Carotid diameter, wall thickness, and parietal stress in essential hypertension.
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Blood Pressure↗
Biomedical subjects
R Pontremoli
Publications and source records attributed to R Pontremoli.
Ultrasonographic imaging and Doppler analysis of renal changes in non-insulin-dependent diabetes mellitus.
RATIONALE AND OBJECTIVES: We used ultrasonographic imaging and Doppler analysis to assess renal changes in patients with non-insulin-dependent diabetes mellitus (NIDDM) and normal renal function, as established by normal serum creatinine levels and the absence of macroalbuminuria. METHODS: Renal parenchymal echogenicity, renal volume, and resistive index (RI) were blindly evaluated for 85 NIDDM patients and 42 age-matched control subjects (C). Results were analyzed and correlated with the following clinical parameters: patient age, duration of diabetes, blood pressure, blood glucose and cholesterol levels, and the presence of microalbuminuria. RESULTS: Normal renal parenchymal echogenicity was seen in all but one NIDDM patient; however, in comparison with C, diabetic patients had significantly higher renal volume (mean +/- standard deviation, 314.01 +/- 72.74 vs 227.64 +/- 58.76) and RI (mean +/- standard deviation, 0.71 +/- 0.05 vs 0.64 +/- 0.02). An RI higher than 0.70 was found in 55 of 85 (65%) NIDDM patients; an increased RI was directly correlated with patient age, whereas an inverse correlation existed between an increased RI and renal volume. No statistically significant differences were observed for the duration of diabetes, arterial hypertension, blood levels of glucose and cholesterol, and the presence of microalbuminuria. CONCLUSIONS: NIDDM patients with normal renal function show a significant increase in renal volume and RI in comparison with C. Demonstration of these findings may aid in the detection of early renal involvement in NIDDM patients. However, further investigations are needed to understand fully the correlation of such changes with the pathology of diabetic nephropathy and to provide an interpretation of the pathophysiologic mechanisms underlying changes in intrarenal vascular impedance in NIDDM patients.
Aged↗
Insulin activation of red blood cell Na+/H+ exchange decreases the affinity of sodium sites.
We have previously reported increased activity of Na+/H+ and Na+/Li+ exchanges in red blood cells (RBC) of patients with hypertension and diabetic nephropathy. The presence in human red blood cells (RBC) of insulin receptors has led us to examine the effects of this hormone on the kinetic parameters of Na+/H+ exchange as a first approach to define its mechanism of action. The antiporter activity was measured as net Na+ influx driven by an outward H+ gradient in acid-loaded, Na-depleted RBCs preincubated with or without (w/wo) insulin (0 to 100 microU/ml) for different time periods. The effects of insulin on the H+ and Na+ activation kinetics of Na+/H+ exchange were examined in RBCs of normal subjects fasted for 12 hours. Insulin (50 microU/ml for 1 hr) increased the Vmax from 28 +/- 6 to 49 +/- 8 mmol/liter cell x hr (N = 10, P < 0.0005) and the Km for Na+ from 72 +/- 10 to 142 +/- 19 mM (N = 4, P < 0.05) but did not change the Km for intracellular H+. Insulin also increased the Vmax of Na+/Li+ exchange at pHi 7.4 (0.34 +/- 0.03 to 0.45 +/- 0.04 mmol/liter cell x hr, N = 9, P < 0.005) as well as the Km for Na+ (31 +/- 3 to 6 +/- 10 mM, P < 0.0003). Therefore, insulin can modulate Na+ sites of Na+/Li+ or Na+/H+ exchanges independent of the occupancy of H+ sites to favor the release of bound Na+ into the cytoplasm. Insulin stimulation of Na+/H+ exchange required endogenous cytosolic Ca2+ levels. The kinetic effects of insulin on Na+/H+ and Na+/Li+ exchanges were imitated by okadaic acid (300 microM), an inhibitor of protein phosphatases which dephosphorylate serine-threonine residues. Okadaic acid increased the Vmax of Na+/H+ and Na+/Li+ exchanges and the Km for Na+ as insulin did. In conclusion, insulin stimulation of the Na+/H+ antiporter occurs by a novel kinetic mechanism leading to a decreased affinity for external Na+ without changes in the affinity for Hi. On the basis that insulin effects were imitated by okadaic acid, we hypothesize that this hormone may increase the phosphorylated state of serine-threonine residues of this antiporter protein.
Adult↗
[Microalbuminuria, hypertension, and cardiovascular risk].
