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

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

All IDDM patients without late complications have blood pressures similar to the nondiabetic background population, and those who develop clinical nephropathy in Denmark have no familial predisposition to hypertension. Blood pressure remains normal until after development of microalbuminuria, indicating no primary role for hypertension in the pathogenesis of nephropathy. When microalbuminuria is present it does, however, play a crucial role in the progression of nephropathy. Sodium retention, possibly induced by hyperinsulinemia, and perhaps glucose-coupled sodium reabsorption in insulin treated patients, seem to play a central role in elevating the blood pressure, but this needs further clarification.
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PMID:Hypertension in the course of insulin dependent diabetes mellitus and its pathogenetic mechanisms. 214 1

Patients with apparent mineralocorticoid excess (AME) have low or absent activity of the enzyme 11 beta OH steroid dehydrogenase (11SD), and inappropriately high intrarenal levels of cortisol resulting in Na+ retention and hypertension. Pseudohypoaldosteronism (PHA), in contrast, is characterized by salt wasting despite hyperaldosteronemia, reflecting low or absent mineralocorticoid receptors (MR). Although AME is presumed to reflect inappropriate cortisol occupancy of MR, several features also suggest inappropriate occupancy of glucocorticoid receptors (GR). To test this possibility, we administered carbenoxolone, which is known to block 11SD, to four patients with PHA, and observed marked mineralocorticoid effects, e.g., antinatriuresis and elevated plasma bicarbonate. To further test the possibility that occupancy of renal GR may induce a classical mineralocorticoid response, we administered the highly specific glucocorticoid RU 28362 to adrenalectomized rats and showed that it has profound antinatriuretic effects. Finally, by selectively blocking MR with RU 28318 or GR with RU 38486, we have shown that corticosterone, the physiologic glucocorticoid in rats, has an antinatriuretic effect in adrenalectomized rats via either MR or GR occupancy. Previous studies have clearly shown that MR are inherently nonselective and have equivalent intrinsic affinity for aldosterone, corticosterone, and cortisol. The present studies suggest that this nonselectivity includes the nuclear response element to which either MR or GR may bind to elicit a mineralocorticoid effect, and further underscore the importance of the enzyme 11SD in the specific mineralocorticoid action of aldosterone.
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PMID:Apparent mineralocorticoid excess, pseudohypoaldosteronism, and urinary electrolyte excretion: toward a redefinition of mineralocorticoid action. 217 62

Based on a review of literature in various fields of research related to hypertension, we develop a new working hypothesis on the pathophysiology of genetically determined increases in blood pressure. According to our hypothesis, the primary defect is located in the kidneys. Renal alpha-adrenergic receptor density is increased in the early stages of the disease, before increases in blood pressure occur. Most renal alpha-adrenergic receptors are located in the proximal tubules and enhance Na+ reabsorption. A genetically determined increase of alpha 1- or alpha 2- or of both alpha-adrenergic receptor subtypes would impair Na+ excretion and, together with increased Na+ intake, would lead to positive Na+ balance. Subsequently, various mechanisms would be activated to restore a neutral Na+ balance, including the secretion of a natriuretic factor that inhibits Na+/K+-ATPase. Inhibition of Na+/K+-ATPase in extrarenal tissues would increase the intracellular concentration of Na+ and, via Na+/Ca2+ exchange, of Ca2+. Elevated intracellular Ca2+ would enhance vascular smooth muscle contractility and neuronal transmitter release, thereby leading to vasoconstriction and to increases in blood pressure. We thus hypothesize that hypertension is a homeostatic response designed to protect blood volume from a genetically determined renal alpha-adrenergic receptor-mediated increase in Na+ retention.
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PMID:Renal alpha-adrenergic receptor alterations: a cause of essential hypertension? 253 29

1. This study investigated the effect of progesterone, which, under certain circumstances, can antagonize both the mineralocorticoid and glucocorticoid activities of steroid hormones, on the development and maintenance of adrenocorticotrophic hormone (ACTH)-induced hypertension in conscious sheep. 2. Progesterone (500 mg/day) alone, for 5 days, had no effect on blood pressure, but increased urinary Na excretion by 38 +/- 10 mmol/day (P less than 0.05) during the first 24 h. 3. Infusion of ACTH (5 micrograms/kg per day), alone, for 3 days, increased arterial pressure by 21 +/- 2 mmHg (P less than 0.001) associated with hypernatraemia, hypokalaemia, urinary Na retention, and increased fasting plasma glucose concentration. 4. Progesterone (500 mg/day) concurrently with ACTH blocked the rise in mean arterial pressure and the mineralocorticoid (urinary Na retention) but not the glucocorticoid (increase in plasma glucose concentration) effects associated with ACTH administration. 5. Progesterone (500 and 1000 mg/day) failed to reverse the hypertension and hypokalaemia in sheep pretreated for 3 days with ACTH. 6. Thus, progesterone blocked the onset but did not affect established ACTH hypertension. The mechanism by which progesterone blocked the development of ACTH hypertension appears to be related to the ability of progesterone to block the essential mineralocorticoid component of the adrenocortical steroids involved in the development of ACTH hypertension.
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PMID:Progesterone antagonizes development but not maintenance of ACTH-induced hypertension in sheep. 255 50

