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

The use of microelectrode techniques for studying oxygen distribution and blood flow in the eye of a physiologically well maintained rat provides a very convenient model in which to study oxygen supply to the retina. The availability of rat models of vascular disease such as diabetes and hypertension, and the existence of several models of retinal degeneration, make studies of oxygen supply in the rat eye of particular relevance. The experiments reported in this paper demonstrate changes in oxygen distribution and blood flow very early in STZ induced diabetes. Thus, we have established a preparation in which the role of changes in oxygen supply can be correlated with the pathological events that are apparent later in the disease.
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PMID:Oxygen tension and blood flow in the retina of normal and diabetic rats. 128 5

The effect of acute streptozotocin-induced diabetes mellitus on the systemic hemodynamic parameters was studied in conscious rats by thermodilution technique. Male Wistar rats were made diabetic with a single intravenous injection of streptozotocin (STZ, 50 mg/kg). The most important finding of this work was the elucidation of the systemic vasodilation and increased cardiac index one day after STZ injection. Such alteration in hemodynamic parameters could result in the increased blood flow and capillary hypertension in some vascular beds and, therefore, be considered as a pathogenic factor in the development of diabetic microangiopathy.
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PMID:[Parameters of systemic hemodynamics in conscious rats with acute streptozotocin diabetes]. 142 Dec 17

To understand the mechanisms of diabetic cardiomyopathy and the consequences of combined hypertension and diabetes, cardiac tissue responses to various inotropic agents were measured in experimental diabetes. Streptozotocin was injected into Wistar rats, spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKYs). Six weeks after the injection diabetic rats showed a subsensitivity to beta adrenergic stimulation in ventricular tissue and a supersensitivity and hyper-responsiveness to Ca++ and alpha adrenergic stimulation (except in WKYs) in ventricular tissues and left atria. A supersensitivity to BAY K 8644 in SHR left atria and a hyper-responsiveness to verapamil in ventricular strips were also noted. These alterations may be due to a change in receptor number or to postreceptor alterations. Diabetic SHRs exhibited greater changes in several of the drug responses (responses to isoproterenol, phenylephrine and BAK 8644) were more hyperlipidemic and had a high mortality as compared with Wistar rats and WKY diabetics. These findings confirm that the combination of hypertension and diabetes results in greater cardiac pathology than is seen with either disease alone.
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PMID:Altered inotropic responses in diabetic cardiomyopathy and hypertensive-diabetic cardiomyopathy. 170 26

Several lines of evidence suggest that hypertension is a contributing factor to diabetic nephropathy, a major cause of mortality in diabetes mellitus patients. The present study tested the hypotheses (1) that insulin dependent diabetes (IDD) causes hypertension, and (2) that simultaneous hypertension and IDD causes greater renal damage than would be expected from the independent contributions of each disease. IDD was induced by injection of streptozotocin (STZ, 65 mg/kg i.p.) into male Wistar rats, causing severe hyperglycaemia within 4 days. Seven days after the STZ treatment, hypertension was initiated by subcutaneous implantation of deoxycorticosterone acetate and administration of 1% saline in the drinking water (DOCA-NaCl). IDD rats not receiving DOCA-NaCl displayed a small elevation of blood pressure one week after STZ treatment, but thereafter displayed significant hypotension. The IDD rats receiving DOCA-NaCl displayed elevated systolic arterial pressure throughout the study, but by the end of the experiment, their mean systolic arterial pressure was significantly lower than that of the rats treated with DOCA-NaCl alone. Only the IDD/DOCA-NaCl rats displayed significant signs of renal dysfunction, i.e. greatly increased proteinuria and morphological renal damage, including marked distension of distal tubules and occasional casts. No other group displayed these abnormalities.
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PMID:Effects of simultaneous diabetes and hypertension in an insulin dependent diabetic model. 176 11

