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Biomedical subjects

H A Struijker Boudier

Publications and source records attributed to H A Struijker Boudier.

At least 19 recordsLinked to original sources
PubMed2004

[Recently published European and American guidelines for the diagnosis and treatment of hypertension].

The European Society of Hypertension in conjunction with the European Society of Cardiology has published new guidelines on the management of hypertension. At about the same time, the Joint National Committee in the United States updated the American hypertension guidelines. Both guidelines agree on a number of issues, such as the importance of systolic blood pressure, the necessity to take into account additional risk factors and the growing emphasis on combination treatment. As far as pharmacotherapy is concerned, however, there are major differences between the guidelines. Whereas the European report permits a choice from among several classes of drugs for initial treatment, the American guidelines still consider diuretics to be the first choice.

Antihypertensive Agents↗
PubMed2001

Anginex, a designed peptide that inhibits angiogenesis.

Novel beta-sheet-forming peptide 33-mers, betapep peptides, have been designed by using a combination approach employing basic folding principles and incorporating short sequences from the beta-sheet domains of anti-angiogenic proteins. One of these designed peptides (betapep-25), named anginex, was observed to be potently anti-angiogenic. Anginex specifically inhibits vascular endothelial cell proliferation and induces apoptosis in these cells, as shown by flow-cytometric detection of sub-diploid cells, TUNEL (terminal deoxyribonucleotidyl transferase-mediated dUTP-nick-end labelling) analysis and cell morphology. Anginex also inhibits endothelial cell adhesion to and migration on different extracellular matrix components. Inhibition of angiogenesis in vitro is demonstrated in the sprout-formation assay and in vivo in the chick embryo chorio-allantoic membrane angiogenesis assay. Comparison of active and inactive betapep sequences allows structure-function relationships to be deduced. Five hydrophobic residues and two lysines appear to be crucial to activity. This is the first report of a designed peptide having a well-defined biological function as a novel cytokine, which may be an effective anti-angiogenic agent for therapeutic use against various pathological disorders, such as neoplasia, rheumatoid arthritis, diabetic retinopathy and restenosis.

Amino Acid Sequence↗
PubMed2001

Non-invasive assessment of local arterial pulse pressure: comparison of applanation tonometry and echo-tracking.

OBJECTIVES: Pulse pressure is not constant throughout the arterial tree. Use of pulse pressure at one arterial site as surrogate for pulse pressure at another arterial site may be erroneous. The present study compares three non-invasive techniques to measure local pulse pressure: (i) internally calibrated readings from applanation tonometry, (ii) alternative calibration of pressure waves obtained with applanation tonometry and (iii) alternative calibration of arterial distension waves obtained with echo-tracking. Alternative calibration assumes mean and diastolic blood pressure constant throughout the large artery tree. DESIGN AND METHODS: Study 1 used invasive measurements in the ascending aorta as a reference method and internally calibrated tonometer readings and alternatively calibrated pressure waves at the common carotid artery as test methods. Study 2 used alternatively calibrated pressure waves as a reference method and alternatively calibrated distension waves and internally calibrated applanation tonometer readings as test methods. RESULTS: In study 1, pulse pressure from internally calibrated tonometer readings was 10.2+/-14.3 mmHg lower and pulse pressure from alternatively calibrated pressure waves was 1.8+/-5.2 mmHg higher than invasive pulse pressure. Pulse pressure from calibrated distension waves was 3.4+/-6.9 mmHg lower than pulse pressure from alternatively calibrated pressure waves. According to British Hypertension Society criteria, pulse pressure from the internally calibrated tonometer achieved grade D and pulse pressure from alternatively calibrated pressure waves achieved grade A. Pulse pressure from calibrated distension waves achieved grade B when alternatively calibrated pressure waves were used as a reference method. CONCLUSIONS: Pulse pressure obtained from alternatively calibrated tonometer-derived pressure waves and echo-tracking-derived distension waves demonstrates good accuracy. Accuracy of pulse pressure from internally calibrated applanation tonometer readings at the carotid artery is poor.

Adult↗
PubMed1999

Is it possible to develop drugs that act more selectively on large arteries?