We have previously shown that weight gain in the dog results in an increase in blood pressure. To study the pathogenesis of the rise in blood pressure associated with weight gain, we compared the serial changes in blood pressure, body weight, sodium balance, plasma volume, and three hormones known to affect sodium balance (norepinephrine, insulin, and aldosterone) in seven dogs fed a high fat diet for 6 weeks and seven dogs fed a control diet. The sodium content of both diets was equal. During a 2-week control period, no differences were noted between the two groups. Weight gain was associated with a progressive increase in blood pressure (mean pressure increased by 18.5 +/- 2.1 mm Hg in the high fat group) and plasma volume (plasma volume increased from 1,426 +/- 202 to 2,053 +/- 250 ml in the high fat group). Sodium retention occurred after 1 week of the high fat diet and persisted. Over the 6-week period, the dogs on the high fat diet increased their cumulative sodium balance by 2,024 +/- 462 meq versus an increase of only 289 +/- 97 meq for the dogs on the control diet. In the high fat diet group of dogs, there was a significant relation between change in cumulative sodium balance and the change in blood pressure and plasma volume. After 1 week of the high fat diet, norepinephrine was the only hormone that significantly increased from baseline. Over the next 5 weeks norepinephrine increased no further, whereas fasting insulin and aldosterone progressively increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1989 Jun
PMID:Pathogenesis of weight-related changes in blood pressure in dogs. 266 33

A retrospective chart review was conducted of 26 organ donors to determine hemodynamic and metabolic derangements encountered and nursing requirements for donor organ maintenance. There were 15 boys and 11 girls with a mean age 6.57 +/- 5.46 years. Mean donor maintenance time was 10.5 +/- 6.7 hours. Cardiorespiratory derangements included hypotension in 16, hypertension in 6, arrhythmias in 17 (premature ventricular contraction in 4, bradycardia in 8, paroxysmal atrial tachycardia in 3, and ventricular tachycardia in 2), asystolic events in 5, pulmonary insufficiency in 6, anemia in 8, and thrombocytopenia in 8. Metabolic and hormonal derangements included hyperglycemia in 18, hypokalemia in 20, hyperkalemia in 4, hyponatremia in 3, hypernatremia in 17, metabolic acidosis in 10, and diabetes insipidus in 15. Hypothermia (temperature 33.3 degrees +/- 0.4 degrees C, mean +/- SD) occurred in 14 donors. The mean physiologic Stability Index score was 22.2 +/- 4.7 and mean Therapeutic Intervention Score was 46.7 +/- 5.8. Total number of nursing hours spent in donor maintenance was 424.5 hours. Therapies offered included diuretics in 10, sodium bicarbonate in 8, antibiotics in 6, insulin in 12, pitressin in 13, verapamil in 3, isoproterenol in 3, dopamine in 17, and intravenous potassium boluses in 14. Of the potential 26 donors, 46 kidneys, 8 hearts, 14 livers, 3 pancreas, and 9 corneas were retrieved in transplantable condition. With appropriate donor maintenance, organs suitable for transplantation can be retrieved despite significant pathophysiologic derangements. Physicians intending to provide donor support should be comfortable with invasive monitoring and cardiorespiratory support and be prepared to provide a nurse to patient ratio of 2:1 at the bedside.
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PMID:Pediatric organ donor maintenance: pathophysiologic derangements and nursing requirements. 278 Jan 31

Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.
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PMID:Idiopathic hyperaldosteronism in a dog. 299 95

A primary role for the kidney in the initiation and maintenance of hypertension has long been recognized, but the pathogenetic interactions among renal hemodynamics, hormonal and hereditary factors, and dietary sodium intake remain enigmatic. Reduction in filtration surface area, whether acquired in the course of intrinsic renal disease or after surgical renal ablation, leads to systemic hypertension as well as to progressive renal insufficiency, sequellae made even more severe by dietary sodium excess. Moreover, hypertension and progressive renal disease eventuate in some individuals born with a solitary kidney, as well as in those with more severe degrees of dysgenesis (ie, oligomeganephronia). Hypertension is also commonly observed in certain inbred rat strains in which filtration surface area is congenitally deficient. Based on these and other lines of evidence reviewed herein, we postulate that a renal abnormality that contributes to essential hypertension in the general population is a reduced number of nephrons. The consequences of this abnormality are limitations in the ability to excrete sodium and thus, salt-sensitive hypertension. Finally, congenital variability in filtration surface area may explain why only some, but not all, patients exposed to potentially injurious renal stimuli eventually manifest chronic nephropathy. This may also account for the susceptibility of subsets of Type I and Type II diabetics to develop overt glomerulopathy.
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PMID:Glomeruli and blood pressure. Less of one, more the other? 1691 17

Several aspects of renal function vary considerably during the 1st year of life and differ markedly from the equivalent values in the adult. Glomerular filtration rate (GFR) increases little, prior to the time an infant reaches a conceptional age of 34 weeks, the point in renal development from which the absolute GFR (ml/min) increases gradually to mature values when linear growth is completed during adolescence. GFR corrected for body size is not comparable with adult normal values until after 12 months of age; therefore, whether GFR is estimated from Scr or measured by timed urine collection, there is no easily recalled range of normal values for infants. One must know the changes in the renal function of normal infants that take place following birth during the 1st year of life. Despite several attempts to do so, renal function during the 1st year of life cannot be assessed from urine flow rate. A urine flow rate of less than 1 ml/kg per hour may be normal and appropriate and may not be harmful either to preterm or full-term infants with normal GFR. Impaired concentrating ability of the neonatal kidney is probably of no clinical significance in all but the most extreme circumstances and is not a major factor in an infant becoming dehydrated, developing hypernatremia or being at greater risk of acute renal injury. Acid-base status in infants must be interpreted appropriately to know when alkali therapy should be introduced to avoid growth failure secondary to true metabolic acidosis. When plasma renin activity is measured in the infant with renal failure of hypertension, one must compare the result with the normal range of values related to postnatal age of normal infants.
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PMID:Postnatal development of renal function during the first year of life. 315 94


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