Biomedical subjects
Publications and source records attributed to R L Luparini.
In this study we observed that carvedilol administration to patients with heart failure improves hemodynamic function, baroreflex sensitivity, and heart rate variability. These findings contribute to improvement in survival in such patients.
Although atrial natriuretic peptide (ANP) levels are often elevated in low-renin hypertensives, the renal and hormonal effects of ANP infusion have never been evaluated in these patients. To address this topic, 27 lean nondiabetic men affected by uncomplicated essential hypertension were studied. Low-renin patients (n = 9, age 42 +/- 3 years) were defined as those individuals in balance on a low NaCl intake (10 mmol NaCl/day for 1 week) who had a plasma renin activity <0.30 ng angiotensin I/l/s, in both the supine and the upright positions. The remaining hypertensives (n = 18, age 41 +/- 4 years) were classified into the normal-renin group. Six age-matched healthy men (age 40 +/- 2 years) served as controls. After plasma renin activity determinations, both patients and controls were replaced on a normal NaCl intake (120 mmol NaCl/day). After 1 week, either ANP (99-126), at a dose (0.7 pmol/kg/min for 3 h) which is known to induce changes in plasma ANP confined to the range of normality, or its vehicle were infused at 1-week intervals, according to a randomized double-blind crossover design. At time 0, low-renin patients had significantly higher (p < 0.05) levels of plasma ANP (12.4 +/- 2.5 fmol/ml) than normal-renin patients (7.2 +/- 2.4 fmol/ ml) and normotensives (7.4 +/- 3.3 fmol/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Nonmodulation seems to represent an inheritable trait characterized by abnormal angiotensin-mediated control of aldosterone release and renal blood supply and salt-sensitive hypertension. Recently, we demonstrated that atrial natriuretic peptide (ANP) response to angiotensin II also is altered in nonmodulators. Moreover, an abnormal ANP response to acute volume expansion has been shown by others in hypertensive patients displaying some features of nonmodulators. These data induced us to hypothesize that nonmodulators. These data induced us to hypothesize that nonmodulation could be characterized by an abnormal ANP response to saline load. METHODS AND RESULTS: Forty-three essential hypertensive men were subdivided into low-renin patients (n = 12), nonmodulators (n = 15), and modulators (n = 16) according to their renin profile and ability to modulate aldosterone and p-aminohippurate clearance responses to a graded angiotensin II infusion (1.0 ng.kg-1.min-1 and 3.0 ng.kg-1.min-1 for 30 minutes each) on both a low- (10 mmol Na+ per day) and a high- (210 mmol Na+ per day) Na+ intake. The intravenous saline load (0.25 mL.kg-1.min-1 for 2 hours) performed on a low-Na+ diet increased plasma ANP levels in low-renin (from 14.30 +/- 4.68 to 23.30 +/- 7.52 fmol/mL at 120 minutes, P < .05) and modulating patients (from 10.95 +/- 3.55 to 18.21 +/- 5.42 fmol/mL at 120 minutes, P < .05), whereas it did not change the hormone levels in nonmodulators (from 10.77 +/- 3.25 to 13.83 +/- 5.70 fmol/mL at 120 minutes, P = NS). When patients switched from a low- to a high-NaCl diet, plasma ANP levels increased significantly in all groups. However, when the saline load was repeated on a high-NaCl intake, ANP levels increased in both low-renin and modulating patients (P < .05), whereas it failed to increase in nonmodulators. CONCLUSIONS: Nonmodulating hypertensive patients showed a reduced ANP response to saline infusion in the presence of a normal increase of plasma ANP with dietary NaCl load. The impaired ANP response to saline infusion could be due to a different distribution of volume load and contribute to determining the reduced ability to excrete sodium that is commonly described in nonmodulators.
To evaluate the atrial natriuretic peptide response to angiotensin II (Ang II) infusion in non-modulating hypertension, we studied 31 men with essential hypertension. These patients were subdivided into groups of low renin patients (n = 8), non-modulators (n = 11), and modulators (n = 12) according to their renin profile and ability to modulate renin and aldosterone responses to a graded infusion of Ang II (1.0 and 3.0 ng/kg per minute) on a low Na+ intake (10 mmol Na+ per day). During basal conditions, plasma atrial natriuretic peptide was higher (p < 0.05) in low renin patients (16.34 +/- 2.67 fmol/mL) than in both modulators (10.59 +/- 4.29 fmol/mL) and non-modulators (9.85 +/- 2.64 fmol/mL). During Ang II infusion, plasma atrial natriuretic peptide significantly increased in both low renin (27.67 +/- 2.61 fmol/mL at 60 minutes, p < 0.01) and modulating (20.36 +/- 3.07 fmol/mL at 60 minutes, p < 0.05) patients, whereas it did not change in non-modulators (13.94 +/- 4.39 fmol/mL, NS). After 5 days on a high sodium intake (200 mmol Na+ per day), plasma atrial natriuretic peptide rose in modulating (20.61 +/- 2.31 fmol/mL, p < 0.01 versus low sodium intake), non-modulating (20.11 +/- 6.48 fmol/mL, p < 0.01 versus low sodium intake), and low renin (26.13 +/- 3.81 fmol/mL, p < 0.001 versus low sodium intake) hypertensive patients. When the Ang II infusion was repeated with a high sodium intake, plasma atrial natriuretic peptide increased again in low renin and modulating patients, whereas it did not change in non-modulators.(ABSTRACT TRUNCATED AT 250 WORDS)
Fractional excretion of lithium (FeLi) is a marker of proximal tubular sodium reabsorption. During different sodium intakes (normal = 120 mEq/day, low = 40 mEq/day and high = 240 mEq/day) fractional lithium excretion was evaluated in essential hypertensive patients (n. 19) and control subjects (n. 5). Our data showed that FeLi was higher in hypertensives than in controls. Dividing hypertensives on the basis of blood-pressure sensitivity, salt resistant patients showed lower FeLi levels as compared to salt sensitive ones. Our findings indicate that proximal tubular sodium reabsorption is decreased in essential hypertension; this behavior is particularly evident in salt sensitive patients, suggesting that factors affecting proximal tubular function are activated in these patients in order to reduce the impairment of renal excretory capability.