BACKGROUND: Patients with high pulse pressures have an increased risk for cardiovascular events. Drugs that selectively decrease high pulse pressure may be of interest for these patients. Such drugs have a more pronounced effect on large arteries than on resistance vessels. OBJECTIVE: To compare the selectivity to large arteries of the new nitric oxide donor sinitrodil with the classic nitrate isosorbide dinitrate in healthy young men in order to investigate whether it is possible to develop drugs that act more selectively on large arteries. DESIGN: The study had a double-blind, 5-way cross-over design. In randomized order, subjects received a single oral dose of 10 mg sinitrodil, 20 mg sinitrodil, 40 mg sinitrodil, isosorbide dinitrate and placebo. Measurements were performed before and 45 min after administration of the drugs. Between each drug administration, at least 3 days of wash-out was allowed. METHODS: The effects of the drugs on large arteries and resistance vessels were assessed by their effects on brachial artery compliance and total peripheral resistance, respectively. RESULTS: Brachial artery compliance increased gradually with increasing doses of sinitrodil (by 10, 20 and 27% with 10, 20 and 40 mg sinitrodil, respectively). Total peripheral resistance index decreased with isosorbide dinitrate (by 11%) and 40 mg sinitrodil (by 7%), while it remained unchanged with 10 mg and 20 mg sinitrodil. CONCLUSIONS: The results of this study show that it may be possible to develop drugs with a higher selectivity for large arteries. Such drugs may be good candidates to decrease high pulse pressure without substantially decreasing mean and diastolic blood pressures.

Adult↗
PubMed1999

Mechanical properties of mesenteric arteries in diabetic rats: consequences of outward remodeling.

Diabetes induces hemodynamic and biochemical changes that can influence mechanical properties of arteries. Structure and mechanics of mesenteric small arteries were investigated in rats with streptozotocin-induced diabetes (duration 7-9 wk). The external diameter of mesenteric artery branches was measured in control (n = 9) and diabetic (n = 7) Wistar Rp rats at baseline and during pressurization in situ (0-150 mmHg) under normal and passive smooth muscle conditions. Mean arterial pressure and mesenteric artery pressure were not significantly different. Baseline mesenteric artery diameter was larger in the diabetes-induced group (439 +/- 12 vs. 388 +/- 18 micrometers, P < 0.05). Media cross-sectional area of arteries from diabetic rats was not significantly increased (0.0149 +/- 0.0015 vs. 0.0122 +/- 0.0007 mm2). Cross-sectional compliance was significantly increased in diabetic rats at intraluminal pressures ranging from 25 to 75 mmHg (P < 0.005), whereas cross-sectional distensibility was not modified. Wall tension and circumferential wall stress were increased in diabetes. These results indicate that mesenteric small arteries of diabetic rats display eutrophic outward remodeling associated with increased wall tension and circumferential wall stress.

Animals↗
PubMed1999

Arteriolar and capillary remodelling in hypertension.

The major haemodynamic abnormality underlying elevated blood pressure in hypertension is an increase in vascular resistance. The microcirculation is a key site of increased vascular resistance in hypertension. A reduced density of arterioles and capillaries is an important common characteristic of various microvascular beds in many forms of hypertension. This microvascular rarefaction has been observed even in very early stages of the development of hypertension. A hypothesis is discussed for early microvascular rarefaction being the result of genetic and fetal mechanisms of decreased small blood vessel growth.

Arteries↗
PubMed1998

Angiogenesis and hypertension.

BACKGROUND: The formation of new blood vessels is an important process in embryonic development and in physiological repair processes. Abnormalities in blood vessel growth have been associated with various pathologies. HYPERTENSION AND IMPAIRED VASCULAR GROWTH: The basic observation underlying the hypothesis that essential hypertension is based on an impaired capacity for vascular growth is the nature of the structural alterations of microvascular beds in essential hypertension. Recent advances in understanding the molecular and cellular mechanisms of vascular growth suggest that the remodeling of individual vessels and vascular networks in hypertension may be a pathological variant of the formation of mature networks. PATHOGENESIS OF IMPAIRED VASCULAR GROWTH: Genetic and fetal influences appear to have significant effects in determining impaired vascular development as an early cause of essential hypertension.

Animals↗
PubMed1998

Arteriolar reactivity in conscious diabetic rats: influence of aminoguanidine treatment.

