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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological studies have revealed, that elevated blood pressure is in diabetics 1.5-3.0-times more frequent that in general population. It is one of the most important factors increasing the morbidity and mortality due to small and big arteries disease. Hypotensive therapy should be commenced in diabetic persons earlier than in patients without diabetes mellitus. In many such diabetic patients blood pressure normalization could be obtained by dietary adaptations and metabolic compensation. In more advanced cases pharmacological treatment should be undertaken. When selecting the drug for a diabetic person one has to balance between positive and adverse actions. The drugs of the first choice are the ACE inhibitors, drugs blocking the slow calcium channel and alpha 1-adrenergic receptors, because they do not influence negatively the carbohydrate and lipid metabolism. On contrary, prazosin and ACE inhibitors increase the tissue sensitivity to insulin. The latter group decrease also intraglomerular pressure and albuminuria. As a routine the treatment begins with small, testing dose of a single hypotensive drug. The dosage may be increased slowly up to the average dose level. If this manipulation does not permit normalization of blood pressure one may combine 2 or 3 hypotensive drugs. Selection of the drug and of its dose rely also on the type and intensity of late diabetic complications--at first nephropathy and autonomic neuropathy.
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PMID:[Principles of hypotension treatment in patients with diabetes]. 836 76

Physicians need to weigh the efficacy, adverse effects and cost of first-line antihypertensive agents. Calcium channel blockers lower blood pressure, improve coronary blood flow and depress cardiac contractility by relaxing smooth muscle and cardiac muscle. They have beneficial or neutral effects in hypertensive patients with angina, asthma, chronic obstructive pulmonary disease, postural hypotension, peripheral vascular disease, depression, sexual dysfunction, diabetes and hyperlipidemia. The major adverse effect of some calcium channel blockers is that they may worsen congestive heart failure in some patients. Because calcium channel blockers are metabolized in the liver, the dosage must be lowered in the elderly and in patients with hepatic disease. Diltiazem, verapamil and nifedipine represent prototypes of the three classes of calcium channel blockers, each with slightly different effects.
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PMID:Calcium channel blockers in the treatment of hypertension. 836 95

In the absence of any other exogenously added fuel, monomethylsuccinate, the methyl ester of succinic acid, at 10-20 mM stimulates insulin release in a biphasic pattern. In quantitative terms, first-phase release evoked by 20 mM MMSucc was comparable to that observed with 20 mM glucose but second-phase release was only 20% of the glucose-induced response. Secretion to both MMSucc and glucose was virtually abolished by the calcium channel antagonist nitrendipine (0.5 microM). In islets that had phosphoinositide pools labeled with [3H]inositol for 2 h, subsequent stimulation with 20 mM MMSucc results in dramatic and sustained increases in [3H]inositol efflux rates. Inositol phosphate levels are also increased. In contrast to secretion, the increase in phosphoinositide hydrolysis caused by MMSucc was largely resistant to nitrendipine, whereas significant reductions in glucose-induced phosphoinositide hydrolysis were observed in the presence of the calcium channel antagonist. MMSucc (2.75-10 mM) substitutes for glucose in that MMSucc supported the insulinotropic effects of the sulfonylurea tolbutamide (200 microM) and the gut hormone cholecystokinin (200 nM). A prior 15-min exposure to 20 mM MMSucc also sensitized islets to the stimulatory effects of 7.5 mM glucose. Finally, a 2-h exposure to 20 mM MMSucc desensitized the islet, in terms of both phosphoinositide hydrolysis and insulin secretion, to a subsequent exposure to 10 mM glucose. Thus, appropriate concentrations of MMSucc can cause qualitatively many of the effects induced by glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Jun
PMID:Comparative effects of monomethylsuccinate and glucose on insulin secretion from perifused rat islets. 838 41

