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

A rare case of nesidioblastosis in an adult arising from heterotopic pancreas and presenting with hypertension is reported. To our knowledge it is the first case to be described in literature. The pathogenic mechanisms to explain hypertension are not clear. The stimulating action of glucagon on the adrenal gland or on peripheral beta receptors could be considered as hypothetical factors.
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PMID:Nesidioblastosis arising from heterotopic pancreas and presenting with hypertension. A clinical, immunohistochemical and ultrastructural study. 268 66

Fasting concentration of the C peptide in serum was estimated in 150 patients with type 2 diabetes treated with insulin because of the late, true ineffectiveness of the sulphonylurea derivatives. In 36 patients selected out of the total group at random the secretion of that peptide was measured after i.v. injection of 1 mg of glucagon. Only 9 patients showed trace amounts of that peptide at morning fast (Group A--0.17 +/- 0.08 nmol/l), in 69 the secretion was normal (Sub-Group B1--0.80 +/- 0.25 nmol/l), in 48 moderately elevated (Sub-Group B2--1.67 +/- 0.10 nmol/l) and in 24 markedly elevated (Sub-Group B3--4.54 +/- 2.57 nmol/l). The increments of the peptide C concentration after glucagon stimulation were parallel to its fasting concentration, which indicated a proper reactivity of the pancreatic beta-cells in patients with normal or increased basal secretion. The patients with only trace secretion of the peptide C differed from the other by their small, normal body mass and by a longer duration of insulin treatment. Very similar insulin needs must be stressed in the patients of the Groups A and B as well as within the Sub-Groups B. In patients with hyperactivity of the beta-cells (Sub-Group B2 and B3) no differences were found, as compared with the other patients, in the prevalence of chronic diabetes complications of the micro- or macroangiopathy type, also prevalence of hypertension was equal. The results presented show that in the most patients with type 2 diabetes, with the late, true ineffectiveness of the sulphonylurea derivatives the secretory function of the pancreatic islets beta-cells remains normal or is even increased.
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PMID:[Functional capacity of pancreatic B cells in patients with diabetes mellitus type 2 with late true ineffectiveness of sulfonylurea derivatives]. 269 67

Hypertension in diabetic patients is more common than in controls, contributes substantially to their increased cardiovascular morbidity and mortality, and should be treated as accurately as diabetes mellitus itself. After appropriate exclusion of secondary forms, the first therapeutic step consists of reduction of overweight, salt intake, and smoking; the omission of interfering drugs; and adequate instruction. Step 2 has usually been the prescription of a diuretic drug, in spite of its known side effects on carbohydrate and lipid metabolism. A new possible alternative may be a calcium antagonist. Results in 10 hypertensive diabetic persons suggest that at a dose that normalizes blood pressure, neither carbohydrate nor lipid metabolism is altered, uric acid decreases, the exaggerated cardiovascular reactivity toward norepinephrine becomes normal, and the pressor dose for angiotensin II tends to rise. Body weight, blood volume, exchangeable sodium, as well as plasma and urinary sodium, potassium, and creatinine levels were unchanged. The third therapeutic step is the addition of a cardioselective beta blocker in a moderate dose. This avoids the disadvantages of beta 2-adrenergic blockade such as decreased insulin output, prolonged hypoglycemia, diminished glucagon secretion, and increased vasospasticity during hypoglycemic states, as well as aggravation of peripheral vascular disease. Alternatives are other sympatholytics with their known tendency to cause or increase orthostatic and sexual problems or, again, a calcium antagonist. In step 4, a hydralazine-type drug or prazosine is added. The fifth step, which adds minoxidil or captopril to the previous drugs, should only be taken after a specialist reevaluates the overall situation.
Hypertension
PMID:Antihypertensive therapy in diabetic patients. 286 38

Hypertensive crisis in a patient with pheochromocytoma can be induced by endoscopy premedication. Opiates, glucagon, and metoclopramide are commonly used in the gastrointestinal laboratory and capable of releasing catecholamines from a pheochromocytoma. Patients who have just had endoscopy can display untoward effects such as nausea, weakness, and diaphoresis. Such patients should probably have their blood pressure carefully recorded. Although hypotension is expected, endoscopists should be alert to the finding of severe hypertension and consider pheochromocytoma. The need for this becomes even greater considering that primary gastrointestinal endoscopy is often being done in doctor's offices away from hospitals and more acute resuscitative resources. In the case reported, a life-threatening hypertensive crisis was induced by fentanyl. The hypertensive crisis was correctly ascribed to pheochromocytoma, enabling institution of lifesaving treatment.
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PMID:Inadvertent diagnosis of pheochromocytoma after endoscopic premedication. 291 Jun 72