The effect of 6 weeks' streptozotocin (STZ)-induced (70 mg/kg) diabetes and aminoguanidine (AG) treatment (50 mg/kg s.c. or 250-750 mg/l given in drinking water) on arteriolar reactivity to vasoactive substances was investigated in conscious rats. Studies were performed in untreated control rats (n = 13), STZ-induced diabetic rats (n = 11), AG-treated control rats (n = 12), and AG-treated diabetic rats (n = 12). Rats were provided with a dorsal microcirculatory chamber that allowed intravital microscopy of striated muscle arterioles of varying diameter (A1, large; A2, intermediate; and A3, small arterioles) in conscious animals. The mean arterial pressure (MAP) and arteriolar diameter responses to intravenous infusion of the following drugs were examined: the endothelium-dependent vasodilator acetylcholine (ACh; 3, 10, and 30 microg x kg(-1) x min(-1)), the potassium-channel opener levcromakalim (LC; 30 microg/kg), and the vasoconstrictor agents ANG II (0.1 and 0.3 microg x kg(-1) x min(-1)) and norepinephrine (NE; 0.2, 0.6, and 2.0 microg x kg(-1) x min(-1)). Baseline MAP was lower in both diabetic groups versus the nondiabetic groups (P < 0.05). AG treatment had no influence on baseline MAP. The absolute change in MAP after drug infusion tended to be lower in the diabetic rats than in their nondiabetic littermates. Arteriolar vasodilatory responses to ACh and LC were attenuated in the diabetic animals (1 +/- 7 vs. 19 +/- 7% [P < 0.05] and 7 +/- 3 vs. 34 +/- 8% [P < 0.01] in A2, respectively). AG treatment of diabetic animals did not prevent the development of this disturbance. Vasoconstrictor responses were not influenced by the diabetic state. In the intermediate arterioles of AG-treated control rats, a hyperresponse was observed after ANG II infusion (-10 +/- 2 vs. -2 +/- 2%; P < 0.05) and a hyporesponse was observed after ACh and LC infusion (2 +/- 3 and 15 +/- 6%, respectively; P < 0.05 vs. untreated control rats). These data indicate that 6 weeks of experimental diabetes is associated with a decreased endothelium-dependent and -independent vasodilatation. AG treatment had no beneficial effect on this disturbance.

Acetylcholine↗
PubMed1997

Ouabain improves cardiac function in vivo in rats with heart failure after chronic but not acute treatment.

Rats are generally believed to be insensitive for cardiac glycosides. However, like in humans, the hemodynamic effects may be related to the pathophysiological condition. Since the hemodynamic effects of cardiac glycosides have never been investigated in rats with heart failure, the aim of the present experiments was to investigate the role of the pathophysiological condition in the rat. Therefore, hemodynamic and cardiac effects of ouabain were investigated both in normal rats and rats with heart failure due to myocardial infarction (MI). Since the effects of ouabain may also depend on the treatment scheme, rats were treated either for a short-term period or a long-term period. Three weeks after sham surgery or ligation of the left coronary artery (MI), Wistar rats were treated for two weeks with ouabain (14.4 mg/kg.d s.c.), either continuously (osmotic minipumps) or intermittently (once daily). A separate group of rats was treated for 45-60 min (1-100 microg/kg.min ouabain; i.v. infusion 5 weeks after MI). Hemodynamic measurements were performed at rest and after volume loading in conscious rats, chronically instrumented with an electromagnetic flow probe and catheters. Induction of MI resulted in a significant increase in total peripheral resistance (TPR), and a significant decrease in basal and maximal cardiac output following volume loading (basal CO: sham, 92 +/- 5; MI, 74 +/- 5 ml/min; maximal CO: sham, 152 +/- 4; MI, 105 +/- 7 ml/min; n = 7-11). Chronic intermittent ouabain treatment further increased TPR in MI rats. In contrast, continuous ouabain treatment normalized TPR in rats. Only in continuously treated MI rats, basal and maximal CO improved significantly (basal: 83 +/- 4; maximal: 134 +/- 7 ml/min; n = 7). Acute treatment dose-dependently worsened the hemodynamic conditions of MI rats, since TPR and MAP increased and CO and stroke volume decreased significantly. These experiments demonstrate that ouabain can improve cardiac function in rats, although only in MI rats and strongly depending on the delivery regimen. Thus, in contrast to the general belief, the presently used rat model is suitable for investigation of cardiac glycosides in heart failure. The preferential improvement of cardiac function in MI rats continuously treated with ouabain may depend upon changes in Na+,K+-ATPase or altered neurohumoral conditions due to MI and chronic treatment.

