PubMed Health⌕ Search

Biomedical subjects

S Coassin

Publications and source records attributed to S Coassin.

18 recordsLinked to original sources

[Incidentalomas of the adrenal glands. Personal cases and review of the literature].

BACKGROUND: The growing use of sensitive non-invasive methods to image the abdomen such as ultrasonography, computed tomography (CT) and magnetic resonance imaging (MRI), have resulted in increasing recognition of adrenal incidentalomas. METHODS: In this study, we report the clinical, endocrine and radiologic evaluation of 75 patients (50 women and 25 men, mean age 56 +/- 14 years) with adrenal incidentaloma (size 1 to 18 cm, mean 3 +/- 2.5 cm). None of the patients showed any symptoms or clinical signs that might indicate the existence of adrenal dysfunction. The patients underwent basal and dynamic evaluation of the hypothalamic-pituitary-adrenal axis, renin-angiotensin-aldosterone system, and adrenomedullary function. Moreover, CT and MRI scan and Iodo-cholesterol (NP-59) scintigraphy were performed. RESULTS: The endocrine evaluation indicated 11 cases of pre-clinical Cushing's syndrome, 2 cases of pheochromocytoma and 62 not-functionally adrenal masses. On the basis of endocrine and morphologic data, 29 patients underwent surgical treatment: 20 adrenocortical adenoma, 2 pheochromocytomas, 2 not-cortisol-secreting adrenal carcinomas, 1 adrenal lymphoma, 1 adrenal metastasis, 1 myelolipoma, 1 hemorrhage and 1 pseudocystis. CONCLUSIONS: In conclusion, patient with an incidentally discovered mass has to be investigated to detect malignancy and subtle hormonal overproduction, to select the cases for surgical treatment.

Adenoma↗

Adrenomedullin levels are high in primary aldosteronism due to adenoma and decline after surgical cure.

The aim of the study was to evaluate the possible changes in plasma adrenomedullin (AM) levels in patients with primary aldosteronism before and after surgical resection. The study included 13 patients affected by aldosterone-producing adenoma (9 women, 4 men; mean age 36.2+/-14.2 years) and 20 healthy control subjects (7 women, 13 M; mean age 31.8+/-12.4 years). Unilateral adrenalectomy was performed in all patients and adrenal mass consisted of a benign adrenal cortical adenoma. The mean plasma AM concentrations in patients with primary aldosteronism (36.2+/-19.3 pg/ml) were significantly (p < 0.0001) higher than those of normal subjects (13.2+/-6.2 pg/ml). In these patients the plasma AM levels significantly (p < 0.0001) reduced after surgical removal of the tumours (14.9+/-7.6 pg/ml). In all patients with aldosterone-producing adenoma, tumour diameter correlated with the plasma AM concentrations (r=0.631; p < 0.021). In conclusion, the present investigation shows that in primary aldosteronism due to adrenal adenoma plasma AM levels are higher at the moment of diagnosis and decline after successful adrenal operation.

Adenoma↗

High plasma endothelin-1 levels in hypertensive patients with low-renin essential hypertension.

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide derived from endothelial cells and may be important in the control of systemic blood pressure (BP) and local blood flow. Immunoreactive ET-1 plasma levels may be normal or elevated in human arterial hypertension, although the exact pathophysiological role of ET-1 remains to be established. The aim of our study was to determine the relationship between the components of the renin-angiotensin-aldosterone system and plasma ET-1 levels in patients with low, normal or high-renin essential hypertension. The study groups included 13 patients with low-renin essential hypertension (average age 43.5 +/- 16.2 years), 16 patients with normal-renin essential hypertension (46.5 +/- 13.4 years), 11 patients with high-renin essential hypertension (40.7 +/- 13.8 years) and 12 healthy subjects (43.1 +/- 11.4 years). Our results demonstrated that the mean ET-1 values of all patients with essential hypertension were 10.4 +/- 3.4 pg/ml; there was not a statistical correlation between plasma renin activity (PRA) and the ET-1 levels of hypertensives; instead there was a statistically significant correlation between plasma ET-1 and plasma aldosterone (PA) (r = 0.393; P < 0.026). In particular mean plasma ET-1 values in patients with low-renin essential hypertension (12.6 +/- 2.1 pg/ml) were significantly higher (ANOVA = 0.000, P < 0.05) than those of normotensive subjects (7.7 +/- 1.7 pg/ml), patients with normal-renin essential hypertension (8.5 +/- 2.8 pg/ml), and patients with high-renin essential hypertension (9.9 +/- 3.8 pg/ml), respectively. There was a statistical correlation between PA and ET-1 levels in patients with low-renin essential hypertension (r = 0.619, P < 0.024). Our study demonstrated that there was an increase of circulating ET-1 levels in patients with low-renin essential hypertension and ET-1 plasma levels correlated with PA. The results suggest that ET-1 may play an important role in this particular form of human essential hypertension.

