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Biomedical subjects

B Fabris

Publications and source records attributed to B Fabris.

At least 19 recordsLinked to original sources
PubMed2001

Haemoconcentration, shear-stress increase and carotid artery diameter regulation after furosemide administration in older hypertensives.

The aim of the present study was to determine whether changes of carotid wall shear stress induced by changes in blood viscosity after diuretic administration cause carotid arterial dilatation in elderly hypertensives, as reported in the cat. Arterial wall shear rate (ultrasound technique, profilmeter FRP III), the systo-diastolic diameter (echotracking technique) and the mean blood flow velocity and volume of the common carotid artery, the blood viscosity (rotational viscometer) and the finger arterial blood pressure (Finapress Ohmeda) were measured in 12 young volunteers (aged 25+/-2 years) and in 12 elderly hypertensives (aged 80+/-4 years) treated with short-acting calcium antagonists up to 24h before the study, both at baseline and after intravenous furosemide infusion (0.5mg/min), when the haematocrit had increased by at least two percentage points. After furosemide administration the mean arterial blood pressure decreased and blood viscosity and carotid systolic shear stress increased in both groups. However, common carotid artery diameter increased only in the young controls but not in the elderly hypertensives. These data show that an increase in carotid shear stress caused by haemoconcentration induces carotid vasodilatation only in young healthy subjects, and not in elderly hypertensives. This effect may be related to impaired endothelium function and/or arterial wall mechanics.

Adult↗
PubMed2001

Modulation of incipient glomerular lesions in experimental diabetic nephropathy by hypotensive and subhypotensive dosages of an ACE inhibitor.

A glomerular permeability defect occurs early in the course of type 1 diabetes and precedes the onset of microalbuminuria and renal morphological changes. Recently, ACE inhibitors have been shown to prevent loss of glomerular membrane permselective function, but the mechanism of this nephroprotective effect is still being debated. The objective of the present study was to evaluate the effects of hypotensive and subhypotensive dosages of the ACE inhibitor quinapril ex vivo and of its active metabolite quinaprilat in vitro on the glomerular albumin permeability (P(alb)) defect in the early phases of experimental diabetes. For the ex vivo study, six groups of male Wistar rats were evaluated for 4 weeks. One group served as a nondiabetic control (C); the other five groups were rendered diabetic and included untreated diabetic rats (D) and diabetic rats receiving quinapril at the dosages of 5 (DQ1), 2.5 (DQ2), 1.25 (DQ3), and 0.625 (DQ4) mg. kg(-1). day(-1). Dosage-dependent effects of quinapril on systolic blood pressure and the glomerular filtration rate were observed. In contrast, control of P(alb) in isolated glomeruli exposed to oncotic gradients, proteinuria, and glomerular and tubular hypertrophy was obtained with subhypotensive dosages (DQ3 and DQ4 groups) of the ACE inhibitor. In the in vitro study, quinaprilat reduced P(alb) significantly in concentration ranges from 10(-6) to 10(-14) mol/l compared with results in control glomeruli. The effect on P(alb) may have occurred by mechanisms different from kidney ACE inhibitor. These study results indicated that ACE inhibitor treatment prevents the early onset of the P(alb) defect in experimental diabetes. This effect seemed to occur independently of systemic or glomerular hemodynamic changes and, at least partially, from kidney ACE inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Mechanics of the carotid artery wall and baroreflex sensitivity after acute ethanol administration in young healthy volunteers.