Animals↗
PubMed1996

Impaired arterial reactivity following cytomegalovirus infection in the immunosuppressed rat.

1. Cytomegalovirus (CMV) is a major pathogen in immunocompromised individuals and may participate in the pathogenesis of atherosclerosis in the general population. We evaluated whether CMV-infection alters the function of arterial smooth muscle. 2. Blood pressure (BP) and arterial reactivity were recorded in immunosuppressed rats that had been infected with CMV (10(5) plaque forming units i.p.). Furthermore, the reactivity of isolated arteries was compared between CMV-infected rats and rats injected with bacterial endotoxin (LPS). 3. Initially resting BP and heart rate (HR) were not modified in CMV-infected rats, but baroreflex control of HR was impaired. By the eighth day post-CMV, BP dropped precipitously and could no longer be raised by phenylephrine (PHE). 4. In mesenteric resistance arteries, isolated at this stage from CMV-infected rats, contractile responses to nerve stimulation, noradrenaline, PHE and 5-hydroxytryptamine (5-HT) were virtually absent while those to high potassium and vasopressin (AVP) were not modified. In aortae of CMV-infected rats, responses to 5-HT and AVP were impaired while those to PHE or potassium were hardly affected. Reduced contractile responses could not be restored by NG-nitro-L-arginine methyl ester (L-NAME). 5. Continuous treatment of CMV-infected rats with prazosin (0.1 mg kg-1 day-1) prevented blood pressure lowering and resistance artery changes. 6. Observations in arteries of LPS-treated rats (5-10 mg kg-1, i.p.) differed markedly from those in vessels of CMV-infected animals. The contractile reactivity of their mesenteric resistance arteries was not altered while in their aortae, responses to PHE, 5-HT and AVP were reduced. With the exception of the AVP responses, this was more pronounced in the presence of 1-arginine and reversed by L-NAME. 7. These findings indicate that CMV-infection results in a reduction of resistance artery reactivity and hypotonia. This seems not to involve cytokine-mediated induction of NO synthase in the vascular wall but may be due to alterations of excitation-contraction coupling in arterial smooth muscle in response to increased sympathetic nervous input.

Animals↗
PubMed1996

The concept of cardioreparation: Part 1. Pathophysiology of remodelling.

PURPOSE: Left ventricular hypertrophy is common in patients with hypertension or congestive heart failure and in survivors of myocardial infarction. It is associated with increased risks of adverse cardiovascular events, including angina, myocardial infarction and congestive heart failure. We aimed to explain these observations in terms of changes in the structure of the heart, collectively described as remodelling. DATA EXTRACTION: Laboratory investigations of animal models of cardiovascular diseases were reviewed. The most prominent features of remodelling are myocyte hypertrophy, excessive accumulation of collagen in the heart (myocardial fibrosis) and pathological changes in the coronary blood vessels. Remodelling disrupts the structure of the heart and impairs its pumping function and blood supply. The reversal of remodelling, termed cardioreparation, could restore cardiac structure and function towards normal and improve the prognosis of patients with cardiovascular diseases. CONCLUSIONS: Cardioreparation implies the regression of myocyte hypertrophy and myocardial fibrosis. Myocyte hypertrophy is primarily a response to chronic pressure or volume overload of the ventricles, whereas myocardial fibrosis depends on activation of circulating and tissue renin-angiotensin-aldosterone systems. Angiotensin converting enzyme inhibitors reduce blood pressure and inhibit these systems. They might therefore induce cardioreparation.

Cardiovascular Diseases↗
PubMed1996

The concept of cardioreparation: Part 2. Medical implications of cardioreparation.

