Effectiveness of nifedipine in the treatment of arterial hypertension in various types of diabetes mellitus

Selection of indications and the general tactics of nifedipine monotherapy of hypertension in diabetic subjects is not clearly established, as yet. It refers specifically to different forms and phases of diabetes mellitus. This was the reason to carry out a respective study. In 4 groups of hypertension: 1) in diabetics without vascular complications, 2) in diabetic nephropathy, 3) in diabetics type II without nephropathy, and 4) in comparative group of subjects without diabetes mellitus, a 6-week controlled, open trial was performed. Before, during and after nifedipine (3 X 10-20 mg p.d.), the following parameters were monitored: 1) systolic, diastolic and mean blood pressures, 2) glycaemic indices of diabetes control, 3) serum cholesterol: total, HDL, LDL, triglycerides, 4) daily albuminuria and GFR, 5) adverse reactions to nifedipine. It could be concluded that nifedipine therapy was relatively most effective and safe in hypertensive diabetics type II without nephropathy. It was less effective in diabetics type I without nephropathy and failed in diabetics type I with nephropathy.     

Genetic Predisposition for Development of Nephropathy in Type 2 Diabetes Mellitus

The aim of the study was to explore the association of the angiotensin-converting enzyme (ACE) gene I/D polymorphism and the methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism with development of diabetic nephropathy in type 2 diabetes mellitus. Three groups were recruited during 2007–2011: 232 normal controls, 185 type 2 diabetics without nephropathy, and 407 type 2 diabetics with nephropathy. The ACE I/D and MTHFR C677T polymorphisms were examined using PCR and PCR-RFLP methods. We found no significant association of the ACE I/D polymorphism with diabetic nephropathy in genotype, allele, dominant, and recessive models. We observed a significant association of MTHFR C677T with development of diabetic nephropathy in type 2 diabetics. The MTHFR C677T polymorphism plays a significant role in predisposition of renal insufficiency in diabetic patients.     

Sodium restriction and blood pressure in hypertensive type II diabetics: randomised blind controlled and crossover studies of moderate sodium restriction and sodium supplementation.

OBJECTIVE--To determine the effect of moderate dietary sodium restriction on the hypertension of non-insulin-dependent (type II) diabetes. DESIGN--Randomised parallel controlled study of moderate sodium restriction for three months compared with usual diabetic diet, followed by randomised double blind crossover trial of sustained release preparation of sodium for one month versus placebo for one month in patients continuing with sodium restriction. SETTING--Patients attending diabetic outpatient clinic of city hospital. PATIENTS--Thirty four patients with established type II diabetes complicated by mild hypertension (systolic blood pressure greater than 160 mm Hg or diastolic pressure greater than 95 mm Hg on three consecutive occasions). Patients already taking antihypertensive agents (but not diuretics) not barred from study provided that criteria for mild hypertension still met. Conditions precluding patients from study were diabetic or hypertensive nephropathy, cardiac failure, and pregnancy. INTERVENTIONS--After run in phase with recordings at seven weeks, three weeks, and time zero patients were allocated at random to receive moderate dietary sodium restriction for three months (n = 17) or to continue with usual diabetic diet. Subsequently nine patients in sodium restriction group continued with regimen for a further two months, during which they completed a randomised double blind crossover trial of sustained release preparation of sodium (Slow Sodium 80 mmol daily) for one month versus matching placebo for one month. END POINT--Reduction in blood pressure in type II diabetics with mild hypertension. MEASUREMENTS AND MAIN RESULTS--Supine and erect blood pressure, body weight, and 24 hour urinary sodium and potassium excretion measured monthly during parallel group and double blind crossover studies. After parallel group study sodium restriction group showed significant reduction in systolic blood pressure (supine 19.2 mm Hg, erect 21.4 mm Hg; p less than 0.001) and mean daily urinary sodium excretion (mean reduction 60 mmol/24 h). There were no appreciable changes in weight, diabetic control, or diastolic pressure. No significant changes occurred in controls. In double blind crossover study mean supine systolic blood pressure rose significantly (p less than 0.005) during sodium supplementation (to 171 mm Hg) compared with value after three months of sodium restriction alone (159.9 mm Hg) and after one month of placebo (161.8 mm Hg). CONCLUSIONS--Moderate dietary restriction of sodium has a definite hypotensive effect, which may be useful in mild hypertension of type II diabetes.     