The effects of ethanol administered orally (300 mg/kg in 250 ml of water) or intravenously (7.5 mg.min(-1).kg(-1) in 250 ml of saline over 40 min) on common carotid haemodynamics, wall mechanics and baroreflex sensitivity were compared with the effects of the intravenous infusion of 250 ml of saline. Ethanol or saline was administered to 10 healthy volunteers after 30 min of supine rest, and measurements were obtained 40 min (median; range 34-46 min) after administration. After ethanol administration, the plasma alcohol level rose from 0 to 0.3+/-0.07 g/l. Mean arterial blood pressure had risen slightly at 20 min, but was normalized by 40 min, the time at which the haemodynamic study was performed. Heart rate decreased after infusion of either saline or alcohol, but was unchanged after oral ethanol administration. Both oral and intravenous ethanol administration were associated with significant decreases in baroreflex sensitivity, carotid shear stress and blood velocity, compared with resting values, while the mean carotid artery diameter was increased, and blood viscosity and mean blood flow were unchanged. No changes were observed in these parameters after saline administration. Ethanol, administered either intravenously or orally, increased the stiffness of the carotid artery and decreased the pulsatility (systo-diastolic changes) of its diameter. A direct, statistically significant correlation was found between the decrease in shear stress and the decrease in baroreflex heart rate control sensitivity after both modes of alcohol administration, while no such correlation was found between the increase in the Peterson elastic modulus and the decrease in carotid diameter pulsatility on the one hand or the decrease in baroreflex sensitivity on the other. In conclusion, reduced shear stress associated with vasodilatation of the carotid artery wall may contribute to the decrease in baroreflex sensitivity observed after acute ethanol administration.

Administration, Oral↗
PubMed2000

Albumin permeability in isolated glomeruli in incipient experimental diabetes mellitus.

AIMS/HYPOTHESIS: The pre-clinical phase of diabetic nephropathy is characterised by increased glomerular filtration rate and episodes of microalbuminuria. The cause of the microalbuminuria has been variably ascribed to alterations of the size or charge selective barriers of the glomerulus or both or as a consequence of the haemodynamic changes. Our aim was to investigate very early albumin permeability alterations in isolated glomeruli which were not subject to perfusion pressure. METHODS: Isolated glomeruli were studied from 120 male Wistar rats, divided into three groups: streptozotocin-treated, streptozotocin-treated with insulin pellet implants, and controls. From each group ten animals were killed at 7, 14, 28, and 56 days after induction. Study variables included blood pressure, proteinuria, iopamidol clearance, albumin permeability and glomerular area. Subsequently, albumin permeability, proteinuria, and iopamidol clearance were determined in an additional group of 40 diabetic animals studied at 24, 72, 96, and 120 h after induction. RESULTS: Albumin permeability increased steadily from induction in streptozotocin-treated animals, reaching a plateau at approximately 120 h. Glomerular filtration rate was shown to increase significantly at approximately 7 days and proteinuria correlated with it. Glomerular hypertrophy was observed both in streptozotocin-treated animals and in streptozotocin-treated rats with insulin pellet implants. Strict blood glucose control delayed the appearance of the permeability defect in isolated glomeruli and inhibited the increase in glomerular filtration in intact animals. It did not prevent glomerular hypertrophy. CONCLUSION/INTERPRETATION: An albumin permeability defect exists early in isolated non-perfused glomeruli from streptozotocin-treated rats and seems to be independent of glomerular filtration rate alterations.

Animals↗
PubMed2000

Effects of prolonged high-altitude exposure on peripheral adrenergic receptors in young healthy volunteers.

The regulation of adrenergic receptors during hypoxia is complex, and the results of published reports have not been consistent. In the present study blood cell adrenoceptor characteristics at sea level (SL) before and after prolonged exposure to high altitude (HA) were measured in seven trained young male lowlanders. Sympathoadrenal activity and clinical haemodynamic parameters were also evaluated before departure (SLB), after 1 week (HA1) and 4 weeks (HA4) at HA and 1 week after return to sea level (SLA). As compared to pre-departure sea level values, urinary norepinephrine excretion increased significantly during altitude exposure [SLB: 10.26 (3.04) microg x 3 h(-1); HA1: 23.2 (4.19) microg x 3 h(-1); HA4: 20.3 (8.68) microg x 3 h(-1)] and fell to pre-ascent values 1 week after return to sea level [SLA: 9 (2.91) microg x 3 h(-1)]. In contrast, mean urinary epinephrine levels did not increase over time at HA. Both systolic and diastolic blood pressures, as well as heart rate, were increased during HA exposure. The circadian blood pressure and heart rate rhythms were preserved during all phases of altitude exposure. Mean maximal binding (Bmax) of the alpha2-adrenoceptor antagonist [3H]rauwolscine to platelet membranes was significantly reduced (P < 0.001) after exposure to chronic hypoxia [SLB: 172.6 (48.5) fmol x mg(-1) protein versus SLA: 136.8 (56.1) fmol x mg(-1) protein] without change in the dissociation constant (K(D)). Neither the lymphomonocyte beta2-adrenoceptor Bmax [SLB: 38.5 (13.6) fmol x mg(-1) protein, versus SLA: 32.4 (12.1) fmol mg(-1) protein] nor the K(D) for [3H]dihydroalprenolol was affected by chronic hypoxia. Cyclic AMP (adenosine 3',5'-cyclic monophoshate) generation in lymphomonocytes by maximal isoproterenol stimulation was not modified after prolonged HA exposure. In conclusion, the down-regulation of alpha2-adrenoceptors appears to be an important component of the adrenergic system response to HA exposure.