PURPOSE: Left ventricular hypertrophy (LVH) caused by systemic hypertension, myocardial infarction and congestive heart failure is associated with pathological changes in the structure of the heart, collectively described as remodelling (see part 1 of this review). The reversal of remodelling, termed cardioreparation, might restore cardiac structure and function towards normal, thereby improving the prognosis of these conditions. We aimed to explore the medical implications of this concept. DATA EXTRACTION: Clinical trials of angiotensin converting enzyme (ACE) inhibitors and other drugs in patients with hypertension, myocardial infarction and congestive heart failure were reviewed. The results showed that ACE inhibitors induce regression of LVH in hypertensive patients, reduce mortality in acute myocardial infarction, and reduce morbidity and mortality in patients with congestive heart failure or left ventricular dysfunction subsequent to myocardial infarction. These observations are consistent with cardioreparation by ACE inhibitors. CONCLUSIONS: ACE inhibitors reduce morbidity and mortality in patients with myocardial infarction or congestive heart failure. Theoretical considerations and some clinical observations suggest that these benefits might result from cardioreparation.

Antihypertensive Agents↗
PubMed1995

Aortic wall properties in normotensive and hypertensive rats of various ages in vivo.

The distensibility of the arterial system, which is partly determined by arterial wall structure, smooth muscle tone, and actual pressure level, decreases with aging and hypertension. Our aim was to compare aortic wall properties in 3- and 6-month-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) at comparable blood pressures in vivo. During ketamine/xylazine anesthesia in rats we performed ultrasound arterial wall tracking and invasive pressure measurements to determine, at the level of the thoracic aorta, diastolic pressure, diastolic lumen area, changes in pressure and lumen area during the cardiac cycle, and indexes of compliance and distensibility. These observations were combined with histological measurements for determination of media cross-sectional area and thickness and the incremental elastic modulus under conditions as expected in situ. Anesthesia abolished the difference in diastolic pressure between SHR and WKY. Between 3 and 6 months of age in WKY, diastolic area and incremental elastic modulus increased significantly, distensibility decreased, and all other recorded variables were not modified. Between 3 and 6 months of age in SHR, diastolic area and incremental elastic modulus increased, distensibility of the aortic wall decreased, and all other mechanical and structural properties did not change significantly. At both ages, diastolic area and compliance were significantly smaller in SHR than WKY. The other mechanical and structural properties measured or calculated at comparable pressure did not differ between strains. Differences between the aorta of 3- and 6-month-old rats and between strains observed in vivo at comparable pressures can largely be attributed to differences in lumen caliber.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1995

Effects of antihypertensive agents on local arterial distensibility and compliance.

Distensibility and compliance are important vessel wall properties. Distensibility is related to elastic properties of the arterial wall, and compliance reflects the buffering function of the artery. Distensibility is a determinant of stress on the vessel wall. A decreased distensibility might increase the risk of arterial wall damage. Therefore, a preserved local distensibility might be important in protecting the arterial wall of each particular artery and especially of those arteries that are more susceptible to vascular disease. Local distensibility and compliance of various large arteries can be measured noninvasively with echo tracking techniques. Studies on local distensibility and compliance revealed that with the calcium antagonist verapamil and the angiotensin-converting enzyme inhibitor perindopril arterial compliance increased mainly because of an increase in distensibility, with only a minor effect on arterial diameter. In contrast, the nitrate compound isosorbide dinitrate increased compliance mainly by increasing arterial diameter, without an increase in distensibility. This indicates that an increase in arterial compliance does not automatically imply an increase in arterial distensibility. The effect of antihypertensive drugs may also depend on the vascular territory. The diuretic amiloride/hydrochlorothiazide increased brachial artery compliance but not common carotid artery compliance. During angiotensin-converting enzyme inhibition the effect on arterial compliance was smaller at the carotid than the femoral artery. However, the opposite held for the nitrate compound. These distinctive effects of antihypertensive drugs on arterial distensibility and compliance and on vascular territories may be relevant to pharmacological prevention and management of arterial disease.

Antihypertensive Agents↗
PubMed1995

Vessel wall properties of large arteries in uncomplicated IDDM.