Short term effect of captopril on microalbuminuria induced by exercise in normotensive diabetics.

OBJECTIVE--To investigate whether captopril has any effect on microalbuminuria induced by exercise in normotensive diabetic patients with early stage nephropathy. DESIGN--Randomised, double blind, crossover trial. SETTING--Outpatient department. PATIENTS--22 diabetics with stage II nephropathy (urinary albumin excretion rate less than 20 micrograms/min; 15 with type I diabetes and seven with type II), 32 patients with stage III nephropathy (urinary albumin excretion rate 20-200 micrograms/min; 14 with type I diabetes and 18 with type II), and 10 normal subjects. INTERVENTIONS--Four exercise tests on a cycle ergometer: the first two under basal conditions and the third and fourth after subjects had received captopril (two 25 mg doses in 24 hours) or placebo (two tablets in 24 hours). END POINT--Exercised until 90% of maximum heart rate achieved. MEASUREMENTS AND MAIN RESULTS--Mean urinary excretion one hour after the first two exercise tests was 21 micrograms/min in normal subjects, 101 micrograms/min in diabetic patients with stage II nephropathy, and 333 micrograms/min in those with stage III nephropathy. Similar results were obtained after placebo. After captopril the urinary excretion rate one hour after exercise was significantly decreased in diabetics with stage II (36 micrograms/min) and stage III (107 micrograms/min) disease compared with placebo but not in normal subjects. Systolic and diastolic pressures were similar in the three groups after placebo and captopril had been given. CONCLUSIONS--Captopril significantly reduces microalbuminuria induced by exercise in normotensive diabetics without affecting systemic blood pressure. Captopril may reduce renal intracapillary pressure.     

Effect of captopril on kidney function in insulin-dependent diabetic patients with nephropathy.

The influence of angiotensin II on kidney function in diabetic nephropathy was assessed by studying the effect of 12 weeks'' monotherapy with captopril (25-50 mg twice a day) in 16 hypertensive insulin dependent diabetic patients with persistent albuminuria. In an initial one week randomised single blind trial of captopril versus placebo, captopril (for nine patients) reduced arterial blood pressure from 148/94 (SD11/6) to 135/88 (8/7) mm Hg (p less than 0.05) and albuminuria from 1549 (range 352-2238) to 1170 (297-2198) micrograms/min (p less than 0.05), while glomerular filtration rate remained stable. No significant changes occurred in seven patients treated with placebo. During the 12 weeks of captopril treatment arterial blood pressure in all patients fell from 147/94 (11/6) to 135/86 (13/7) mm Hg (p less than 0.01), albuminuria fell from 1589 (range 168-2588) to 1075 (35-2647) micrograms/min (p less than 0.01), and glomerular filtration rate fell from 99 (SD19) to 93 (25) ml/min/1.73 m2 (p less than 0.01). The renin-angiotensin system showed suppressed plasma concentrations of angiotensin II and increased concentrations of angiotensin I and renin. The study showed that glomerular filtration rate is not dependent on angiotensin II, that captopril reduces albuminuria, probably by lowering glomerular hypertension, and that captopril represents a valuable new drug for treating hypertension in diabetics dependent on insulin with nephropathy.     