A growing interest in the study of microalbuminuria (Mi) in essential hypertension (EH) has recently emerged. While clinical proteinuria is found with a low frequence (between 4 and 16%) in patients with EH, a variable but generally higher prevalence (10-40%) of Mi has been reported, even in the absence of diabetes and nephropathy. Mi is defined as an abnormal urinary excretion of albumin (20-200 micrograms/min), undetectable by conventional tests. Variations in the prevalence of Mi in different studies may be attributed to different selection criteria, techniques for detection of albuminuria, the severity of hypertension, age, race, coexistence of renal disease as well as the number of patients studied and the presence or absence of antihypertensive treatment. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and target organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis. Mi has been associated with higher blood pressure levels, a worse lipid profile as well as the presence of target organ damage, namely peripheral artery disease and left ventricular hypertrophy in patients with EH. Several studies have shown a correlation between Mi and/or proteinuria and cardiovascular diseases independently of other risk factors and cardiovascular mortality to be ten times higher in patients with Mi than in normoalbuminuric patients. Long-term prospective studies are needed in order to clarify the exact prevalence of Mi, its predictive value for the development of clinical proteinuria and renal function deterioration as well as the effect of different antihypertensive drugs.
Albuminuria↗
Cardiac diastolic abnormalities and atrial natriuretic factor in essential hypertension.
Cardiac function and plasma levels of atrial natriuretic factor (ANF) were studied in a group of 38 patients with untreated essential hypertension and in a group of 31 well matched normotensive controls. ANF was slightly but significantly higher in hypertensives and was directly correlated with mean arterial pressure and inversely with plasma renin activity (PRA). Hypertensives showed normal systolic function and higher cardiac mass compared to controls. ANF was inversely correlated to echocardiographic indexes of left ventricular performance in the former group. At Doppler echocardiographic evaluation, hypertensives showed an impairment in diastolic function which was correlated to the increase in ANF levels. Stepwise multiple regression analysis performed with ANF as the dependent variable and several biohumoral and echocardiographic parameters as the independent variables showed that only cardiac diastolic function and PRA significantly affect ANF levels in hypertensives. In conclusion, an impairment in cardiac diastolic function may be responsible together with other factors for the increased ANF levels encountered in essential hypertension.
Adult↗
Effects of a protein meal on blood amino acid profile in patients with chronic renal failure.
Arterial whole blood levels of amino acids were determined in patients with chronic renal failure and in healthy subjects before and after 270 min after the ingestion of a grilled beefsteak (4 g/kg). In patients, total nonessential amino acids increased significantly more (+46%) than in controls owing to an exaggerated rise of serine, glutamine, proline, glycine, cyst(e)ine and alanine. Total essential amino acids increased as much as in controls; however, threonine, histidine and phenylalanine showed greater increases, while tryptophan had a smaller increment. Abnormalities in amino acid levels were even more evident in the postprandial period than in the postabsorptive state owing to reduced levels of valine, leucine, tryptophan, tyrosine, aspartate and glutamate and higher levels of glutamine, proline, glycine, cyst(e)ine, threonine, histidine and phenylalanine. Moreover, after the meal, the ratios total essential amino acids/total nonessential amino acids, valine/glycine, and branched-chain amino acids/total amino acids rose but persisted to be reduced whereas tryptophan/total amino acids and tyrosine/phenylalanine ratios increased in controls, but did not change in patients. In conclusion, in chronic renal failure, protein ingestion enhances the imbalance in amino acid levels already present in the postabsorptive state. The all data indicate that in patients with chronic renal failure, the metabolism of exogenous protein is impaired and the flow of amino acids to the organs is altered during the phase of body nitrogen replenishment.
Adult↗
Regional cerebral blood flow in chronic hypertension. A correlative study.
BACKGROUND AND PURPOSE: Cerebral hypoperfusion has occasionally been reported during essential hypertension. We explored regional cerebral blood flow in a large series of neurologically asymptomatic hypertensive patients to determine relations among cerebral blood flow, concomitant main vascular risk factors, and the most common signs of end-organ damage. METHODS: Regional cerebral blood flow was measured by the 133Xe inhalation method in 101 hypertensive patients without clinically apparent central nervous system involvement, including 39 mild to moderate untreated and 62 mild to severe treated patients. RESULTS: Compared with age- and sex-matched normal control subjects, cerebral blood flow was significantly reduced in untreated hypertensive patients (P < .01) and to a lesser extent in treated patients (P = .047). Both regional and global cerebral blood flow reductions were observed in approximately one third of patients in both groups. Analysis of variance failed to show significant correlations between cerebral blood flow and total cholesterol concentration, mean arterial blood pressure, duration of disease, or the presence of retinopathy or left ventricular hypertrophy. In the treated group, the quality of control of hypertension significantly influenced both global cerebral blood flow (P = .007) and cerebrovascular resistance (P < .0001). CONCLUSIONS: Focal or diffuse cerebral hypoperfusion is present even in neurologically asymptomatic hypertensive patients, especially when untreated; good control of blood pressure may preserve cerebral perfusion and reduce cerebrovascular resistance. Regional cerebral blood flow examination represents a relatively simple and low-cost technique to explore the perfusional condition of the brain, one of the main target organs of hypertensive disease.
