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

This study investigated hemodynamic changes in diabetic rats and their relationship to changes in vascular albumin permeation and increased metabolism of glucose to sorbitol. The effects of 6 wk of streptozocin-induced diabetes and three structurally different inhibitors of aldose reductase were examined on 1) regional blood flow (assessed with 15-microns 85Sr-labeled microspheres) and vascular permeation by 125I-labeled bovine serum albumin (BSA) and 2) glomerular filtration rate (assessed by plasma clearance of 57Co-labeled EDTA) and urinary albumin excretion (determined by radial immunodiffusion assay). In diabetic rats, blood flow was significantly increased in ocular tissues (anterior uvea, posterior uvea, retina, and optic nerve), sciatic nerve, kidney, new granulation tissue, cecum, and brain. 125I-BSA permeation was increased in all of these tissues except brain. Glomerular filtration rate and 24-h urinary albumin excretion were increased 2- and 29-fold, respectively, in diabetic rats. All three aldose reductase inhibitors completely prevented or markedly reduced these hemodynamic and vascular filtration changes and increases in tissue sorbitol levels in the anterior uvea, posterior uvea, retina, sciatic nerve, and granulation tissue. These observations indicate that early diabetes-induced hemodynamic changes and increased vascular albumin permeation and urinary albumin excretion are aldose reductase-linked phenomena. Discordant effects of aldose reductase inhibitors on blood flow and vascular albumin permeation in some tissues suggest that increased vascular albumin permeation is not entirely attributable to hemodynamic changes. We hypothesize that 1) increases in blood flow may reflect impaired contractile function of smooth muscle cells in resistance arterioles and 2) increases in vascular 125I-BSA permeation and urinary albumin excretion reflect impaired vascular barrier functional integrity in addition to increased hydraulic conductance secondary to microvascular hypertension associated with decreased vascular resistance.
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PMID:Prevention of hemodynamic and vascular albumin filtration changes in diabetic rats by aldose reductase inhibitors. 250 78

Chronic lead exposure resulting in blood lead concentrations that exceed 1.93 mumol/l (40 micrograms/dl) or chelatable urinary lead excretion greater than 3.14 mumol (650 micrograms) per 72 h has been associated with renal disease. A previous study had found greater chelatable urine lead excretion in subjects with hypertension and renal failure than in controls with renal failure due to other causes, although mean blood lead concentrations averaged 0.92 mumol/l (19 micrograms/dl). To determine if chelatable urinary lead, blood lead, or the hematologic effect of lead (zinc protoporphyrin) were greater in hypertensive nephropathy (when hypertension precedes elevation of serum creatinine) than in other forms of mild renal failure, we compared 40 study subjects with hypertensive nephropathy to 24 controls having a similar degree of renal dysfunction due to causes other than hypertension. Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l). We conclude that subjects from a general population with hypertensive nephropathy do not have greater body burdens of lead than renal failure controls.
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PMID:Body burdens of lead in hypertensive nephropathy. 251 Jun 13

Renal perfusion has been shown to be preserved or improved during treatment by tertatolol in patients with arterial hypertension. The aims of the present study were (1) to document the central and renal hemodynamic effects of tertatolol in normal subjects and (2) to look for a possible interaction between tertatolol and products of the cyclooxygenase pathway of arachidonic acid metabolism. Five mg of tertatolol, 1 g aspirin, 5 mg tertatolol together with 1 g aspirin, and placebo were administered to 8 healthy volunteers at 1 week intervals in a random order and in a double-blind fashion. Cardiac output was measured by cardiac Doppler echography and renal blood flow and glomerular filtration rate by constant infusion techniques using I123-iodohippurate and Cr51-EDTA respectively. Measurements were performed before and then successively 2 and 4 h after oral intake of drugs or placebo. Tertatolol alone or with aspirin significantly decreased heart rate and cardiac output (P less than .05) without change in blood pressure, renal blood flow or glomerular filtration rate. The renal fraction of cardiac output was increased by tertatolol alone or with aspirin (P less than .05). Either placebo or aspirin alone had no effect. Thus tertatolol redistributes cardiac output to the kidneys in normal subjects as previously reported in hypertensive patients. This favorable effect on renal hemodynamics appers unlikely to be mediated by a local release of vasodilating prostaglandins.
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PMID:Redistribution of cardiac output to the kidneys by tertatolol does not involve prostaglandins. 257 71