Gene polymorphisms in patients with type 2 diabetes and diabetic nephropathy

A considerable variability in the incidence and prevalence of diabetic nephropathy (DN) coheres with an important contribution of multigenetic predisposition in the development of DN. Some genes, which probably participate in the pathogenesis of diabetic nephropathy, also play a role in the regulation of blood pressure, familial hyperlipidemia, familial hypertension and other diseases of the cardiovascular system. We have examined the association of diabetic nephropathy, nephropathy of non-diabetic origin, hypertension and of type 2 diabetes itself with several genetic polymorphisms (the insertion/deletion polymorphism in the gene for angiotensin-converting enzyme, the G/T polymorphism in the glucose transporter 1 gene, the G/T (894) polymorphism and the T/C (−786) polymorphism in the eNOS gene in three groups of patients with diabetes mellitus: 1) patients without diabetic nephropathy (DM); 2) patients with DN; 3) patients with nephropathy of non-diabetic origin (NDRD). Angiotensin-converting enzyme is an important factor in a development of arterial hypertension, but in our groups of Central European diabetic patients the I/D polymorphism was not associated with diabetic nephropathy. Furthermore, we have confirmed that the T/C (T786C) polymorphism in the eNOS gene is associated with metabolic syndrome including type 2 diabetes.     

Protection of kidney function and decrease in albuminuria by captopril in insulin dependent diabetics with nephropathy.

STUDY OBJECTIVE--To assess whether long term inhibition of angiotensin converting enzyme with captopril and frusemide or bendrofluazide protects kidney function in diabetic nephropathy. DESIGN--Non-randomised controlled before-after trial of matched hypertensive insulin dependent diabetics with nephropathy treated with captopril and frusemide or bendrofluazide. SETTING--Outpatient diabetic clinic in tertiary referral centre. PATIENTS--Treatment group of 18 hypertensive insulin dependent diabetics with nephropathy (mean age 33), who had not been treated previously. Control group of 13 patients (mean age 32) fulfilling the same entry criteria from a prospective study. INTERVENTIONS--Treatment group was given daily captopril 37.5-100.0 mg and frusemide (mean) 98 mg (10 patients) or bendrofluazide (mean) 4 mg (seven). Treatment was continued for about two and a half years. Controls were not treated. END POINT--Measurement of arterial blood pressure, albuminuria, and glomerular filtration. MEASUREMENTS AND MAIN RESULTS--Baseline values were identical in treated and untreated groups respectively: mean blood pressure 146/93 (SE 3/1) mm Hg v 137/95 (2/1) mm Hg; geometric mean albuminuria 982 (antilog SE 1.2) micrograms/min v 936 (1.2) micrograms/min; and mean glomerular filtration rate 98 (SE 5) ml/min/1.73 m2 v 96 (6) ml/min/1.73 m2. Mean arterial blood pressure fell by 8.7 (1.3) mm Hg with captopril and rose by 6.6 (1.5) mm Hg in controls, (p less than 0.001); Albumin excretion decreased to 390 (1.1) micrograms/min with captopril and rose to 1367 (1.3) micrograms/min in controls (p less than 0.001). The rate of decrease in glomerular filtration rate was lower with captopril (5.8 (0.7) ml/year v 10.0 (1.3) ml/year) (p less than 0.01). Rate of fall in glomerular filtration rate and mean arterial blood pressure were significantly correlated (n = 31, r = 0.37, p less than 0.05). CONCLUSIONS--Captopril is a valuable new drug for treating hypertension in insulin dependent diabetics with nephropathy.     

A correlation between microalbuminuria and anti-insulin antibodies in type I diabetics

A link between circulating anti-insulin antibodies and diabetic glomerulopathy has been suggested. This paper presents two different studies aiming to detect a relationship between incipient nephropathy (indicated by microalbuminuria) and anti-insulin antibodies. In 64 type I diabetics, overnight urinary albumin excretion during an exercise-test was found to be correlated with systolic blood pressure (r = 0.258 p less than 0.05), anti-insulin antibodies (r = 0.258 p less than 0.05), and glycosylated hemoglobin (r = 0.258 p less than 0.05) whereas no correlation was found among these three parameters. In another group of 80 type I diabetics, urinary albumin excretion during a standardized exercise-test was also correlated with anti-insulin antibodies (r = 0.360 p less than 0.001). In this latter group, diabetics with elevated (greater than 200 microU/ml) levels of anti-insulin antibodies had higher values of microalbuminuria after exercise (p less than 0.001) when compared to those with lower or undetectable levels, although they did not differ with respect to blood pressure and glycemic control. Therefore, we confirm preliminary reports indicating a statistical relationship between anti-insulin antibodies and microalbuminuria. We hypothesize that anti-insulin antibodies may be an additional factor of risk in the pathogenesis of early (reversible) stages of diabetic nephropathy.     