Adult↗
Red cell sodium-proton exchange is increased in Dahl salt-sensitive hypertensive rats.
To investigate the relationship between red blood cell Na+/H+ exchange (EXC) and genetic factors in hypertension, we studied the maximal rate of the antiporter (mmol/liter cell x hr; flux units = FU) in three strains of genetically hypertensive rats. Salt-resistant Dahl rats (DR) were normotensive under low (0.02%) and high (8%) NaCl diets, while salt-sensitive Dahl rats (DS) became markedly hypertensive after four weeks on the high-NaCl diet. Na+/H+ exchange did not differ between DR and DS rats when both were fed with the low-NaCl diet (mean +/- SE, 31 +/- 3, N = 15, vs. 29 +/- 3 FU, N = 14). On the high-NaCl diet, the DR strain did not exhibit significant changes in blood pressure and antiporter activity, but the DS rats significantly increased their blood pressure and Na+/H+ exchange (57 +/- 4 FU, N = 13) versus DR rats (38 +/- 3 FU, N = 15, P < 0.02). DS rats also significantly increased blood pressure and antiporter activity when fed with high-NaCl diet for one week. These data indicate that high NaCl intake per se does not increase Na+/H+ EXC because the control DR strain did not exhibit transport and blood pressure alterations as observed in the DS strain. Milan hypertensive and spontaneously hypertensive rats (Charles River substrain) had higher blood pressures than Milan and Wistar-Kyoto normotensive rats when they were maintained for four weeks on a 1.5% NaCl diet; however, no differences were seen among normotensive and hypertensive strains in Na+/H+ exchange activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
The calpastatin defect in hypertension is possibly due to a specific degradation by calpain.
Calpastatin activity, significantly reduced in erythrocytes of patients affected by essential hypertension, is restored to normal values by appropriate therapeutical treatments in a time-dependent fashion and in parallel with the decline in blood pressure. Evidence is also presented indicating that red cell calpastatin is degraded in human and rat red cells by homologous calpain, and that the rate of degradation is approx. 5-times higher in rat erythrocytes. Thus, increased proteolytic degradation catalyzed by calpain could explain both the decrease in the amount of calpastatin activity and the profound difference between the intracellular level of the calpain inhibitor observed in erythrocytes from patients with essential hypertension and the genetically hypertensive rats.
Animals↗
Renal ammoniagenesis in humans with chronic potassium depletion.
Renal ammonia production and distribution and ammonia precursor utilization were evaluated in eight patients with chronic potassium depletion (CPD) and aldosterone-producing adenoma and in 20 controls. In CPD, urinary ammonia excretion and ammonia added to renal venous blood were about twofold higher than in controls; thus, total ammonia production was significantly augmented (88.0 +/- 10.3 mumol/min.1.73 m2 vs. 45.0 +/- 2.6 in controls). Total ammonia production was inversely correlated with serum potassium and directly correlated with urine flow. Stepwise multiple regression analysis showed that both factors, mainly serum potassium, significantly influence ammonia production and account for 61.4% of variations in ammonia production. Renal extraction of glutamine was significantly increased (56.6 +/- 5.9 mumol/min.1.73 m2 vs. 34.6 +/- 3.1 in controls), and this could account for ammonia production. The ratio of urinary ammonia excretion to total ammonia production, an index of the intrarenal ammonia distribution, was similar in patients and controls, and was significantly correlated with urine pH and true renal blood flow (RBF). Stepwise multiple regression analysis showed that RBF, urine pH and urine flow also significantly affected ammonia distribution. However, these factors accounted for only 41.7% of variations in intrarenal ammonia partition, urine pH having a minor role. We conclude that in patients with CPD other factors besides urine pH, urine flow and RBF intervene in the ammonia partition between urine and blood.
Acid-Base Equilibrium↗
Changes in blood pressure, plasma triglyceride and aldosterone concentration, and red cell cation concentration in patients with hyperinsulinemia.