Adenylyl Cyclases↗
PubMed2000

Systemic and regional haemodynamic effects of aortofemoral angiography.

UNLABELLED: The aim was to investigate the regional and systemic haemodynamic consequences of bolus injection of fluids with different physical properties in the course of routine aortography. Iopamidol was compared with an equiosmolar solution of mannitol and with a 0.9 N saline solution. Continuous blood flow and Pulsatility Index (PI), as an index of regional vascular resistance, were measured by Doppler technique. Finger arterial pressure and heart rate were monitored at the time and for 3 min following each intraaortic bolus injections. The patients who underwent routine aortography were grouped according to the site of the flow measurements: common femoral artery, common carotid artery and brachial artery. Flow changes induced by the bolus infusion were evident for all the fluids but only at the femoral artery level. After an immediate (3 +/- 2 s) and brief (2 +/- 2 s) but marked reduction of flow and in-phase increase of PI following the bolus, further haemodynamic changes were observed only in the femoral artery, with a peak at 35 +/- 10 s and returning to baseline values after 70 +/- 15 s, in terms of both increased mean blood velocity and decreased PI. Saline and mannitol induced overall blood velocity alterations of 54% and 80%, respectively, and PI reductions of 44% and 57% compared with those induced by iopamidol. In the other vascular areas there was only a 17 +/- 2% increase of the physiological early diastolic backflow at the brachial artery level. Blood pressure decreased and heart rate increased in phase with the flow changes of the femoral artery. IN CONCLUSION: (1) a dramatic rheodynamic perturbation at the site of injection induces a vasodilating stimulus; (2) the haemodynamic response following injection results in marked vasodilation of only the tributary vascular bed; (3) flow steal may occur from other beds towards the lower limb vascular beds owing to vascular impedance imbalance; (4) a reduction of systemic arterial pressure is induced in phase with the regional vascular events and a reflex increase of the heart rate; and (5) the physical properties of the injected fluids influence the intensity of the perturbation, although the decisive triggering factor is the counterflowing bolus per se.

Aortography↗
PubMed1999

Baroreceptor-heart rate reflex sensitivity enhancement after urinary bladder distention in essential hypertensives.