Adult↗

Circulating endothelin-1 in non-insulin-dependent diabetic patients with retinopathy.

Endothelin-1 (ET-1), a novel 21-amino acid vasoconstrictive peptide secreted by endothelial cells, has been thought to play a role in various forms of vascular disease. Diabetes mellitus is well known for its association with microvascular damage. To investigate whether ET-1 levels may be related to microangiopathy in diabetes mellitus, plasma ET-1 levels were measured in two groups of diabetic patients: A) 47 patients with non-insulin dependent diabetes mellitus (NIDDM) and retinopathy (28 M, 19 F; mean age 60.7+/-8.5 yrs) but without nephropathy (microalbuminuria < 30 mg/day) and hypertension (SBP < 140, DBP < 90 mmHg); group A was divided in three subgroups based on the severity of retinopathy: a) 16 with background retinopathy; b) 21 with pre-proliferative retinopathy; c) 10 with proliferative retinopathy. B) 8 patients with insulin-dependent diabetes mellitus (IDDM) recently diagnosed (6 M, 2 F; 16.4+/-3.8 yrs) without complications. C) 28 healthy subjects (HS) (16 M, 12 F; 47.8+/-11.8 yrs) as controls. In the NIDDM group the ET-1 concentration was significantly higher (17.3+/-2.4 pg/ml) than both in the HS (8+/-4.7 pg/ml) and IDDM patients (10.2+/-3.7 pg/ml) (p < 0.0001). In the subgroups with retinopathy the ET-1 levels were a) 15.1+/-4.3 pg/ml; b) 22.2+/-6.8 pg/ml and c) 16.6+/-5.1 pg/ml. These values were significantly elevated as compared to HS (p<0.001; p < 0.0001; p < 0.002, respectively), being the highest levels of ET-1 observed in the NIDDM patients with pre-proliferative retinopathy. In conclusion our study revealed that the ET-1 concentrations are elevated in NIDDM patients with retinopathy especially in those patients with pre-proliferative retinopathy.

Aged↗

Plasma endothelin-1 concentrations in patients with coronary artery disease during stress test before and after nisoldipine administration.

The purpose of this study was to determine the response of plasma levels of endothelin-1 (ET-1) to dynamic exercise in patients with coronary artery disease and chronic stable angina pectoris and positive exercise tolerance test, before and after treatment with the calcium antagonist nisoldipine (20 mg/day buccally for 7 days). Plasma ET-1 levels and hemodynamic parameters (blood pressure and heart rate) were determined at rest, at peak exercise and recovery. All patients had a positive electrically and clinically stress test and all of the eight patients did not developed ECG signs of myocardial ischemia after nisoldipine administration. Before nisoldipine treatment the plasma ET-1 levels did not increase significantly during exercise. After nisoldipine treatment the plasma ET-1 levels were significantly lower at rest and during exercise compared with those revealed before calcium antagonist treatment. In conclusion our results suggest that in patients with chronic stable angina pectoris the treatment with calcium antagonist nisoldipine reduced ischemia and plasma ET-1 levels.

Adult↗

Serum concentrations of osteocalcin in pregnant women with multinodular thyroid goiter undergoing treatment with levothyroxine.

In this study we measured serum osteocalcin (Bone Gla-Protein) to investigate bone metabolism in pregnant women with multinodular thyroid goiter undergoing treatment with levothyroxine (L-T4). Serum concentration of BGP was measured in 18 pregnant women and in 20 non-pregnant women (ages raging from 21-34 years) receiving L-T4 (75-125 micrograms/day). Venous blood samples for RIA determination of serum BGP, plasma thyroid hormone (T3, T4, free T3, free T4) and TSH were collected from the two groups. The samples of the pregnant women group were collected before pregnancy (at the moment the disease was diagnosed without L-T4 therapy) during pregnancy (at the 3rd, 6th and 9th month) and one month after delivery. The normal TSH levels (measured with Irma method) before pregnancy, were significantly reduced during treatment with L-T4 during pregnancy and after delivery (p < 0.005), respectively. Also in the control group TSH levels were reduced during treatment. Serial measurement of serum BGP before pregnancy, (3.4 +/- 1 ng/ml) during pregnancy (3rd: 4.2 +/- 1.5 ng/ml; 6th: 4.2 +/- 1.4 ng/ml; 9th: 2.8 +/- 1.6 ng ml, month respectively) and one month after delivery (3.5 +/- 1.3 ng/ml) did not demonstrate significant variations. Furthermore, in the control group the BGP levels were 3.2 +/- 1.7 ng/ml. There was no correlation between BGP, thyroid hormones and TSH in these groups. These data indicate that the administration of moderate doses of L-T4 in pregnant and in non-pregnant women did not modify the serum BGP levels.