Fifty-seven patients with chronic renal failure (CRF) of diverse etiology entered a prospective, randomized study to evaluate the effect of a low protein diet on the progression rate of CRF. All patients were followed for a control period of 12 or 24 months before randomization into two groups, one permitted unrestricted protein intake and the other prescribed a diet containing 0.4 g/kg body wt/day of protein and 0.1 g/kg body wt/day of essential amino acids, (LPD + EAA). During both the control and study periods, patients were clinically evaluated and had serum biochemistry and 24-hour clearance of creatinine, urea and protein excretion checked monthly. The 51Cr-EDTA clearance (plasma slope and urinary clearance) was determined every third month. The progression of renal failure was evaluated from the regressions of the reciprocal of serum creatinine (SCr-1), creatinine clearance and urinary 51Cr-EDTA clearance against time. Having defined criteria for progression, only patients in whom renal failure had progressed over 12 or 24 months were randomized. In 28 patients, data were available, permitting a comparison of the progression of renal failure (estimated from regression of SCr-1 and of creatinine clearance against time) during the retrospective and prospective periods. There was a significant correlation between the change in progression rate and the change in mean arterial pressure, a relationship which was also present in patients with mild hypertension or those with blood pressure within the "normal" range. The urinary protein excretion also correlated with the change in mean arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stockholm clinical study on progression of chronic renal failure--an interim report. 263 44

Hypertension may eventually develop in response to chronic slight retention of sodium and expansion of the extracellular fluid volume, either due to intrinsic pathology or to neurohormonal influences of the kidneys. As almost half of all juvenile diabetic patients sooner or later will develop diabetic nephropathy and hypertension, data are discussed which tend to indicate that renal sodium metabolism is altered already early during the course of diabetes. Compared to healthy subjects the absolute total tubular sodium reabsorption is increased by approximately 30-40 per cent, as is the filtered sodium load. Insulin may stimulate sodium reabsorption in man through an effect on the distal nephron segment. However, by means of combined lithium and 51Cr-labelled EDTA clearances it has been clearly demonstrated that the excess sodium reabsorption in ambulatory insulin-dependent diabetics exclusively takes place in the proximal tubules, while the distal tubular function appears normal. In these studied patients the extracellular fluid volume was also significantly increased. The increased fractional sodium reabsorption of the proximal tubules remains unaffected by increasing duration of diabetes and is also demonstrable in patients with overt diabetic nephropathy. Glucose is reabsorbed in the early portion of the proximal tubules coupled to Na+ transport, utilizing a common carrier protein. An increased load of glucose will therefore be expected to induce an increase in the proximal tubular reabsorption rate of sodium and water, at least as long as the proximal tubular reabsorption capacity for glucose is not exceeded to a degree inducing significant osmotic diuresis. This deviation from normal in proximal renal sodium and fluid handling may be relevant to the development of hypertension in long-term insulin-dependent diabetes.
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PMID:Renal sodium metabolism in relation to hypertension in diabetes. 269 46