Progressive renal failure is a significant complication of hypertension, a major cause of end-stage renal disease. In hypertensive patients, the markers of impaired renal function are abnormal levels of serum creatinine and microalbuminuria. Serum creatinine measurements, which can be adjusted for age and gender by using a simple formula, are used to estimate creatinine clearance and glomerular filtration rate. Microalbuminuria is an early sign of renal damage found in 20% to 30% of cases of essential hypertension and foretells the development of nephropathy and other complications. Current general guidelines for managing hypertension associated with renal impairment recommend controlling blood pressure, pharmacologically if necessary; adding a diuretic, if initial monotherapy is not effective; and reducing dietary sodium intake. Diuretic drugs remain the cornerstone of antihypertensive therapy for patients with renal failure, whereas beta-blockers, calcium channel blockers, and angiotensin-converting enzyme inhibitors have varying effects and continue to be investigated intensively. In a study undertaken by the National Institute of Diabetes and Digestive and Kidney Diseases, the different classes of antihypertensive drugs are currently being evaluated for their ability to slow progressive renal failure.
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PMID:Renal issues in the management of hypertension. 839 8

Recent investigations using experimental models of diabetes mellitus have emphasized the importance of impaired blood flow for the development of nerve dysfunction. Other observations suggest that this may also be the case for patients. A number of studies have revealed that several types of vasodilators can prevent or successfully treat early conduction abnormalities in diabetic rodents. These include alpha 1-adrenoreceptor antagonists, calcium channel blockers, agents that inhibit the renin-angiotensin system, and vasomodulator prostanoids. Other treatments applied to animal models, such as omega-6 essential fatty acids, aldose reductase inhibitors, aminoguanidine which prevents the formation of advanced glycation end-products, and anti-oxidants all appear to have vascular-related effects that lead to improvements in nerve conduction. These findings suggest that endothelial dysfunction and oxidative stress could be important factors in the aetiology of diabetic neuropathy. Studies have also focused on deficits in axon growth and regeneration, their relation to impaired neuronal synthesis and transport of growth-related chemicals, and neuronotrophic abnormalities. Taken together, the data give rise to the notion that an optimal therapeutic strategy could consist of improving the microenvironment of damaged nerve fibres by manipulating nerve blood flow while concurrently encouraging repair with trophic agents.
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PMID:Potential therapeutic approaches to the treatment or prevention of diabetic neuropathy: evidence from experimental studies. 840 19

Data are presented concerning the basal levels of parathormone and calcitonin and the effect of dihydropyridine derivatives on the characteristics of haemodynamics as well as pancreatic secretory activity in patients with diabetes mellitus. It is shown that in diabetic patients with hypertension a single administration of the drugs induces vasodilatation which causes lowering of systolic and diastolic blood pressure. In patients with diabetes mellitus in combination with hypertension, heart coronary disease and obvious peripheral angiopathy (similar procedure) no peripheral vasodilatation was observed. No negative effects were observed on the compensatory processes (and obviously on pancreatic secretory activity in patients with both insulin-dependent and insulin-independent diabetes mellitus even during long-lasting administration of drugs. A conclusion is made that calcium channel antagonists should be recommended to patients with diabetes mellitus taking into account the state of their peripheral vessels.
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PMID:[Effect of calcium antagonists on the hemodynamic and pancreatic secretory parameters in diabetes mellitus]. 840 42

Medicine has long recognized an association between hypertension and the kidney. The kidney may be a culprit or a victim in the process. As a culprit, the kidney may be responsible for the pathogenesis of hypertension in many patients, and in virtually all patients the renal response to antihypertensive therapy is a major determinant of its success or failure. In some patients, hypertension can lead to renal injury and even end-stage renal disease. Indeed, 25% of patients entering dialysis or transplant programs in the United States today have hypertension as the primary or sole mechanism, and another 25% have the complex combination of diabetes and hypertension as the cause. Antihypertensive therapy appears to be successful in preventing or arresting the renal response in accelerated hypertension, regardless of the treatment used to reduce blood pressure. However, treatment appears to be less successful in preventing the progression of moderate hypertension to end-stage renal disease. Substantial evidence suggests that angiotensin-converting enzyme inhibition and calcium channel blockade may prevent this progression when other antihypertensive therapy does not. The renal response to an angiotensin-converting enzyme inhibitor or a calcium channel-blocking agent appears to be determined by the pathogenetic features of the hypertension, and this may be an important determinant of the efficacy of the agents selected. Although still indistinct, the guidelines favoring selection of a specific antihypertensive agent are gradually emerging.
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PMID:Hypertension and the kidney: determinants of the response to antihypertensive therapy and their implications. 843 Jun 5