Our objective was to determine if urinary bladder distention modifies the sensitivity of the baroreceptor-heart rate reflex in hypertensive and control subjects. The baroreceptor-heart rate reflex sensitivity was measured in 15 male patients (mean age 37+/-8 years) with mild untreated hypertension (mean 163+/-8/ 95+/-12 mmHg) and 17 age- and sex-matched control subjects before and after urinary bladder distention. Bladder filling was performed infusing saline heated to 37 degrees C via a urinary catheter; the volume infused in each patient corresponded to that which caused the urge to void without reaching the pain threshold. The baroreceptor-heart rate reflex sensitivity was determined correlating the variations of the systolic pressure and of the peak blood flow velocity in the common carotid artery with the variations of the ECG RR' interval of the following heart beat, both during spontaneous and phenylephrine-induced fluctuations of the haemodynamic variables. After bladder distention the diastolic pressure of the hypertensive subjects increased significantly (95+/-12 vs. 100+/-12 mmHg: P < 0.02), whereas the heart rate decreased (RR= 873+/-70 vs. 926+/-80 ms; P < 0.005). These parameters were unchanged in the normotensive subjects (84+/-9 vs. 83+/-8 mmHg and 914+/-158 vs. 913+/-140 ms, respectively). The baroreceptor-heart rate reflex sensitivity, measured on the basis of spontaneous pressure and carotid blood flow velocity fluctuations in relationship to RR changes, decreased in the normotensive subjects after bladder distention (10.7+/-4.6 vs. 9.4+/-2.7 ms/mmHg; P < 0.05 and 423+/-99 vs. 356+/-102 ms/kHz; P < 0.01, respectively), whereas it increased in the hypertensive patients (6.9 +/- 3.6 vs. 8.3 +/- 2.8 ms/mmHg; P < 0.03, and 332 +/- 86 vs. 381+/-97 ms/kHz; P < 0.03 respectively). After bladder distention and phenylephrine administration the baroreceptor-heart rate reflex sensitivity, measured by the correlation between systolic pressure and RR interval, increased only in the hypertensive group (10.2+/-5.4 vs. 15.2+/-7.7 ms/mmHg; P < 0.005). In conclusion urinary bladder distention provokes in hypertensives but not normotensive controls a brisk parasympathetic response of the component of the baroreceptor-heart rate reflex which controls heart rate.

Adult↗
PubMed1999

Control of glomerular hyperfiltration and renal hypertrophy by an angiotensin converting enzyme inhibitor prevents the progression of renal damage in hypertensive diabetic rats.

OBJECTIVE: Glomerular hyperfiltration and renal hypertrophy are both considered important in the progression of diabetic nephropathy. The aim of this study was to compare the effects of an equivalent reduction in blood pressure produced by the angiotensin-converting enzyme (ACE) inhibitor spirapril (SPI) and an antihypertensive triple drug combination of hydralazine, reserpine and hydrochlorothiazide (HRH) on kidney function, proteinuria and renal structure in hypertensive diabetic rats. DESIGN AND METHODS: Four groups of animals were evaluated in short-term and long-term studies. In both studies one group served as a non-diabetic hypertensive control (H). The other three groups were rendered diabetic and were allocated to one of the following groups: the first diabetic group received no specific therapy (HD), the second diabetic group was treated with SPI (HD-SPI) and the third diabetic group was treated with HRH (HD-HRH). In each of the two studies the systolic blood pressure (SBP), 24 h urinary total protein, glomerular filtration rate (GFR), glomerular area, proximal tubular area and glomerular sclerosis were evaluated. RESULTS: The blood pressure reduction was equal in rats receiving either SPI or HRH. The GFR, proteinuria, glomerular area and tubular area were significantly increased in the HD group, both in the short-term and the long-term study. In the HD-SPI group the diabetic hyperfiltration and renal hypertrophy responses were prevented. In the HD-HRH group the GFR and proteinuria were slightly reduced in the later phases of diabetes, while the glomerular area and tubular area were not affected. Semiquantitative analysis of renal lesions showed that SPI was more effective than HRH in the prevention of the development of glomerulosclerosis. CONCLUSIONS: The results of this study suggest that the control of early adaptive hyperfiltration and renal hypertrophy by SPI may be relevant in the prevention of glomerulosclerosis.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Regional and systemic haemodynamic response to aortography in hypertensives.

