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

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

Adrenergic receptor response coupling pathways have been shown to differ in hypertrophied hearts in different models of hypertension. To mimic this, chronic subcutaneous infusions of epinephrine (80 nmol/h for up to 13 days) and angiotensin II (AII) (4.3 nmol/h for up to 4 weeks) were given. Myocardial-, basal-, and isoproterenol-, glucagon-, forskolin-, and Gpp(NH)p-stimulated adenylate cyclase were measured. No changes in enzyme activity were seen following AII infusion, even though myocardial hypertrophy was significant. After epinephrine infusion for 6 days, there was a decrease in isoproterenol stimulated enzyme. After 13 days of infusion, cyclase activity, both basal and stimulated, was reduced. We conclude that in hearts from different models of experimental hypertension associated with cardiac hypertrophy, there are different biochemical alterations in the beta-adrenergic receptor response coupling mechanism.
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PMID:Adenylate cyclase activity in rat myocardium following chronic infusions of angiotensin II and epinephrine. 620 77

Normotensive (WKY) and spontaneously hypertensive (SHR) male rats were treated orally, one week after weaning and for 9 weeks, with alpha-methyldopa (100 mg/kg per day), propranolol (30 mg/kg per day) or hydralazine (10 mg/kg per day). Untreated WKY and SHR rats served as controls. The development of hypertension in SHR rats were attenuated by treatment but none of the drugs was able to restore the impairment in isoproterenol, secretin and glucagon responsiveness of cardiac adenylate cyclase activity which is characteristic of these animals. In heart membranes from both WKY and SHR rats, alpha-methyldopa treatment increased the number of beta-adrenoceptors by 20-32% and the maximal response of adenylate cyclase activity to isoproterenol and glucagon by 20-34%. By contrast, the beta-blocker propranolol was ineffective on these parameters. The results obtained are consistent with the hypothesis that the change in adenylate cyclase seen in SHR rats is genetic in origin and is not a consequence of hypertension.
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PMID:Comparative effects of alpha-methyldopa, propranolol and hydralazine therapy on cardiac adenylate cyclase activity in normal and spontaneously hypertensive rats. 626 48

The autopsy findings in a 58 year old female with the typical glucagonoma syndrome with heart muscle hypertrophy are described. Despite remission of a skin rash and hyperglucagonemia following removal of metastatic liver tumors, the patient died of massive cerebral hemorrhage caused by uncontrolled hypertension and septic cerebral angiitis. On the basis of surgical and autopsy materials, the tumors in the pancreas and liver were defined as malignant glucagonoma by histological, histochemical, immunohistochemical, and ultrastructural studies. The pathohistological changes in several organs that might be related to the hypersecretion of pancreatic glucagon are discussed.
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PMID:A postmortem study of malignant glucagonoma with heart muscle hypertrophy, including chemical, histochemical, immunohistological and ultrastructural observations. 627 84

Fourteen patients having cholecystectomies under general anesthesia were divided into two groups in a double-blind study. All had intraoperative cholangiograms, before which half had glucagon hydrochloride given intravenously in a dose of 1 mg; the others received only normal saline solution. There was a consistently superior visualization of the biliary tree in those given glucagon, and the difference was statistically significant. No significant changes in blood glucose level, heart rate, or ECG patterns were noted in either group. One patient with preoperative hypertension had a brief rise in BP after the glucagon was given. This study confirms previous anecdotal reports suggesting that glucagon in low dose enhances the quality of cholangiography without producing side effects.
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PMID:Glucagon enhancement of cholangiography. A preliminary report. 633 45

To the extent that they have deficient glucagon secretory responses to plasma glucose decrements, as they commonly do, patients with insulin-dependent diabetes mellitus (IDDM) are dependent on epinephrine-mediated beta-adrenergic mechanisms to promote recovery from hypoglycemia. Thus, they are at increased risk for prolonged hypoglycemia if treated with a nonselective beta-adrenergic antagonist such as propranolol. If the hyperglycemic actions of epinephrine are mediated through beta 2-adrenergic mechanisms, therapeutic efficacy (e.g., for hypertension or ischemic heart disease) could be accomplished without increased risk of hypoglycemia by selective beta 1-adrenergic blockade in such patients. However, oral administration of the relatively selective beta 1-adrenergic antagonist metoprolol (100 mg) and of the nonselective beta-adrenergic antagonist propranolol (80 mg) both impaired recovery from insulin-induced hypoglycemia in patients with IDDM. Thus, at a dose of 100 mg, oral metoprolol is not safer than oral propranolol with respect to recovery from hypoglycemia in patients with IDDM.
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PMID:Oral propranolol and metoprolol both impair glucose recovery from insulin-induced hypoglycemia in insulin-dependent diabetes mellitus. 637 17

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

The hemodynamic effects of intravenous labetalol (a combined alpha- and beta-blocking agent) were studied in 11 patients during early post-open heart surgery hypertension. With a mean dosage of 15 mg, labetalol reduced both systemic arterial pressures and the heart rate by an average of 21 percent (p < .001). The patients failed to compensate for the decline in pressure and pulse rate by elevation of their stroke volume, and even the cardiac index (CI) was severely depressed (from 2.30 to 1.67 L/min/m2, ie, 27 percent; p < .001). Neither left ventricular filling pressure nor vascular resistance was affected by labetalol early after open heart surgery. In four patients, 3 mg of glucagon after administration of labetalol elevated pulmonary arterial pressures and increased the CI by 16 percent. Two patients were observed on the preoperative day, and their response to labetalol was similar to that described in earlier studies: during blood pressure decline, CI was slightly augmented, and the systemic vascular resistance was greatly reduced (26 percent). The results indicate that after open heart surgery, patients are highly sensitive to the beta-blocking effects of labetalol, and although labetalol can greatly reduce myocardial oxygen consumption, it cannot be recommended for the treatment of post-open heart surgery hypertension.
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PMID:Combined alpha- and beta-blockade with labetalol in post-open heart surgery hypertension. Reversal of hemodynamic deterioration with glucagon. 700 97

Nine prepubertal obese boys ages 9 1/2 to 12 yr followed moderately restricted diets and moderate exercise routine for 31 wk. Foods were selected from the family's basic diet and the physical activities were tailored to the home environment. This dietary (approximate decrease of 600 kcal/day) and activity (approximate increase of 300 kcal/day) intervention program was sufficient to stop weight gain and normalize key metabolic indices for prediction of atherosclerosis, hypertension, and diabetes. Throughout the treatment period serum lipid responses included significantly lower (p less than 0.05) total cholesterol, low-density lipoprotein-cholesterol and triglycerides. High-density lipoprotein-cholesterol was constant throughout the period. Responses in carbohydrate metabolism included significantly lower (p less than 0.05) fasting insulin and glucose. Insulin and glucose levels were positively correlated with total caloric consumption and insulin was also positively correlated with sucrose consumption (p less than 0.05). Fasting insulin/glucose ratios and glycosylated Hb decreased throughout the treatment period, but serum glucagon levels remained constant. In response to a glucose load, insulin and glucose decreased significantly by wk 31 of treatment. A practical approach for normalizing metabolism in obese male children is presented.
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PMID:Moderate diet control in children: the effects on metabolic indicators that predict obesity-related degenerative diseases. 704 93

Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.
Hypertension
PMID:Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma? 729 31


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