Streptozotocin (STZ) treatment on neonatal rats produces a non-insulin-dependent diabetes mellitus (NIDDM) model in adulthood. Applying this model to spontaneously hypertensive rats (SHR), we designed the present study to develop a new model of NIDDM with genetic hypertension. Two-day-old male and female SHR were intraperitoneally injected with 25.0-75.0mg/kg STZ, and two-day-old Wistar Kyoto rats (WKY) of both sexes, which are a normotensive control strain for SHR, were similarly injected with 75.0-150.0mg/kg STZ. Control rats received vehicle alone. The relationships between the doses of the STZ injected and the changes of the metabolic variable and blood pressure were examined for 12 weeks following the treatment. Plasma glucose levels in male SHR increased in a dose-dependent manner at 12 weeks, control 122 +/- 8 (SEM) mg/dl, 25.0mg/kg STZ 139 +/- 13mg/dl (ns), 37.5mg/kg STZ 240 +/- 51mg/dl (ns), 50.0mg/kg STZ 359 +/- 39mg/dl (p less than 0.01), 62.5mg/kg STZ 419 +/- 33mg/dl (p less than 0.001) and 75.0mg/kg STZ 513 +/- 10mg/dl (p less than 0.001), whereas in male WKY, only mild hyperglycemia developed in case of the higher doses of STZ given, control 112 +/- 4mg/dl, 75.0mg/kg STZ 136 +/- 18mg/dl (ns), 100.0mg/kg STZ 204 +/- 40mg/dl (ns), 125.0mg/kg STZ 219 +/- 37mg/dl (p less than 0.05), and 150.0mg/kg STZ 177 +/- 12mg/dl (p less than 0.01). The development of hypertension was not affected by the neonatal STZ treatment in male SHR at 11 weeks, systolic blood pressure being control 210 +/- 7mmHg, 25.0mg/kg STZ 217 +/- 5mmHg (ns), 37.5mg/kg STZ 202 +/- 3mmHg (ns), 50.0mg/kg STZ 216 +/- 6mmHg (ns), 62.5mg/kg STZ 210 +/- 6mmHg (ns), and 75.0mg/kg STZ 209 +/- 5mmHg (ns). For the long-term observation, STZ-treated male SHR were divided into mild diabetes group (plasma glucose at 12 weeks less than 300mg/dl, mean 195 +/- 21mg/dl) and severe diabetes group (greater than or equal to 300mg/dl, mean 445 +/- 18mg/dl). Hyperglycemia in both groups was maintained until 28 weeks, plasma glucose being control 112 +/- 4mg/dl, mild diabetes group 161 +/- 10mg/dl (p less than 0.01), and severe diabetes group 419 +/- 25mg/dl (p less than 0.001) but it later gradually ameliorated, plasma glucose at 52 weeks being control 120 +/- 3mg/dl, mild diabetes group 131 +/- 7mg/dl (ns), and severe diabetes group 220 +/- 43mg/dl (ns). However, hypertension persisted in both diabetes groups until 52 weeks, systolic blood pressure being control 209 +/- 6mmHg, mild diabetes group 199 +/- 9mmHg (ns), and severe diabetes group 221 +/- 6mmHg (ns).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A new animal model of non-insulin-dependent diabetes mellitus with hypertension: neonatal streptozotocin treatment in spontaneously hypertensive rats. 183 97

The influences of hypertension and hypothyroidism on diabetic cardiomyopathy are not clear. We studied this problem further by characterizing the effects of chronic triiodothyronine (T3) treatment on cardiac performance of diabetic renovascular hypertensive (RVH) rats. Hypertension was effected by clipping the left renal artery of Wistar-Kyoto (WKY) rats, and diabetes was induced 2 weeks later by streptozotocin (STZ; 55 mg/kg i.v.). The WKY strain was selected because it is relatively resistant to the cardiodepressant effects of diabetes, so that the influence of superimposed hypertension would be more apparent. Performance of working Krebs-Henseleit buffer perfused hearts was quantified by measuring left ventricular pressure and flow characteristics. The results showed that renovascular clipping caused a marked hypertension and left ventricular hypertrophy (LVH) but had no effect on perfused heart performance after 10 weeks. They also showed that diabetes during the final 8 weeks (i) caused a marked impairment in the performance of perfused hearts ex vivo of hypertensive rats but had no measurable effect in the normotensive WKY, (ii) had no effect on arterial pressure of either the normotensive or the hypertensive rats but reduced heart rate of hypertensive animals in vivo, and (iii) caused equivalent hyperglycemia, hypoinsulinemia, and hypothyroidism (depressed serum T3 and T4 levels) of hypertensive and normotensive rats. Treatment of diabetic RVH rats with T3 (10 micrograms.kg-1.day-1) in vivo was nearly as effective as insulin therapy (10 U.kg-1.day-1) in preventing the cardiac dysfunction ex vivo and was as effective as insulin therapy in preventing the bradycardia in vivo and the decline loss.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac function of the diabetic renovascular hypertensive rat: effects of insulin and thyroid hormone treatment. 205