Adult↗

Dynamic exercise induces elevation of plasma levels of endothelin-1 in patients with coronary artery disease.

In this investigation the response of endothelin-1 plasma levels to dynamic exercise in patients with coronary artery disease (CAD) was studied. The study population consisted of 20 patients with CAD, 16 men and 4 women (mean age 53 +/- 8.6 years). Seven normal volunteers all men (mean age 53.4 +/- 4.4 years) were studied as a control group. Seven patients had prior myocardial infarction. All patients and controls exercised on a multi-stage bicycle ergometer; plasma endothelin-1 levels and hemodynamic indices were measured at rest, at peak exercise, and at two and six minutes after exercise. Of the 20 patients examined, 7 (35%) showed electrocardiogrpahic (ECG) signs of myocardial ischemia during the stress test. The mean plasma endothelin-1 concentration increased significantly from 7.8 +/- 3.0 to 13.6 +/- 3.5 pg/mL at exercise peak (P < 0.05) only in patients who did not show ECG signs of myocardial ischemia and returned to baseline values during recovery (six minutes) (9.4 +/- 2.1 pg/mL). In normal subjects baseline endothelin-1 levels (9.4 +/- 4.2 pg/mL) were not significantly altered at peak exercise (10.8 +/- 4.7 pg/mL) and at recovery (11.3 +/- 3.6 pg/mL). The hemodynamic parameters were not correlated with the plasma endothelin-1 levels before, during, and after exercise in all groups. The present study demonstrated that the plasma levels of endothelin-1 in patients with CAD increased significantly during stress testing.

Adult↗

Circulating endothelin-1 levels increase during euglycemic hyperinsulinemic clamp in lean NIDDM men.

OBJECTIVE: To evaluate whether or not insulin stimulates endothelin (ET)-1 secretion in vivo. RESEARCH DESIGN AND METHODS: Plasma ET-1 levels were evaluated in 16 lean normotensive men with non-insulin-dependent diabetes mellitus (NIDDM) (mean age 50.3 +/- 4.1 years) during either a 2-h euglycemic hyperinsulinemic clamp (40 mU insulin.m-2.min-1) or placebo infusion (50 ml isotonic saline) according to a single-blind randomized crossover protocol. RESULTS: Circulating ET-1 levels increased during the euglycemic hyperinsulinemic clamp (from 0.88 +/- 0.38 pg/ml at time 0 to 1.66 +/- 0.22 pg/ml and 1.89 +/- 0.99 pg/ml at 60 and 120 min, respectively [P < 0.05 vs. time 0]) and returned to baseline levels after the discontinuation of insulin infusion (0.71 +/- 0.22 pg/ml after a 30-min period of recovery [NS]). Compared with placebo, the euglycemic hyperinsulinemic clamp induced a significant increase in plasma ET-1 levels at 60 min (P < 0.0001) and 120 min (P < 0.0001). Changes in basal insulin levels and corresponding changes in circulating ET-1 levels after a 2-h euglycemic hyperinsulinemic clamp were significantly correlated (r = 0.771, P < 0.0001). A possible unfavorable effect of ET-1 on the tissue sensitivity to insulin-stimulated glucose uptake was suggested by the presence of a negative correlation between total glucose uptake and baseline ET-1 levels (r = -0.498, P < 0.05). CONCLUSIONS: Our findings indicate that circulating ET-1 levels significantly increase during euglycemic hyperinsulinemic clamp in men with NIDDM. The negative correlation between total glucose uptake and circulating ET-1 levels suggests that the peptide might exert negative effects on the insulin sensitivity of target tissues. The consequent increase in insulin secretion as well as the insulin-related ET-1 release from endothelial cells could favor the development of diabetes-related vascular lesions.

Blood Glucose↗

Plasma endogenous digoxin-like substance levels are dependent on blood O2 in man.