OBJECTIVE: To study the effects of aortography and of aortic counterflow bolus injection per se on regional and systemic haemodynamics in hypertensives in comparison to normotensive matched controls. DESIGN AND METHODS: Mean blood velocity (MBV) and pulsatility index (PI)--as an index of regional vascular resistance--by the Doppler technique, at the femoral, common carotid and brachial arteries, finger arterial pressure and electrocardiographic R-R' interval were monitored beat-by-beat, before, during and for 3 min following counterflow bolus injections into the abdominal aorta of 40 ml/2.6 s of iopamidol (I), iso-osmolar mannitol (M) and 0.9 N saline (S), in 11 hypertensive and nine normotensive patients. RESULTS: After bolus injection of iopamidol, MBV increased to a peak at 35+/-5 s, both in normotensive (deltaMBV versus baseline +16.7+/-9.9 cm/s; P < 0.01) and in hypertensive subjects (deltaMBV versus baseline: +13.9+/-6.6 cm/s; P < 0.01). At the same time, the PI decreased both in normotensive (deltaPI versus baseline: -4.05+/-2.49; P < 0.01) and in hypertensive subjects (deltaPI versus baseline: -3.02+/-2.25; P < 0.01). After M boluses, the haemodynamic changes were of the same direction and magnitude as I for both groups, while after S the magnitude was approximately 50% lower. No significant differences were observed between normotensive and hypertensive subjects. In other vascular circulations, a 15% increase of the early diastolic backflow in the brachial artery, in phase with the femoral artery haemodynamic changes, was the only evidence of the procedure. Mean arterial pressure decreased and heart rate increased in phase with flow changes of the femoral artery. CONCLUSIONS: (1) The regional flow and systemic pressure changes observed during aortography seem, at least partially, to be due to the hydrodynamic perturbation induced by bolus injection per se. (2) The physical and chemical properties of the contrast media and therefore the probable different shear-stress modifications induced by the fluid injected could explain why the haemodynamic changes were greater after I compared to S and were more similar to M. (3) Hypertensive subjects did not show a different vasoreactive response in comparison to normotensive subjects during aortography.

Aged↗
PubMed1997

[Role of Doppler color ultrasonography and of flowmetric analysis in the diagnosis and follow-up of Grave's disease].

Hyperthyroidism in Graves' disease is caused by the presence of circulating autoantibodies to the THS receptors on the thyroid cells. Thyroid-suppression therapy prevents hormone production directly, without affecting the pathogenetic process. We performed color Doppler US of the thyroid gland and pulsed Doppler analysis of thyroid artery flow in 21 patients with Graves' disease before and during medical treatment. US results were compared with those of a control group of 40 healthy subjects and correlated with the values of thyroid hormones, TSH, and thyroid microsomal and thyroglobulin antibodies. The thyroid gland was hypovascularized in the control group. Pulsed Doppler examination of the thyroid arteries exhibited peak systolic velocity of PSV 20 +/- 4 cm/s, diastolic velocity of 8 +/- 1 cm/s, and resistive index of 0.60 +/- 0.04. The thyroid gland of Graves' disease patients was hypervascularized. Pulsed Doppler examination of the thyroid arteries exhibited peak systolic velocity (PSV = 51 +/- 12 cm/s), end diastolic velocity (VD = 15 +/- 4 cm/s), and resistive index (RI = 0.71 +/- 0.04) significantly higher than in normal subjects (p < 0.001). Circulating thyroid hormones and flow parameters normalized after 6-8 months of medical therapy (PSV = 20 +/- 6 cm/s, VD = 9 +/- 3 cm/s, RI = 0.58 +/- 0.07). Conversely, the color Doppler patterns normalized only in a patient with normal TSH and antibodies. Sampling of the thyroid arteries proved more repeatable than sampling of parenchymal vessels.

Blood Flow Velocity↗
PubMed1996

Relationship between mechanical properties of the carotid artery wall and baroreflex function in acutely treated hypertensive patients.