The effects of calcium channel blockers (CCB)-verapamil, nifedipine, diltiazem on metabolic control in streptozotocin-induced long-term diabetes in rats were investigated. Diabetes mellitus was induced by single intravenous injection of streptozotocin (65 mg/kg body wt.). The animals were divided into five groups: a healthy control group, a diabetic group and three diabetic groups treated with one of the calcium channel blockers (verapamil, 25 mg/kg/day, nifedipine, 20 mg/kg/day, and diltiazem, 30 mg/kg/day, respectively). Body weight, glycemia, glycated hemoglobin and total serum protein levels of these animals were measured at the beginning and at the end (after 13 weeks) of the experiment. It was observed that diabetic animals who were not treated with CCB had lost weight at the end of the experiment (P < 0.01). The blood glucose and glycated hemoglobin levels were increased in the diabetic group in comparison to the healthy control group (P < 0.001). However, the calcium channel blockers seem to have beneficial effects on body weight, glycated hemoglobin and blood glucose levels.
Diabetes Res Clin Pract 1995 Jun
PMID:The effects of calcium channel blockers, verapamil, nifedipine and diltiazem, on metabolic control in diabetic rats. 852 99

Hypertension is common in patients with non-insulin-dependent diabetes mellitus and is also an early sign of diabetic nephropathy in those with insulin-dependent diabetes. Hypertension contributes to the progression of both macrovascular disease and nephropathy in patients with diabetes. Certain antihypertensive agents can adversely affect carbohydrate and lipid metabolism. Angiotensin-converting enzyme inhibitors and calcium channel blockers may slow the progression of renal complications in patients with diabetes. The pharmacologic approaches to treatment of hypertension in patients with diabetes potentially differ from those in nondiabetic persons. On the basis of a review of the recent literature related to antihypertensive therapy for patients with diabetes, we describe an empiric approach to treatment of hypertension in such patients. The proposed approach must be modified as new data from randomized clinical trials become available.
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PMID:A practical guideline for management of hypertension in patients with diabetes. 853 34

Many cells are equipped with so-called potassium (K+) channels which have an important role in maintaining transmembrane potential. Closure of these channels leads to membrane depolarization, which can be followed by cell-specific activity such as contraction of vascular smooth muscle, or secretion of insulin from pancreatic beta-cells. Therefore, it is not surprising that a number of drugs have been introduced which influence K+ channels by either blocking or opening them. The treatment of type 2 (non-insulin-dependent) diabetes mellitus with sulphonylurea derivatives (SU), which exert their insulinotropic effect by closing the K+[ATP] channels of the pancreatic beta-cell, is customary. Slight differences are described in the insulinotropic action of the various SU. Claims in the past that treatment with SU increases cardiovascular mortality are not supported by sound evidence. SU may even reduce cardiovascular mortality by protecting against ventricular arrhythmias during cardiac ischaemia. K+[ATP]-channel-opening drugs are under investigation for the treatment of essential hypertension and angina pectoris. They are at least as effective in achieving adequate blood pressure control as calcium channel blockers. The recently introduced coronary vasodilating drug, nicorandil, exerts its effect by two mechanisms of action: opening K+[ATP] channels in vascular smooth muscle cells of coronary arteries and activation of guanidyl cyclase by its nitro-group in these cells. A proarrhythmic effect of K+[ATP] channel openers has only been observed at very high doses, but not in the low doses used in angina pectoris and hypertension. In vivo no negative effect of K+[ATP]-channel-opening drugs on insulin secretion is found.
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PMID:Clinical relevance of ATP-dependent potassium channels. 854 97


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