1985
DOI: 10.1136/pgmj.61.717.563
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The choice of antihypertensive therapy in the diabetic patient

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Cited by 25 publications
(6 citation statements)
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“…In accordance with other studies carried out in hypertensive NIDDM patients, 46 -47 treatment with the ACE inhibitor during the present study did not adversely influence grycemic control and lipid profile. On the other hand, our results do not confirm previous observations 48 - 52 that treatment with diuretics in NEDDM patients worsens glycemic control or plasma lipid profile. However, the short duration of these studies may be the explanation, as most long-term studies showed no overall changes or short-term adverse effects that waned with time, occasionally to values below baseline.…”
contrasting
confidence: 99%
“…In accordance with other studies carried out in hypertensive NIDDM patients, 46 -47 treatment with the ACE inhibitor during the present study did not adversely influence grycemic control and lipid profile. On the other hand, our results do not confirm previous observations 48 - 52 that treatment with diuretics in NEDDM patients worsens glycemic control or plasma lipid profile. However, the short duration of these studies may be the explanation, as most long-term studies showed no overall changes or short-term adverse effects that waned with time, occasionally to values below baseline.…”
contrasting
confidence: 99%
“…Blood-pressure lowering drugs that act directly on the renin-angiotensin system are therefore the treatments of choice for blood-pressure lowering in patients with the metabolic syndrome. In contrast, betablockers and thiazide diuretics may worsen glucose tolerance [35]. …”
Section: Prevention Of Diabetes In Patients With the Metabolic Syndromementioning
confidence: 99%
“…However, the metabolic effects of those agents in diabetic and hypertensive patients are not well understood. Almost all studies on this subject have investigated the effects of calcium‐channel blockers on glycaemic control, plasma lipid levels and systemic blood pressure in patients with type 2 diabetes (Sruthers, 1985; Murad, 1991).…”
Section: Discussionmentioning
confidence: 99%
“…It has been shown that intracellular deposition of calcium increases in streptozotocin (STZ)‐induced diabetic models (Bhatnagar et al., 1984; Cruz, 1985). This situation has been explained with the action of hyperglycaemia which, through its inhibitory effect on Ca 2+ ATP‐ase, increases intracellular calcium concentrations (Bhatnagar et al., 1984; Sruthers, 1985). Increased intracellular calcium levels induce non‐enzymatic glycation, which leads to diabetic complications (Özden et al., 1989; Faure et al., 1993).…”
Section: Introductionmentioning
confidence: 99%