Blood pressure, plasma concentration of triglyceride, aldosterone, renin activity (PRA), and atrial naturietic peptide (ANP), and red blood cell, urine, and plasma sodium and potassium concentration were determined in 24 healthy individuals divided into two groups defined as being either hyperinsulinemic or normoinsulinemic. The results demonstrated that the hyperinsulinemic group had significantly higher values for both systolic (P less than .01) and diastolic (P less than .05) blood pressure. In addition, plasma concentrations of triglyceride (P less than .02), aldosterone (P less than .05) and potassium (P less than .05) were higher in hyperinsulinemic individuals as compared to those who were normoinsulinemic. Furthermore, red cell potassium was lower (P less than .01) and red cell sodium higher (P less than .01) in the hyperinsulinemic group. Finally, the magnitude of hyperinsulinemia correlated directly with systolic (r = 0.50, P less than .01) and diastolic (r = 0.44, P less than .05) blood pressure, concentration of plasma triglyceride (r = 0.55, P less than .01) and aldosterone (r = 0.46, p less than .05), and erythrocyte sodium concentration (r = 0.57, p less than .01). In contrast, plasma insulin response was negatively correlated with erythrocyte potassium concentration (r = 0.40, P less than 0.05). These observations provide further support for the view that hyperinsulinemia, presumably secondary to resistance to insulin-stimulated glucose uptake, is associated with a cluster of variables that may play important roles in the etiology and clinical course of hypertension.
Aldosterone↗
Renal ammoniagenesis in man with chronic potassium depletion.
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Adult↗
[Captopril-induced changes in renal flow: evaluation using Doppler echography].
It is well known that angiotensin antagonists cause increase of renal blood flow. We have examined, using duplex Doppler sonography, the changes of renal blood flow velocity induced by oral administration of 50 mg. of Captopril. We examined 19 kidneys in 17 subjects without hypertension. Both peak systolic and diastolic velocities were measured at renal hilum and at arcuate arteries, and the resistive index (RI) was calculated. In conclusion duplex Doppler sonography shows significant increase of blood flow velocities both at the hilum and at the arcuate arteries, without variation of the RI, thus showing that changes affect the whole Doppler wave, both in systole and diastole.
Blood Flow Velocity↗
Long-term minoxidil treatment in refractory hypertension and renal failure.
Twenty-two patients with severe or accelerated hypertension refractory to conventional hypotensive therapy have been treated with minoxidil for an extended period. Patients were divided in three groups according to different degrees of renal function or the presence of accelerated hypertension. In the first group (8 patients with normal or slightly decreased renal function) BP fell from 197 +/- 11/118 +/- 3 before minoxidil therapy to 157 +/- 7/98 +/- 2 after six months (p less than 0.001), and remained steady during the following eighteen months. In the second group (9 patients with creatinine clearance of 30 +/- 3 ml/min.1.73 m2) BP decreased from 192 +/- 9/119 +/- 4 to 147 +/- 6/91 +/- 4 at six months (p less than 0.001); renal function did not show any significant modification during the eighteen months of the study. In the third group (5 patients with accelerated hypertension) BP fell from 243 +/- 14/137 +/- 6 to 166 +/- 13/99 +/- 7 at six months (p less than 0.01). Seven patients, four in the first and three in the second group, were followed for more than six years; these patients, with mild renal insufficiency (creatinine clearance 50 +/- 4 ml/min) before minoxidil therapy, were on a protein unrestricted diet for the entire length of the study. In this group of patients BP fell from 182 +/- 9/115 +/- 3 to 150 +/- 6/96 +/- 2 after one year (p less than 0.01) and remained well controlled for the following six years or more. Renal function did not show any significant worsening over the years (monthly decrement in creatinine clearance 0.08 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Acute renal failure due to acute bilateral renal artery thrombosis: successful surgical revascularization after prolonged anuria.
Acute bilateral renal artery thrombosis is a rare but surgically correctable cause of acute renal failure. A middle-aged woman with acute renal failure and anuria due to atherosclerotic occlusion of the abdominal aorta and both renal arteries was surgically treated 42 days after the onset of anuria. Revascularization resulted in the reversal of renal failure and complete recovery of renal function in spite of prolonged anuria. An aggressive diagnostic and therapeutic approach is important whenever this condition is suspected.
Acute Kidney Injury↗
Abnormalities in amino acid metabolism in chronic renal failure.
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Amino Acids↗
Multiple venous sampling for catecholamine assay in the diagnosis of malignant pheochromocytoma.
Malignant pheochromocytoma is a rare cause of hypertension and still has a high mortality rate. The most accurate way to localize a malignant pheochromocytoma is by a combination of scans, both CT and scintigraphy. Selective sampling of venous blood from multiple sites for plasma catecholamine levels is a safe and reliable technique and may be used successfully in some patients. A case is presented where venous sampling proved to be useful in preoperatively localizing a malignant pheochromocytoma and its metastatic lesions which both CT and ultrasound had failed to demonstrate.
Adrenal Gland Neoplasms↗
Hypernatremia associated with severe rhabdomyolysis.
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Humans↗