile by increasing blood pressure.
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PMID:Smokeless nicotine administration is associated with hypertension but not with a deterioration in glucose tolerance in rats. 928 88


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