OBJECTIVE: Patients with insulin-dependent diabetes mellitus (IDDM) are at high risk for cardiovascular disease. Arterial distensibility and compliance are vessel wall properties of large arteries. Altered large artery wall properties can be an early feature of vascular dysfunction. This study investigates vessel wall properties in 30 patients with uncomplicated IDDM and 30 matched healthy control subjects. RESEARCH DESIGN AND METHODS: Vessel wall properties of the elastic common carotid (CCA) and the muscular femoral (FA) and brachial arteries (BA) were measured with a vessel wall movement detector system. Blood pressure and heart rate were recorded simultaneously with a semiautomated device. Aortic pulse wave velocity was estimated from the carotido-femoral transit time. RESULTS: Blood pressure (IDDM patients: 118 +/- 10/69 +/- 5 mmHg), pulse pressure (IDDM patients: 49 +/- 8 mmHg), and heart rate (IDDM patients: 65 +/- 9 beats/min) were similar in IDDM patients and control subjects. No statistically significant changes between IDDM patients and control subjects were found for diameter, distensibility, and compliance of the elastic CCA and the muscular BA. Distensibility (IDDM patients: 16.9 +/- 6.4 10(-3)/kPa; control subjects: 22.4 +/- 11.8 10(-3)/kPa) of the muscular FA was decreased in IDDM (P < 0.05). However, FA compliance (IDDM patients: 0.80 +/- 0.23 mm2/kPa; control subjects: 0.94 +/- 0.41 mm2/kPa) and FA diameter (IDDM patients: 7.87 +/- 1.10 mm; control subjects: 7.57 +/- 1.11 mm) did not differ statistically between IDDM patients and control subjects. Aortic pulse wave velocity was the same in IDDM patients and control subjects (IDDM patients: 5.1 +/- 0.6 m/s). No relation was found between vessel wall properties and duration of disease, actual glucose level, and HbA1c for all three arteries (CCA, BA, and FA). But the groups might have been too small to draw conclusions. CONCLUSIONS: The results of the present study show that in this group of patients with uncomplicated IDDM, vessel wall properties of elastic and muscular large arteries were not obviously reduced when compared with healthy control subjects. However, distensibility of the FA was lower in IDDM patients. Early atherosclerotic changes in IDDM frequently occur at this site. A difference related to the duration of diabetes could not be excluded.

Adolescent↗
PubMed1994

Short term effect of withdrawal of diuretic drugs prescribed for ankle oedema.

OBJECTIVE: To determine the effect of withdrawing diuretic drugs on oedema in patients prescribed them for only ankle oedema, excluding patients with cardiac, hepatic, or renal failure. DESIGN: Randomised controlled trial. SETTING: 15 general practices in the Netherlands. PATIENTS: 1202 patients aged 65 years or older and taking diuretic drugs, 63 of whom were eligible for the trial. MAIN OUTCOME MEASURE: Change in volumetrically determined ankle oedema (oedema index) over six weeks. RESULTS: 34 patients were randomised to stop diuretics and 29 to the control group. In eight patients diuretics had to be restarted. Among patients who had diuretics withdrawn successfully, rebound oedema caused a temporary increase in mean oedema index. The peak level (3.5% (95% confidence interval 1.5% to 5.2%) was reached in the third week, after which the oedema seemed to be returning to the baseline level. CONCLUSION: Few patients who have been prescribed diuretics for only ankle oedema clearly have no contraindications to withdrawing diuretics. If patients are unlikely to have cardiac insufficiency and careful monitoring is provided, withdrawal of diuretics seems to be feasible, though moderate rebound oedema may occur for a short time.

Aged↗
PubMed1994

Aminoguanidine reduces regional albumin clearance but not urinary albumin excretion in streptozotocin-diabetic rats.

Advanced glycation end-product-formation is thought to play a role in the development of diabetic angiopathy. By altering the structure of different extracellular matrix components advanced glycation end-products might affect vascular and glomerular permeability. In this study we investigated the effect of treatment with an inhibitor of advanced glycation end-product-formation, aminoguanidine, on vascular permeability and the development of albuminuria in streptozotocin-induced diabetic rats. Male Wistar Rp rats were randomized into a control group, a diabetic group, and an aminoguanidine-treated diabetic group. After 8 weeks, 24-h urine collections were taken and rats were implanted with an arterial and a venous catheter. mean arterial blood pressure was determined by intra-arterial measurement. Regional albumin clearances were assessed in the eye, ileum, lung, skeletal muscle and skin using an isotope technique. Mean arterial pressure in the diabetic group was significantly lower in the control and aminoguanidine-treated groups (p < 0.02). Regional albumin clearances were significantly increased in all tissues of diabetic rats compared to control rats (p < 0.05). Aminoguanidine treatment of diabetic rats resulted in a significant decrease of regional albumin clearance in all tissues except the lung (p < 0.05, lung p = 0.07). The development of albuminuria in diabetic rats however, was not affected by aminoguanidine.

Albuminuria↗