In order to evaluate the effects of atrial natriuretic factor (ANF) infusion on plasma insulin (IRI) in hypertension, 32 essential hypertensives (aged 40 to 62 years) were studied. After 1 week of pharmacologic washout under normal sodium intake (120 mEq of Na+/day), patients were randomly assigned to receive either ANF (0.04 micrograms/kg/min) or its vehicle (50 mL of isotonic saline) over a 60-min period in supine position. Plasma IRI and glucose were measured at -60, 0, 20, 40, 60, 120, 180, and 240 min (infusion time: from 0 to 60 min). Plasma levels of IRI and glucose did not change significantly during ANF infusion. On the contrary, after ANF discontinuation plasma IRI rose from levels of 13.5 +/- 6.4 microU/mL at 60 min to values of 20.1 +/- 11.3 microU/mL at 240 min (P less than .0001 v time 0). Plasma glucose showed a similar behavior, increasing from values of 100.4 +/- 5.0 mg/dL at 60 min to values of 120.0 +/- 5.1 mg/dL at 240 min (P less than .02 v time 0). Our findings suggest that ANF did not influence insulin release in hypertensives. The increase of plasma glucose and IRI observed after ANF discontinuation could be due to the relapse of sympathetic activity, suppressed during ANF infusion.
Approved for clinical use in peptic ulcer in 1983, ranitidine competitively inhibits the interaction of histamine with H2 receptors. The incidence of adverse reactions has been low and generally minor. After reviewing the literature on hepatitis associated with ranitidine use, we report the case of a young woman, affected by multiple sclerosis, who developed severe liver injury associated with the intake of this drug. This case meets the principal criteria necessary to establish a causal relationship between the administration of a drug and the verification of an adverse reaction. The singularity of our case with respect to others reported in the literature arises from the demonstration of an anatomo-pathological picture suggestive of toxic or idiosyncratic hepatitis after the initial administration that, at rechallenge, evolved into a histologic picture of autoimmune hepatitis. We believe that physicians should be aware of the potential hepatotoxicity of ranitidine.
Our study was intended to verify the efficacy and the side effects of intraluminal dilatation of the distal urinary tract with vascular balloon catheter in a group of patients with urethral stenosis. In 6 out of 10 patients, there was a significant increase in urethral diameter (by 70% to 150%). In 4 patients, the stenosis was only slightly improved (increase in urethral diameter by 10% to 20%). Only 5 patients, all belonging to the group in which dilatation was anatomically effective, have been having normal micturition and have been asymptomatic. According to data in our possession, transurethral dilatation does not seem to be very effective, since it restores adequate micturition in only 50% of cases. In view of the absence of severe side effects, however, this technique may be indicated in patients with medical problems that preclude surgery.
Reduced kallikrein excretion has been demonstrated in essential hypertension, suggesting an impairment of the renal kallikrein-kinin system. Therefore, we evaluated the efficacy and safety of oral kallikrein administration (glandular kallikrein derived form porcine pancreas) in 20 essential hypertensives (14 males and 6 females) aged between 34 and 62 years. Kallikrein was administered (150 U.I. three times daily) over a period of eight days, under normal sodium intake (120 mEq of Na+/day). After the kallikrein administration period, urinary kallikrein resulted increased (from 0.9 +/- 0.4 U/24h, normal value greater than 1.2 U/24h, to 1.6 +/- 1 U/24h; p less than 0.05). Blood pressure decreased (systolic: from 154.6 +/- 13.8 mmHg to 140.3 +/- 12.5 mmHg; p less than 0.01--diastolic: from 92.5 +/- 1.5 mmHg to 86 +/- 3.9 mmHg; p less than 0.025), while urinary excretion of sodium (from 96.7 +/- 16 mEq/24h to 119.1 +/- 32.2 mEq/24h; p less than 0.05) and potassium (from 36.7 +/- 11 mEq/24h to 43.5 +/- 12.8 mEq/24h; p less than 0.05) increased after kallikrein administration. We observed only a transient episode of gastric pain. In conclusion, kallikrein administration has a mild hypotensive effect in hypertensive patients, and is generally well tolerated. The antihypertensive action is probably due to the natriuretic effect of kallikrein.
The effects of active changes in posture, from recumbency to upright position (60 minutes), on the circulating levels of atrial natriuretic peptide (ANP) in healthy human subjects were studied by using a radioimmunoassay method. In supine position, plasma ANP levels ranged from 12 pg/ml to 51.5 pg/ml, with an average level of 35.3 +/- 11.5 pg/ml. After 1 hour of orthostatic position, plasma ANP levels varied from 10 pg/ml to 35 pg/ml, with an average level of 21 +/- 11.5 pg/ml. These results suggest that ANP is involved in the hemodynamic modifications following postural stimuli. Thus, postural changes can be taken in to account for evaluating plasma ANP behaviour properly.