Streptozotocin (STZ)-induced diabetes depresses the rate of vascular collagen synthesis in the spontaneously hypertensive rat (SHR), but it also reduces arterial pressure (SAP) in this strain. We investigated this phenomenon further by comparing the SHR with the renovascular hypertensive (RVH) rat, because diabetes does not affect SAP in the latter model of hypertension. Renovascular hypertension was induced by clipping the left renal artery of Wistar-Kyoto (WKY) rats; sham-operated WKY were included as normotensive controls. Collagen synthesis of arterial tissue in vitro was quantified as prolyl hydroxylase activity and the rate of radioactive proline incorporation into collagen. Arterial collagen synthesis of nondiabetic SHR and RVH animals was elevated compared to that of the nonhypertensive WKY controls. STZ-induced diabetes (8 weeks) reduced SAP of SHR, but had no effect on SAP of either RVH or normotensive WKY rats. However, diabetes significantly depressed vascular collagen synthesis of both SHR and RVH rats, and, less consistently, of the WKY. The results strongly suggest that STZ-induced diabetes in SHR impairs arterial collagen synthesis independent of associated changes in arterial pressure.
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PMID:STZ-induced diabetes in SHR and renovascular hypertensive rats: dissociation between changes in arterial pressure and vascular collagen synthesis. 224 11

This study has evaluated the effects of the angiotensin converting enzyme inhibitor Enalapril on glomerular ultrastructure and albuminuria in normotensive and hypertensive diabetic rats. Streptozotocin-diabetes was induced in Wistar Kyoto and spontaneously hypertensive rats. Enalapril was administered in drinking water in diabetic normotensive, control hypertensive and diabetic hypertensive rats. Enalapril therapy prevented an increase in glomerular basement membrane thickness in diabetic normotensive, control hypertensive and diabetic hypertensive rats without any significant effect on fractional mesangial volume. Enalapril decreased albuminuria in diabetic normotensive, control hypertensive and diabetic hypertensive rats. Thus, enalapril retards the development of glomerular basement membrane thickening and albuminuria in the rat, in the presence or absence of hypertension.
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PMID:Enalapril retards glomerular basement membrane thickening and albuminuria in the diabetic rat. 255 9

To evaluate whether hypertension is a cause or just an association with diabetic renal disease, diabetes was induced in both normotensive Wistar-Kyoto and spontaneously hypertensive rats (WKY and SHR). Animals were assessed monthly for 8 months before sacrifice. When compared to normotensive diabetic rats (WKY-STZ), hypertensive diabetic rats (SHR-STZ) had an earlier and more rapid rise in urinary albumin excretion. In addition, SHR-STZ had increased glomerular basement membrane thickness when compared to WKY-STZ or SHR. In a separate experiment, Enalapril therapy (35 mg/L) was administered in drinking water to WKY-STZ and SHR-STZ. Enalapril significantly reduced blood pressure in both animal groups, and this was associated with a decrease in urinary albumin excretion. The SHR-STZ model has accelerated nephropathy as determined by both functional and structural parameters. Angiotensin-converting enzyme inhibition is associated with a reduction in albuminuria in both hypertensive and normotensive models of diabetic nephropathy.
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PMID:Genetic hypertension accelerates nephropathy in the streptozotocin diabetic rat. 283 66

Streptozotocin-diabetic rats kept moderately hyperglycaemic by daily injections of ultralente insulin for 4-6 weeks (group DM) demonstrated a higher glomerular transcapillary hydraulic pressure gradient (delta P), glomerular plasma flow rate and single-nephron glomerular filtration rate (GFR) than was observed in age- and weight-matched non-diabetic controls (group C). This rise in delta P was prevented by therapy with the angiotensin I converting enzyme inhibitor enalapril (15 mg/l drinking water, group DM + E) even though glomerular hyperperfusion and hyperfiltration persisted. Fourteen months after induction of diabetes, animals in group DM displayed high levels of albuminuria and an increased incidence of focal glomerular sclerosis; treatment with enalapril maintained these parameters at levels which did not differ from those observed in group C. We conclude that prevention of glomerular capillary hypertension with enalapril therapy obviates functional and structural glomerular injury in experimental diabetes mellitus.
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PMID:Prevention of glomerular capillary hypertension in experimental diabetes mellitus obviates functional and structural glomerular injury. 303 78


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