Glomerular filtration and renal volume in type II diabetes (non-insulin-dependent): study in normal and microalbuminuria patients]

In type 2 diabetes elevated glomerular filtration rate (GFR) and increased renal volume (RV), often accompanied to normo or microalbuminuria, were demonstrated. This condition is considered a pathogenetic factor for clinical nephropathy. As this topic is little studied in type 2 diabetes, we have investigated 73 type 2 diabetic patients (34 normo and 39 microalbuminuric), looking for a correlation between GFR, RV, hypertension, duration of diabetes and indexes of metabolic control. GFR was measured by a scintigraphy, after infusion of 99Tc-DTPA. Renal volume was determined by ultrasound scanning. Between the groups GFR and RV weren't different; elevated GFR was demonstrated in 3 patients; increased RV in 1 patient. In the hypertensive group GFR was lower than in normotensive group and in controls. Multivariate analysis in stepwise demonstrated that GFR presents a negative correlation to systolic blood pressure as in normo as in microalbuminuric patients. In the normotensive group GFR didn't correlate to the other variables. The present data suggest that in type 2 diabetes there is a little prevalence of glomerular hyperfiltration and increased renal volume and that hypertension plays a role on GFR of hypertensive diabetic patients.     

Comparative studies on the effects of propranolol and acebutolol on blood pressure, serum lipids and lipoproteins in patients with primary hypertension]

A comparative studies on the effect of propranolol and acebutolol on blood pressure, cardiac function, blood serum lipids and lipoproteins were carried out in 48 patients with the primary hypertension double-blind method was applied. Tested drugs were given for 12 weeks. It was found, that both drugs are potent and comparable hypotensive agents normalizing blood pressure in the majority of treated patients. No significant difference in the effect on heart rate and adverse reactions has been noted. Acebutolol did not change lipid metabolism parameters whereas propranolol slightly but statistically significantly increased serum triglycerides.     

Thyroid dysfunction in type 2 diabetics seen at the University College Hospital, Ibadan, Nigeria

Thyroid dysfunction complicates the metabolic derangement observed in Diabetes Mellitus (DM). It is necessary to recognize and treat it when present in order to achieve stability of metabolic control in these patients. The prevalence of thyroid dysfunction in type-2 diabetics in our environment is not known. This study was therefore designed to determine the prevalence of thyroid dysfunction in Type 2 diabetics seen at the Metabolic Research Unit of University College Hospital, Ibadan, Nigeria. Serum TSH, Free T3 and Free T4 assays were performed using Automated Enzyme Immunoassay platform on fresh sera from volunteers comprising 64 adult type 2 diabetics and 36, age matched, non diabetic controls; weight, height and blood pressures were measured in all subjects. In addition, past lipid profile results of type 2 diabetics were retrieved from medical records. Thyroid dysfunction was present in 19 (29.7%) of 64 type 2 diabetics and 1 (2.8%) of 36 non diabetic controls.The prevalence of thyroid dysfunction is 32.4% in females and 25.9% in males.  Secondary hypothyroidism was seen in 78.9%, sub-clinical hypothyroidism in 15.8%, and sub-clinical hyperthyroidism 5.2% of subjects with thyroid dysfunction. Abnormal lipid profiles were seen in 35.4% of euthyroid type 2 diabetics and 100% of hypothyroid type 2 diabetics. 87.5% of type 2 diabetics and 38.8% of controls were hypertensive. 7.8% of type 2 diabetics and 50% of controls were obese. The prevalence of thyroid dysfunction in type 2 is higher in type 2 diabetics than in controls. More of Type 2 diabetics were obese and more of them were hypertensive compared to controls. The approach of using TSH first in screening for thyroid dysfunction is not sufficient in type 2 diabetics. Routine screening for thyroid dysfunction should be carried out in type 2 diabetics.Keywords: Thyroid dysfunction, Diabetes, Ibadan, Nigeria.     