OBJECTIVE: To evaluate the relationship between the mechanical properties of the carotid artery wall and baroreflex function after acute reduction of blood pressure with lacidipine in essential hypertension. DESIGN: After 15 days of placebo washout, the hypertensive patients underwent a single-blind haemodynamic study before and 90 min after administration of 4 mg lacidipine (a dihydropyridine calcium antagonist). METHODS: Brachial intra-arterial blood pressure was recorded in eight mild-to-moderate essential hypertensive patients aged 40-53 years (mean +/- SEM 46.8 +/- 4.7 years). The carotid pulse diameter was recorded simultaneously by an echo-tracking technique. The mechanical properties of the carotid artery wall were evaluated by calculating Peterson's incremental elastic modulus (Ep) both as an averaged value of 10 heart cycles with stable blood pressure and was the dynamic correlation, on a beat-to-beat basis, of Ep and the systolic blood pressure during a 20 mmHg increase in blood pressure following a bolus injection of phenylephrine. The elastic properties of the carotid artery were investigated further by determining the correlation between the systolic pressure and systolic diameter, beat by beat, during a ramped increase of blood pressure after phenylephrine administration. The baroreceptor reflex sensitivity was measured simultaneously by the Oxford method and by correlating Ep and the electrocardiographic R-R' interval on a beat-to-beat basis during phenylephrine injections. RESULTS: After lacidipine administration Peterson's elastic modulus, measured under resting steady-state conditions, was reduced (18.7 +/- 7.4 versus 16.4 +/- 6 x 10(5) dyne/cm2), whereas the baroreflex sensitivity was unchanged (6.6 +/- 3.3 versus 6.3 +/- 0.2 ms/mmHg) and resetting of the baroreflex had occurred. At the same time, the correlations between the systolic blood pressure and Ep and between the systolic blood pressure and carotid systolic diameter over a 20 mmHg increase in blood pressure were unchanged. Moreover, the correlations between the systolic blood pressure and the R-R' interval and between Ep and R-R' interval during the phenylephrine-induced blood pressure increase did not differ statistically. CONCLUSIONS: The results suggest that the resetting of the baroreflex after the acute reduction in blood pressure caused by lacidipine is dissociated from mechanical changes in the carotid artery wall.

Adult↗
PubMed1995

Contribution of systemic blood pressure to myocardial remodeling in uremic rats.

Left ventricular hypertrophy with diffuse intermyocardiocytic fibrosis is a feature of uremia. The role of blood pressure and/or other cardiovascular uremic risk factors in cardiac remodeling is still uncertain. To determine the extent to which improvement of kidney function and the control of uremia-related risk factors are associated with a reduction of myocardial injury, we evaluated the effect of dietary protein restriction or the angiotensin-converting enzyme inhibitor lisinopril on cardiac structure in remnant kidney rats. One week after subtotal nephrectomy, Wistar rats were allocated to receive drinking water solution (group 1), 5 mg/kg per day lisinopril (group 2), or a low-protein diet (6%) (group 3) for 12 weeks. Group 2 and 3 showed a comparable efficacy in preventing the expected rise in creatininemia, urinary protein excretion, and glomerulosclerosis. However, hypertension development was prevented only in group 2. Groups 1 and 3 developed a significant (P < .01) increase in left ventricular weight (2.45 +/- 0.1 and 2.5 +/- 0.5 mg/g body wt, respectively) compared with group 2 (1.9 +/- 0.06 mg/g body wt). Cardiac hydroxyporline concentration was also lower in group 2 compared with group 1 (2.07 +/- 0.16 versus 2.73 +/- 0.17 mg/g left ventricular weight, P < .05) but not compared with group 3 (2.59 +/- 0.19 mg/g left ventricular weight). The effect of angiotensin-converting enzyme inhibition on left ventricular mass and intracardiac collagen content appeared to be dissociated from anemia, sympathetic activity, and hyperlipidemia. There was a close relationship between systolic pressure and left ventricular mass; however, no relationship between the degree of cardiac fibrosis and systolic pressure could be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

A new ultrasonographic instrument for measuring vessel wall shear stress.