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

The metabolic effects of calcium channels blockers have already been studied both in normal and diabetic humans and results were quite controversial, depending on the drug used, the dose administered, and the type of patient. Little information exists on the use of Ca2+ antagonists in obese people, even if these persons are a population risk group for developing diseases in which these drugs may be requested for treatment. Thus, we evaluated, in obese humans, the metabolic effects of two Ca2+ antagonist drugs recently made commercially available to treat diseases such as hypertension and ischemic heart disease: nicardipine and diltiazem. Sixteen obese subjects were submitted to an intravenous glucose tolerance test (0.33 g/kg) (IVGTT) and an arginine test tolerance (30 g in 30 minutes) (ATT) before and after a week of oral treatment with nicardipine (60 mg/day) or diltiazem (360 mg/day). Plasma values of glucose, insulin, and C-peptide during IVGTT, and of glucose, insulin and glucagon during ATT did not show any modification during treatment with either drug. Thus the Ca2+ antagonists, nicardipine and diltiazem, at therapeutic doses in obese subjects do not significantly affect glucose tolerance or insulin and glucagon release.
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PMID:Lack of effect of nicardipine and diltiazem on glucose- and arginine-induced insulin release in obese subjects. 315 42

Inotropic responses to isoproterenol of hypertrophied hearts have been shown to be decreased. We have previously reported that in 13-week-old spontaneously hypertensive rats (SHR) this decrease is probably due to decreased beta-adrenergic receptor number, while in hearts from two kidney-one clip renal hypertensive rats (2K-1C RHR), this is due to a decreased nucleotide regulatory protein activity. We now show that changes in 2K-1C RHR are time dependent. One week after instituting development of hypertension the heart is already hypertrophied. Biochemical changes consistent with decreased glucagon receptors are seen, as well as beginning changes consistent with decreases in the nucleotide regulatory protein activity. By two weeks this is more evident. Hypertrophy and biochemical changes can be reversed up to six weeks, but by ten weeks the activity of the catalytic subunit of the adenylate cyclase system is decreased. In 1K-1C RHR, biochemical changes in the cyclase system are accelerated as compared with the 2K-1C model. In SHR, changes in 24-week-old rats are the same as in the 13-week-old rats. It is concluded that in cardiac hypertrophy associated with different models of hypertension the decreased inotropic responsiveness to isoproterenol is associated with different biochemical defects in the beta-adrenergic receptor response coupling pathway, and that reversal in function occurs only when there is no apparent change in the catalytic subunit of the adenylate cyclase complex.
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PMID:Adenylate cyclase activity during development and reversal of cardiac hypertrophy. 316 Aug 64

Corticotropin-releasing factor (CRF) has been identified in brain regions that participate in the regulation of the autonomic nervous system and behavioral responses. This paper summarizes the central nervous system as well as the peripheral effects of CRF that are different from those on the anterior pituitary. CRF acts within the brain to increase plasma concentrations of adrenaline and noradrenaline resulting in increased plasma concentrations of glucagon and in hyperglycemia. In the dog, CRF also acts within the brain to increase plasma concentrations of vasopressin. The intracerebroventricular administration of CRF results in a decrease of gastric acid secretion stimulated exogenously by pentagastrin and 2-deoxy-D-glucose or stimulated endogenously by a protein meal. CRF also acts within the brain to decrease gastric emptying and small intestinal transit but to increase large bowel transit and fecal excretions. The central administration of CRF produces hypertension, tachycardia and an elevated oxygen consumption. The effects of CRF on behavior are numerous. CRF induces a reduction in food intake, increases grooming behavior, locomotor activity, vocalization and induces an aroused state but decreases sexual receptivity. Intravenous administration of CRF decreases gastric acid secretion, gastric emptying and blood pressure but increases heart rate, plasma vasopressin concentrations, mesenteric and aortic blood flow, venous return to the heart and pancreatic bicarbonate and protein secretions. The physiological significance of these peripheral actions of CRF on various organ systems is not known.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Extrapituitary effects of corticotropin-releasing factor. 332 96

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.
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PMID:Role of glucagon in splanchnic hyperemia of chronic portal hypertension. 377 72

The aim of this prospective, randomized, double-blind, placebo controlled study was to investigate the effect of nifedipine on carbohydrate metabolism in diabetic patients after a 3-day and a 3-month course of treatment. Sixteen non obese, well controlled non-insulin dependent diabetics, (HbA1 less than 10%), with moderate untreated hypertension were divided in two groups: nifedipine (group N, 8 patients) and placebo (group P, 8 patients). An oral glucose tolerance test (OGTT, 75 g glucose) and an arginine infusion were performed before, after a 3-day, and a 3-month course, either of nifedipine 30 mg/D or placebo. Blood samples obtained during OGTT were assayed for glucose and insulin, and during arginine infusion for insulin, glucagon and growth hormone. The differences between basal and peak values during tests were compared between both groups before and after treatment using Wilcoxon's rank sum test. Neither acute nor chronic administration of nifedipine or placebo modified the glucose tolerance. However, basal insulin levels were reduced by 3 month-administration of nifedipine (from 19 +/- 2 micromicrons/ml to 10 +/- 1 micromicrons/ml, p = 0,01). Otherwise the basal and peak hormonal values during tests were not significantly affected by nifedipine either at the start of after 3 months of treatment. These results suggest that nifedipine, when given in standard dosage for 3 months, has minor effects on carbohydrate metabolism in non-insulin dependent diabetic patients.
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PMID:[Effects of nifedipine on carbohydrate metabolism in the non-insulin dependent diabetic]. 389 85


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