Treatment with an angiotensin converting enzyme (ACE) inhibitor in renovascular hypertension produces acute effects on renal function; however, the long-term consequences of this are not known. We have studied the effect of chronic enalapril treatment on renal structure and function in the two-kidney, one clip model of renovascular hypertension in the rat. Four weeks after the left renal artery was clipped, the hypertensive rats were randomly allocated to treatment with enalapril, minoxidil or to no treatment. The drug dose was titrated for maximal hypotensive effect. After 4 months of treatment blood pressures were 129 +/- 3 mmHg (enalapril), 193 +/- 5 mmHg (minoxidil) and 220 +/- 4.8 mmHg (no treatment). Twelve months later survival was 84% (enalapril group), 48% (minoxidil group) and 15% (untreated group). Split kidney function (51Cr-EDTA clearance, ml/min) of the clipped kidneys was 0.0 (enalapril group), 0.26 +/- 0.23 (minoxidil group) and 0.74 +/- 0.13 (untreated group). The clipped kidney from enalapril-treated rats weighed 0.46 +/- 0.1 g, much less than in the minoxidil-treated group (1.2 +/- 0.07) or the untreated group (1.14 +/- 0.10). Enalapril treatment was withdrawn for 2 weeks in five rats, but the clipped kidney remained small and non-functional. Histological examination revealed marked interstitial fibrosis and tubular atrophy in clipped kidneys from both enalapril groups, in contrast to minor changes in the minoxidil-treated and the untreated groups. We conclude that chronic enalapril treatment of two-kidney, one clip hypertension in the rat improved survival and preserved total renal function, but was associated with irreversible fibrotic atrophy of the clipped kidney.
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PMID:Chronic angiotensin converting enzyme inhibition in the two-kidney, one clip hypertensive rat. 285 50

1. Twenty-four patients with primary hyperparathyroidism were studied before and 18 restudied 6.5 months (mean) after parathyroidectomy, to investigate the pathogenesis of the hypertension which may accompany this condition. Comparison was made with age-matched patients with essential hypertension and with normotensive control subjects. 2. There was a significant inverse relationship between mean arterial pressure and 51Cr-labelled ethylene-diaminetetra-acetate (51Cr-EDTA) clearance in patients with hyperparathyroidism both before and after parathyroidectomy, but not in patients with essential hypertension. 3. Creatinine clearance appeared to overestimate glomerular filtration rate in some patients with hyperparathyroidism, falling significantly after surgery while 51Cr-EDTA clearance was unchanged. This observation may explain the failure of some previous studies to relate hypertension to impairment of renal function. 4. Plasma renin activity, plasma aldosterone and whole-body exchangeable sodium did not differ between normotensive and hypertensive patients with primary hyperparathyroidism and were unchanged after surgery. 5. Parathyroidectomy did not result in any change in blood pressure or in glomerular filtration rate measured by 51Cr-EDTA clearance.
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PMID:Hypertension and renal dysfunction in primary hyperparathyroidism: effect of parathyroidectomy. 292 21

Male spontaneously hypertensive rats (SHR) and age matched Wistar Kyoto normotensive (WKY) rats of 5 weeks, 16 weeks, and 52 weeks of age were used to determine whether duration of hypertension has any effect on contractile protein ATPase and myosin isoenzyme distribution. Myofibrils, actomyosin, and myosin were isolated from the left ventricles of WKY rats and SHR and assayed for myosin ATPase activity and myosin isoenzyme distribution. Myofibrillar ATPase activity was assayed at various free [Ca++] ranging from 10(-7) to 10(-5) mol X litre-1. Ca++ stimulated actomyosin ATPase activity was determined at several Ca++ concentrations both at low ionic strength, which favours actin-myosin interaction, and at high ionic strength, which diminishes actin interaction with myosin. Purified myosin ATPase activity was assayed in the presence of K+-EDTA and in the presence of several concentrations of Ca++. Actin activated myosin ATPase activity was assayed using 26 mumol X litre-1 skeletal muscle actin. Under all these assay conditions no differences were observed in the contractile protein ATPase activity between SHR and WKY rats in any age group. On the other hand, in both SHR and WKY rats the contractile protein ATPase activity under all assay conditions was significantly decreased in 52 week old rats compared with 5 week old rats. The predominant myosin isoenzyme was Vi in 5 week and 16 week old WKY rats and SHR. In 52 week old WKY rats and SHR, however, significant amounts of isoenzymes V2 and V3 were present along with V1. Percentage distribution of V1, V2, V3 isoenzymes calculated from densitometric scans of gels did not show any differences between WKY rats and SHR in any age group. These results suggest that neither myosin ATPase activity nor myosin isoenzyme distribution is altered in the moderately hypertrophied left ventricles of SHR. Moreover, the data indicate that the myocardium of SHR, despite the persistence of pressure overload, undergoes a similar decrease in myosin ATPase activity and an increase in myosin isoenzyme V3 to age matched normotensive WKY rats.
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PMID:Age dependent changes in myosin ATPase activity in the myocardium of spontaneously hypertensive rats. 293 54

