Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study is to explore whether the renal and cardiovascular response to clonidine in type II diabetic patients is different from that in control subjects, and to clarify the role of central alpha 2-receptor in the regulation of cardiovascular response and sodium handling in type II diabetes mellitus (DM). Thirty-five diabetic inpatients aged 30-71 years (54.1 +/- 9.7) and ten control subjects (N) were enrolled in this study after their fasting plasma glucose had been improved. To evaluate the peripheral sympathetic nerve activity, 24-hour urinary catecholamine was measured, and pulse rate (PR) responses to a 30-second standing test was determined. On another day, blood pressure (BP), PR, plasma norepinephrine (PNE), cyclic AMP (p-cAMP), renin activity (PRA), aldosterone (PAC) and growth hormone (p-GH) were measured at 0, 30, 60, 90, 120, 150, 180 minutes following the oral administration of clonidine (150 micrograms). Type II DM were classified as DM with hyper-response (DM-HR, n = 12) when their PR decreased after clonidine more than that of N, and if not, they were classified as DM with normal response (DM-NR, n = 23). Urinary catecholamine excretions in type II DM were within the normal range. BP, PNE and p-cAMP were markedly decreased with clonidine in similar fashion in DM-NR, DM-HR and N. The percent changes of PNE were correlated positively with the changes of p-cAMP in both N and DM-NR (r = 0.660 and 0.449, respectively), but not in DM-HR. No significant difference in the changes of p-GH (delta p-GH) and integral of GH (the area under the curve) following clonidine administration was observed in the three groups. The decrease in PR was correlated with neither delta p-GH (N: r = 0.082, DM-NR: r = -0.400, DM-HR: r = 0.242) or integral of GH (N: r = 0.191, DM-NR: r = 0.382, DM-HR: r = 0.162). The fractional excretion of sodium (FENa) decreased in N (p < 0.01), increased in DM-NR (p < 0.05) and did not change in DM-HR. The changes of FENa were not correlated with those of PRA and PAC.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Altered responses of heart rate, renal sodium handling and plasma growth hormone to clonidine in type II diabetic patients]. 133 89

Ten noninsulin dependent diabetic patients (NIDDM) without baseline hyperkalemia and with normal aldosterone levels when given 100 g of glucose orally revealed heterogeneous responses in serum potassium changes. Six diabetics had paradoxical increases in serum potassium levels averaged 0.44 mEq/L (range, 0.1 to 1.1 mEq/L) and were accompanied by increases in plasma aldosterone levels. On the contrary, four other noninsulin dependent diabetics and four nondiabetic control subjects had gradual decreases in serum potassium levels with simultaneous decreases in plasma aldosterone levels. These rises and falls in serum potassium concentrations coincided with changes in serum osmolality related mostly to the degree of increases in serum glucose following oral glucose administration. pH of venous blood didn't show any relevant and significant changes with changes of serum potassium levels following oral glucose load. This finding suggests that osmotic mechanisms with various degree of well known abnormal insulin secretion and resistance to insulin action in target tissues in NIDDM patients may account for these heterogeneous responses in serum potassium changes after glucose load, and normal aldosterone levels may not be sufficient to prevent glucose induced increases in serum potassium in NIDDM patients.
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PMID:Heterogeneous changes of serum potassium levels in NIDDM patients on oral glucose load. 147 29

We studied whether or not neonatal streptozotocin (STZ) treatment would alter mean arterial pressure (MAP) and blood pressure regulating factors in conscious and unrestrained spontaneously hypertensive rats (SHR). Neonatal STZ administration to SHR resulted in type 2 diabetes mellitus with reduced MAP and heart rate. Plasma glucose was markedly increased in these diabetic animals and was inversely correlated with MAP. In the diabetic SHR, the hypotensive responses to captopril (SQ) or enalapril, administered intravenously, were diminished, regardless of preceding administrations of vasopressin V1-antagonist (AVPA) or hexamethonium (C6), when compared to findings in control rats. In contrast, the C6-induced hypotension was similar in rats with diabetes and control animals. AVPA led to no decrease in MAP in either group. Hypotensive responses to SQ following AVPA and C6 inversely correlated with the plasma levels of glucose in the diabetic group. The combined blockade of the renin-angiotensin system (RAS), sympathetic nervous system and vasoconstrictive action of vasopressin (AVP) abolished the differences in MAP between the groups. Pressor and bradycardic responses to intravenous noradrenaline, angiotensin II and AVP were practically identical in the diabetic and control SHR. Urinary aldosterone excretion rate was not altered by neonatal STZ treatment. In conclusion, a decrease in MAP in SHR with neonatal STZ treatment may be attributed to the suppressed pressor activity of RAS.
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PMID:Suppression of the renin-angiotensin system induced by streptozotocin treatment in neonatal spontaneously hypertensive rats. 197 12

Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
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PMID:Insulin and blood pressure regulation. 204 23

Eighteen patients with non-insulin dependent diabetes mellitus and hypertension were treated during two 4 week periods with the calcium antagonist felodipine or placebo in a double-blind, randomised, cross-over study. Mean systemic blood pressure was significantly lower on felodipine, without producing a deleterious effect on diabetic control. Felodipine was associated with an increment in plasma renin concentration but plasma aldosterone and the renal outputs of sodium and dopamine were similar on both treatments. Plasma atrial natriuretic peptide levels were significantly reduced following felodipine treatment.
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PMID:Effects of felodipine on atrial natriuretic peptide in hypertensive non-insulin dependent diabetes mellitus. 214 57

This investigation was performed in 15 adult patients: 6 with type I and 9 with type II diabetes mellitus, all with arterial hypertension. Captopril (12.5 to 100 mg daily, mean 34 mg) was administered for a month and was effective as monotherapy in all patients. The supine arterial pressure changed from: 177 +/- 19 mm Hg to 141.7 +/- 7.7 mm Hg systolic and 106 +/- 7.6 mm Hg to 87.3 +/- 5.3 mm Hg diastolic; and upright: from 162.7 +/- 16 mm Hg to 139 +/- 11.4 mm Hg systolic and from 101.7 +/- 11.6 mm Hg to 87.3 +/- 6.5 mm Hg diastolic. The differences were statistically significant (p less than 0.001). The mean blood glucose was changed significantly at the end of the study (from 11.1 +/- 3.4 mmol.l-1 to 8.1 +/- 1.0 mumol.l-1, p less than 0.001), while the daily insulin dose (respectively glybenclamide) remained unchanged. No alterations in serum creatinine, HbA1 (glycohemoglobin), urinary excretion rate of albumin, beta 2-microglobulin, glomerular filtration rate were observed during follow-up. No important change in plasma aldosterone was found, while plasma renin activity was significantly increased (p less than 0.05) as expected. No side effects were reported during the therapy. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients without affecting renal function.
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PMID:Captopril in treatment of hypertensive diabetic patients. Preliminary study. 266 Jun 16

Hypertension is more frequently found in patients with diabetes mellitus than in subjects with normal glucose tolerance. On the other hand, concomitant hypertension accelerates the progression of diabetic nephropathy. To examine whether human atrial natriuretic peptide (human ANF-[99-126], hANP) is involved into the pathogenesis of hypertension and nephropathy of diabetic patients and to find out whether the detection of increased hANP levels can serve as an early marker, helping to identify diabetic patients at increased risk of developing these diabetes complications, we studied 107 randomly selected patients with Type 1 or Type 2 diabetes mellitus (53 women, 54 men). There were no differences between patients with normal hANP levels and patients with hANP levels above normal range regarding age, diabetes duration, metabolic control, kidney function (creatinine clearance and proteinuria), electrolytes, and in plasma renin activity, aldosterone, epinephrine and norepinephrine levels in plasma. However, higher blood pressure was measured and antihypertensive therapy was found more frequently in patients with increased hANP levels (p less than 0.05). This was confirmed by analyzing the subgroup of patients with normal blood pressure without antihypertensive therapy: Again, diastolic blood pressure was found to be higher (p less than 0.05) in patients with elevated hANP than in patients with normal hANP levels. In this subgroup, increased creatinine clearance tended to be found more frequently among patients with increased hANP levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[What pathophysiologic significance does increased plasma levels of human atrial natriuretic peptide have in patients with diabetes mellitus?]. 297 Jan 66