Hypertension and Diabetes—A Toxic Combination

ObjectiveTo assess the relationship of diabetes and hypertension and the effect on cardiovascular outcomes.MethodsA review of the English-language literature regarding the effects of diabetes and hypertension published between January 1, 1980, and April 30, 2008, was performed.ResultsIn type 2 diabetes, the prevalence of hypertension due to both hyperglycemia and insulin resistance is increased. High insulin levels are associated with left ventricular hypertrophy and decreased ventricular function. The growth factor effects of insulin on the myocardium are worsened by hypertension. The diabetic hypertensive patient is exquisitely sensitive to blood pressure lowering as it relates to cardiac events and mortality. Because of this, the blood pressure goals for diabetic hypertensive patients are lower than those for their nondiabetic hypertensive peers. Cardiac events have a stronger association with systolic hypertension and the pulse pressure than with diastolic hypertension. The presence of microalbuminuria not only signifies a higher risk of developing diabetic nephropathy, but also increased mortality and incidence of cardiovascular events. Thus, when microalbuminuria is detected, intensification of hypertensive therapies, especially suppression of the renin-angiotensin-aldosterone system, is essential.ConclusionThe effects of hypertension in persons with diabetes increase the frequency and severity of cardiac events, especially when microalbuminuria is present. (Endocr Pract. 2008;14:1031-1039)     

Choice of antihypertensive drug in the diabetic patient

The hypertensive patient with type 2 diabetes is especially at risk of adverse cardiovascular events. The United Kingdom Prospective Diabetes Study (UKPDS) and Hypertension Optimal Treatment (HOT) studies suggested that treatment to a lower target blood pressure resulted in better prevention of clinical disease in these patients. Most trials comparing antihypertensive drugs have shown only minimal differences between the various agents. The evidence from the trials suggests that diuretics, beta-blockers, calcium channel blockers (CCBs), angiotensin-converting enzyme (ACE) inhibitors, and the angiotensin-receptor antagonists (ARBs) will all successfully reduce adverse clinical events. The largest of the comparative hypertensive drug trials, the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), demonstrated that a diuretic has a better hypotensive effect, and was more successful in preventing many aspects of cardiovascular disease compared with CCBs and ACE inhibitors. The importance of good blood pressure control and the general equivalence of antihypertensive drugs were again shown in the Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial, which compared an ARB with a CCB. Choice of antihypertensive agent should be individualized and guided by the presence of concomitant clinical disease and the need to protect any specific target organ system in the diabetic hypertensive. Diuretics, being potent hypotensive drugs with clearly demonstrated clinical benefit, should form part of the antihypertensive regimen of most diabetic hypertensives. ACE inhibitors and ARBs are especially useful in preventing nephropathy. Most patients will require a combination of antihypertensive drugs to achieve tight blood pressure control of under 130/80 mm Hg in the diabetic hypertensive. The clinician should concentrate on seeking this lower target blood pressure rather than be excessively concerned about which is the best antihypertensive agent.     