A new ultrasonographic machine (FRP II) has been developed to measure vessel wall shear stress. A multigate ultrasound probe sends an ultrasound beam simultaneously focused in subsequent points 0.2 mm from each other along the transverse axis of a blood vessel. Blood velocity is measured by cross-correlation technique, which allows a rapid and economical analysis. Thus, the instantaneous (every 5 msec) blood velocity profile is reconstructed for the duration of the entire cardiac cycle. In order to verify the precision and sensitivity of the FRP II in measuring shear stress, 36 measurements were performed on the common carotid artery in 9 hypertensive subjects in different hemodynamic conditions. The FRP II-measured shear stress (the product of the shear rate and blood viscosity) was compared to that calculated by the Womersley's mathematical model (Y = 2K.Vcl/D, where Y = shear rate, Vcl = vessel center line blood velocity, D = vessel diameter). A good correlation (r = 0.77, p < 0.0001) was found between the peak systolic shear stresses measured by FRP II and that calculated by the Womersley's mathematical model, although an underestimation for higher values was observed with the latter method. In conclusion, we propose a new ultrasonographic instrument to measure "in vivo" the vessel wall shear stress.

Aged↗
PubMed1993

The cardiac renin-angiotensin system in heart failure.

The success of angiotensin-converting enzyme (ACE) inhibitors in reducing cardiovascular morbidity and mortality rates has led to a reexamination of the role of the renin-angiotensin system in pathophysiology. Ventricular dysfunction leading to congestive cardiac failure is associated with sequential activation of the sympathetic system and increases in plasma atrial natriuretic peptide; however, increases in plasma renin and aldosterone do not occur until very late. The renin-angiotensin system is now regarded as both a circulating and tissue hormonal system. All components of the renin-angiotensin system have been detected in the heart. ACE is localized in discrete areas of the heart, including the cardiac valves, coronary vessels, atria, and myocardium. After experimental myocardial infarction in the rat, although plasma renin and aldosterone levels are not increased, ACE in the myocardium is markedly increased. Treatment with ACE inhibitors suppresses cardiac ACE and is associated with hemodynamic improvement, reversal of the neurohumoral activation, prevention of ventricular dilatation, and remodeling and reduction in mortality rates. These results suggest that the beneficial effects of ACE inhibitors in treating congestive cardiac failure, preventing ventricular remodeling, and regressing left ventricular hypertrophy may involve not only reducing preload and afterload but also suppressing the local cardiac renin-angiotensin system.

Angiotensin II↗
PubMed1993

Intrarenal renin-angiotensin system in renal physiology and pathophysiology.

It has now been demonstrated by several techniques that all components of the renin-angiotensin system reside within the kidney. It is likely that angiotensin II is formed within interstitial renal tissue, as well as intracellularly, and acts locally in an autocrine, paracrine or intracrine manner. It has been difficult to dissect the different renal physiological roles of circulating angiotensin II as opposed to intrarenal generated angiotensin II. Angiotensin converting enzyme (ACE) inhibitors have played an important role in helping distinguish the effects of intrarenal angiotensin. Apart from hemodynamic actions and effects on glomerular filtration rate and renal tubular function, the intrarenal renin angiotensin system probably plays an important role as a regulator of renal sympathetic activity, modifies mesangial cell function, acts as a renal growth promoter, maintains endothelial cell function, and may be an important inflammatory mediator in the kidney. The renoprotective action of ACE inhibitors in reducing proteinuria and in slowing the fall in glomerular filtration rate in experimental and human renal disease may involve any of the above mechanisms. However, a prerequisite for the renoprotective action of ACE inhibitors is reduction of systemic blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Ace inhibition in renal disease: risks and benefits.

The kidney is one of the principal target organs of hypertension and most diseases of the kidney are associated with blood pressure elevation. Studies in animal models of hypertensive renal disease have provided insights into the complex relationship between systemic and glomerular hypertension. The intrarenal renin-angiotensin system (RAS) appears to play an important role in the pathogenesis of progressive glomerular injury. Thus, angiotensin converting enzyme inhibitors (ACEi) may have a specific therapeutic advantage in the treatment of hypertension associated with progressive renal disease. However, in contrast to their possible renoprotective effect in diabetic nephropathy or in renal hypertension, there are increasing evidence that, in the presence of a reduction in renal perfusion, intrarenal haemodynamic effect of ACEi may lead to compromised renal function. ACEi appear to have dual effects on renal function depending on the setting in which they are administered.

Angiotensin-Converting Enzyme Inhibitors↗