Thirty patients (21 F, 9 M) of mean age 55.3 years with non-insulin dependent diabetes mellitus of mean duration 10.8 years and hypertension (blood pressure 160/95 mm Hg) of 0.3 to 4.0 years were randomly allocated to either a twice daily regimen of captopril (50 mg twice daily, Group A) or a once daily captopril schedule (50 mg once daily, Group B). Good glycaemic control (HbA1c, mean 7.63%) had been achieved with sulphonylureas in 22 patients and insulin in 8 patients. There were no statistical differences in baseline values between the two groups. For the 15 patients in Group A, blood pressure fell significantly from a baseline of 177 +/- 13.2/106 +/- 7.8 mm Hg to 161 +/- 14.3/91 +/- 6.9 after one month (P less than 0.05) and continued to decrease at 3 and 6 months. In Group B the blood pressure changed from 179 +/- 19.0/110 +/- 15.6 to 169 +/- 21.0/98 +/- 7.2 at 1 month (P less than 0.05) with further reductions again seen at 3 and 6 months. Nine patients had poorer response than the other 21 but there were no demographic differences between these subgroups nor were there any differences in plasma renin activity or aldosterone responses. There were no statistically significant changes in haematological or biochemical values in either group during treatment. In particular, HbA1c and fasting glucose were unaffected by captopril treatment. No side effects were encountered during the 6 months of follow-up. In conclusion, captopril is an effective antihypertensive in non-insulin dependent diabetes mellitus with mild to moderate hypertension and a once daily regimen could improve compliance.
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PMID:Effect of captopril at two different dosage regimens in hypertensive non-insulin dependent patients. 307 99

This investigation was performed in two groups of adult patients, 10 with type I and 10 with type II diabetes mellitus, all with arterial hypertension (160 to 200 mm Hg systolic and 95 to 120 mm Hg diastolic). Captopril, 50 mg twice a day, was administered for 12 weeks and was effective as monotherapy in 16 patients. Mean arterial pressure (+/- s.d.) in type I patients changed from 121.4 +/- 9.6 to 100.2 +/- 10.1 after 4 weeks and to 102.0 +/- 3.8 mm Hg after 12 weeks; in type II patients it changed from 132.8 +/- 5.7 to 123.9 +/- 13.5 after 4 weeks and to 109.1 +/- 11.1 mm Hg after 12 weeks. The differences were statistically significant. In only 4 patients was it necessary to add a thiazide after the first month of therapy. No significant change was induced by captopril in urine output, osmolar clearance, free water clearance inulin, and PAH clearances. No significant change was observed in serum and urine Na+, Cl-, Ca++ and Mg++, whereas a statistically significant reduction was found in the renal clearances of K+ and PO4-. No important change in serum aldosterone was found, while plasma renin activity was increased, as expected. No alterations in urine protein, glucosaminoglycans, gamma GT, and N-acetyl-beta-glucosaminidase were observed during follow-up. All patients maintained good metabolic control of their disease. No neutropenia and orthostatic hypotension were seen. Captopril appears to be an effective and safe drug for lowering blood pressure in diabetic patients, without affecting renal function, electrolyte balance and the metabolic control of diabetes.
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PMID:Captopril in the treatment of hypertension in type I and type II diabetic patients. 353 66

A 62-year-old patient with non-insulin dependent diabetes (NIDDM) was admitted to our hospital for blood pressure control. He had been treated with angiotensin converting enzyme inhibitor (ACEI) for 7 years and showed marked hypokalemia with increased urinary potassium excretion. Hormonal examination revealed a normal plasma aldosterone concentration and increased plasma renin activity (PRA, 13.4 ng/ml/h), so potassium losing nephropathy was suspected. After discontinuation of the ACEI, PRA decreased to normal. An adrenal adenoma was found on abdominal magnetic resonance imaging (MRI) and adrenalectomy was performed to confirm aldosterone producing adenoma (APA). Although ACEIs are said not to alter PRA in APA, this drug was primarily responsible for the increased PRA in this case. This is a rare case of APA, which showed markedly increased PRA during ACEI treatment.
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PMID:A case of aldosterone producing adenoma associated with high PRA after long-term angiotensin converting enzyme inhibitor treatment. 795 96


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