Plasma endothelin-1 levels and albumin excretion rate in normotensive,microalbuminuric type 2 diabetic patients

BACKGROUND: Endothelin-1 (ET-1) is able to determine functional and structural renal alterations and plasma levels of this vasoconstrictor peptide are increased in diabetic patients. In a selected group of type 2 normotensive diabetic patients with microalbuminuria, we investigated circulating ET-1 levels compared to a control group and verified whether there is a relationship between ET-1 levels and albumin excretion rate in diabetics. SUBJECTS AND METHODS: Thirty-two microalbuminuric type 2 diabetic patients (12 males and 20 females; mean age 57 +/- 8 years) without hypertension, renal failure, hypercholesterolemia or atherosclerotic damage were selected. The control group was made up of 28 healthy subjects matched for sex and age. Blood pressure, creatinine clearance, serum cholesterol and plasma ET-1 values were determined in diabetic and control group. In diabetic patients, glycosilated hemoglobin and urinary albumin excretion rate were also assayed. Mean ET-1 values in diabetics and controls were compared using Student's t-test. Linear regression test was done to relate two variables. Statistical significance was set at p<0.05. RESULTS: Mean ET-1 values were significantly higher in the diabetic group than in controls (11.77 +/- 1.16 pg/ml vs 8.9 +/- 2.1 pg/ml; p<0.05). No relationship (p>0.05) was found between circulating ET-1 and blood pressure, creatinine clearance, serum cholesterol and metabolic control in diabetics. There was a significant positive correlation (r=0.403; p=0.03) between plasma ET-1 levels and albumin excretion rate in diabetic patients. CONCLUSIONS: Our results showed that circulating ET-1 values were increased in microalbuminuric, normotensive, type 2 diabetic patients and correlated with albumin excretion rate. These findings confirm that endothelial dysfunction, as expressed by ET-1 levels, occurs early in these patients and support the hypothesis of a potential role for this peptide in development of microalbuminuria in diabetic nephropathy.     

老年高血压患者健康管理的效果分析

目的：对社区老年高血压病人实行健康管理,探讨其在高血压治疗中的临床效应。方法：对老年高血压患者分为实验组和对照组。对照组未实施健康管理,实验组实施健康管理,两组治疗药物方案相同,观察降压效果。结果：统计处理,两组老年高血压病人在相同时间里的降压效果差异具有显著性,实验组血压控制较前好（P〈0．05）。结论：健康管理在老年高血压治疗中效果明显。（健康管理能减少老年高血压患者的,降低医疗经济负担）     

Effects of streptozotocin and dietary fructose on delta-6 desaturation in spontaneously hypertensive rat liver

We have investigated the effects of hypertension associated with diabetes mellitus on polyunsaturated fatty acid biosynthesis. For this purpose, two rat models for these pathologies have been established: a type 1 diabetic hypertensive model obtained by streptozotocin injection to spontaneously hypertensive rat (SHR), followed or not by insulin treatment (experiment 1); a type 2 diabetic hypertensive model by feeding SHR with a fructose enriched diet (experiment 2). Liver gene expression of delta-6 desaturase (D6D), microsomal D6D activities and fatty acid composition of total lipids were estimated. In experiment 1, an increase of linoleic acid (18:2 n-6) level was observed in the streptozotocin group. D6D gene expression appeared depressed in both experimental groups. Insulin did not reverse the streptozotocin effect in SHR, as it does in insulin-dependent diabetic rats. In experiment 2, the results showed a decrease of 18:2 n-6 and of long chain products of desaturation in rats fed on fructose diet. Delta-6 n-3 desaturase activity was significantly increased, whereas gene expression tended to decrease. Feeding fructose induced a significant increase in delta-9 desaturated products, suggesting a stimulation of stearoyl-CoA desaturase. These changes in monounsaturated fatty acids strongly differ from those observed in the streptozotocin experiment, indicating that the effects on lipogenesis of hypertension linked to diabetes differ according to the type of diabetes. Then, these results indicate that the liver steatosis observed during genetic hypertension was reinforced by fructose feeding. All together, the present results showed that hypertension associated to type 1 or type 2 diabetes exacerbated the damage caused by diabetes or hypertension alone on liver lipid metabolism. The metabolic effects induced by fructose being very similar to those found in human NIDDM, SHR fed a fructose-rich diet appears to be an appropriate model for studying the consequences of the combination of hypertension and NIDDM in the metabolic syndrome diseases.     