We investigated whether the glomerular synthesis of prostaglandins modulates the glomerular filtration rate and urinary albumin excretion in incipient diabetic nephropathy (defined as urinary albumin excretion between 30 and 300 mg/24 h (microalbuminuria) in two out of three sterile ketone-free 24-h urine collections in patients having insulin-dependent diabetes mellitus (IDDM) without hypertension or other kidney disease). The urinary excretion of prostaglandin E2 was significantly elevated in 8 insulin-dependent diabetic patients with incipient nephropathy as compared with 9 normoalbuminuric IDDM patients and 11 healthy controls: 317 (182-1273); 95 (67-225); 132 (54-263) pg/min, respectively (2p less than 0.01). Glomerular filtration rate (single bolus 51Cr-EDTA technique) and albuminuria (radioimmunoassay) were measured twice within 2 weeks in 8 females having IDDM with incipient nephropathy. The study design was a randomized double-blind trial with the patients receiving either indomethacin (150 mg/day) or placebo for 3 days prior to the kidney function studies. Indomethacin treatment induced a significant reduction in urinary prostaglandin E2 excretion (73%) (2p less than 0.01), urinary albumin excretion rate diminished from 207 (63-253) to 87 (49-147) mg/24 h (2p less than 0.01), fractional clearance of albumin declined (70%) (2p less than 0.01). Glomerular filtration rate remained stable (108 (88-133) versus 110 (95-142) ml/min). Blood glucose and blood pressure were comparable during the placebo and indomethacin treatment (12.6 +/- 3 versus 13.4 +/- 5 mmol/l and 122/79 +/- 3/9 versus 122/82 +/- 4/10 mmHg, respectively). Our results suggest that enhanced glomerular synthesis of vasodilating prostaglandins may accelerate microalbuminuria in incipient diabetic nephropathy.
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PMID:Elevated urinary prostaglandin excretion and the effect of indomethacin on renal function in incipient diabetic nephropathy. 296 80

A noninvasive single injection technique for the measurement of glomerular filtration rate (GFR) using technetium99m diethylene triamine pentaacetic acid (DTPA) was developed for use in the rat. GFR measurements obtained by the technique correlated well with those obtained by Cr51 EDTA infusion (R = 0.95, n = 7). The coefficient of variation was 8.4%. GFR was measured over 4 weeks in diabetic and control rats. GFR increased with time in both groups, with no difference between the groups; however, when corrected for body weight, diabetes was associated with an increased GFR (diabetic 13.6 +/- 1.7 vs. control 10.4 +/- 0.1 ml/min/kg p less than 0.001). Insulin treated rats had higher GFRs than untreated diabetics (p less than 0.05), but GFR/kg was reduced to that of nondiabetic controls. High protein intake in diabetic rats caused an increase in GFR after 1 week of diabetes, but this was not sustained by the fourth week. Genetic hypertension and angiotensin converting enzyme (ACE) inhibition with ramipril had no effect on GFR in diabetic rats. We conclude that serial measurement of GFR in the diabetic rat is accurate and reproducible. Genetic hypertension, high protein intake, and ACE inhibition have little effect on GFR in experimental diabetes.
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PMID:Glomerular filtration rate in early experimental diabetes. 296 59


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