MTHFR gene variant is not associated with diabetic nephropathy in Japanese.

Genetic predisposition has been implicated in diabetic nephropathy. The C677T variant of the MTHFR gene has been suggested to play a role in the development of not only vascular diseases but also diabetic microangiopathies. By using polymerase chain reaction-restriction length polymorphism (PCR-RFLP) method using Hinf I, we investigated whether this variant is associated with diabetic nephropathy in Japanese. By analysing 274 unrelated Japanese patients with type II DM with or without nephropathy, there was no significant difference in the genotype distribution of this variant. The distribution of the three genotypes were not different among patients with micro- or macroalbuminuria and those without nephropathy. Although previous reports suggest a role of this variant with diabetic microangiopathies, our observations suggest that this variant is does not play an important role in the pathogenesis of diabetic nephropathy in Japanese.     

Serum N-acetyl-beta-D-glucosaminidase (NAG) activity in patients with diabetes mellitus with reference to diabetic microangiopathy]

In 110 diabetics type I and type II and in 30 control subjects the total serum activity of NAG as well as of its isoenzymatic forms A and B was determined. In cases with diabetic nephropathy the GFR and serum creatinine was also analysed. It was found that NAG activity is correlated to the degree of clinical symptoms of diabetic vascular changes. Therefore it could be suggested that NAG plays a role in development of microangiopathy. NAG determination may also serve as an index differentiating the diabetic microangiopathy from other forms of microvessels.     

Increased vasodepressor effect of prostaglandins A1 and E1 in renal hypertensive rabbits.

In order to determine whether cardiovascular reactivity to exogenous prostaglandins is altered in hypertension, the hypotensive effects of increasing intravenous doses of PGA₁ and PGE₁ were assessed in conscious normotensive rabbits and in rabbits made hypertensive by wrapping both kidneys with cellophane. Similar experiments were carried out with nitroglycerin. Depressor responses to the prostaglandins, but not to nitroglycerin, were greater in hypertensive than in normotensive animals. The possibility of this enhanced responsiveness being related to the prostaglandin deficiency believed to exist in hypertension was explored in normotensive rabbits treated acutely with indomethacin. The prostaglandin synthesis inhibitor did not affect blood pressure responses to PGA₁ or PGE₁. Although these experiments do not rule out the possible influence of more prolonged prostaglandin deficiency on cardiovascular reactivity, a more apparent adrenergic inhibitory component of the hypotensive effect of prostaglandins in hypertensive animals was considered a likely alternative explanation for the phenomena observed.     

Scores of coronary calcification determined by electron beam computed tomography are closely related to the extent of diabetes-specific complications.

This study was aimed at investigating the degree of calcification of coronary arteries in type II diabetes mellitus for the purpose of examining as risk factors for coronary disease as well as parameters of diabetic complications. One hundred and three patients with type II diabetes were studied by the newly developed noninvasive technology of electron beam computed tomography, in which the degree of calcification was expressed as coronary calcification scores. The mean +/- SE value of coronary calcification scores were 247.5 +/- 48.1, which were significantly greater than the control patients without diabetes (148.9 +/- 48.3, p<0.05). In the diabetics, the coronary calcification scores had a significant (p < 0.01) correlation with patient age and duration of diabetes. The scores also had a significant (p<0.05) difference between patients who did and did not smoke cigarettes, and between patients with and without hypertension. The scores were significantly (p < 0.01) different between patients with and without hypertension. The scores were significantly (p < 0.01) different between presence and absence of diabetes-specific complications including retinopathy, neuropathy, and nephropathy. In a subgroup of patients without any signs of coronary disease, the scores showed a significant (p<0.01) difference between presence and absence of diabetes-specific complications, but no significant difference with smoking or hypertension. These data suggest that the extent of coronary calcifications and the development of ischemic heart disease seem to be closely related to the association of diabetic complications. Use of electron beam computed tomography seems to be useful in obtaining the information to predict future development of diabetic-specific complications.