1. Recently, we have demonstrated that hypoxic breathing is followed by an increase in plasma digoxin-like substance in normal men. 2. This study was undertaken in order to evaluate whether or not a low arterial O2 partial pressure is combined with an increase in plasma digoxin-like substance in chronic pathological conditions also. 3. Sixteen male patients (mean age 53.1 +/- 3.7 years) affected by chronic obstructive pulmonary disease of a mild stage were studied. They were further subdivided according to their arterial O2 partial pressure into 'mild hypoxic' (n = 8, mean age 52.5 +/- 2.7 years), with an arterial O2 partial pressure between 66 and 75 mmHg, and 'severe hypoxic' (n = 8, mean age 54.3 +/- 5.1 years), with an arterial O2 partial pressure < or = 65 mmHg, groups. Seven healthy men (mean age 48.5 +/- 4.8 years) voluntarily participated as the control group. 4. Plasma digoxin-like substance levels were significantly higher in 'severe hypoxic' patients (203.5 +/- 9.9 pg/ml) than in both 'mild hypoxic' patients (169.5 +/- 31.4 pg/ml, P < 0.02) and normal subjects (158.9 +/- 12.4 pg/ml, P < 0.0001) and were directly correlated with urinary Na+ excretion (severe hypoxic group, r = 0.756, P < 0.007; mild hypoxic group, r = 0.789, P < 0.02). Considering the two hypoxic groups together, plasma digoxin-like substance levels were negatively correlated with arterial O2 partial pressure (r = -0.740, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Abnormal atrial natriuretic peptide and renal responses to saline infusion in nonmodulating essential hypertensive patients.

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.

Adult↗

Unilateral adrenal hypersecretion of both aldosterone and cortisol in two first cousins with a syndrome of mineralocorticoid excess but without signs of hypercortisolism.

A 38 year old woman and her first cousin, a 41 year old man, presented both with hypertension, hypokalemia, hyperaldosteronism, and low plasma renin activity in our Hospital. In both patients, plasma and urine aldosterone were constantly above the normal range, even on a high NaCl diet (250 mEq/day), while the plasma aldosterone response to postural changes was normal. In the female patient abdominal ultrasonic scan, CT scan, MRI, and adrenal gland phlebography were normal, but blood from the left adrenal vein contained 1002 pg/ml of aldosterone, versus 91 pg/ml in the contralateral one. Interestingly, the secretion of cortisol was also lateralized (plasma cortisol levels being of 28.8 mcg% in the left, 2.3 mcg% in the right adrenal gland), although neither clinical nor laboratory signs of hypercortisolism were present. Spironolactone treatment (100 mg/daily) completely reversed the syndrome of mineralocorticoid excess. After 2 years, patient has normal blood pressure and serum K+ levels.

Adrenal Glands↗

Effects of atrial natriuretic factor infusion on plasma prorenin levels in hypertensive males.

To evaluate the influence of atrial natriuretic factor (ANF) infusion on circulating prorenin, 20 essential hypertensive males, aged between 40 and 60 years, were studied. After 2 weeks under normal sodium intake (120 mmol NaCl per day), patients were randomly assigned to receive either ANF (0.01 fmol/Kg/min) (n.12 patients) or its vehicle (50 mL of isotonic saline) (n.8 patients) over a period of 60 minutes. Blood samples for plasma renin activity (PRA), prorenin and aldosterone (PAC) were taken at time -60, 0, 20, 40, 60, 120, 180, 240 minutes (infusion time: from 0 to 60 minutes). PRA and PAC decreased during the ANF infusion (PRA: from 0.33 +/- 0.05 ng/L/s at time 0 to 0.10 +/- 0.06 ng/L/s at 60 minutes, p < 0.0001; PAC: from 389.2 +/- 99.8 pmol/L at time 0 to 148.7 +/- 44.3 pmol/L at 60 minutes, p < 0.0001), while returned immediately to baseline levels after the infusion was stopped (PRA: 0.37 +/- 0.11 ng/L/s at 180 minutes, PAC: 251.6 +/- 72.1 pmol/L at time 180 minutes). On the contrary, plasma prorenin increased during ANF infusion (from 1.66 +/- 0.58 ng/L/s at time 0 to 2.44 +/- 0.72 ng/L/s at 60 minutes, p < 0.05), and returned to baseline levels after the end of the infusion (1.86 +/- 0.83 ng/L/s at 180 minutes). These data indicate that ANF infusion may alter only the circulating levels of active renin, without affecting plasma prorenin secretion.

Adult↗

Renal sodium excretory function during acute oxygen administration.

To evaluate the effect of O2 administration and O2 removal on renal Na+ excretion, 12 hypoxemic eucapnic patients affected by chronic obstructive pulmonary disease (COPD) and 9 normal subjects were studied. After 1 h in the supine position, O2 was administered for 3 h by a tight-fitting face-mask. Urine and blood samples for renal Na+ excretion evaluation were taken at times 0, 60 and 180 min. After O2 removal both the blood and the urine samples were taken again for a further 3 h. In normal subjects, urinary Na+ excretion did not vary after both O2 administration and removal. On the contrary, in patients affected by COPD renal Na+ excretion significantly increased during O2 administration (from basal values of 0.08 +/- 0.01 to 0.17 +/- 0.02 mEq/min at 180 min, p < 0.05), and returned to baseline levels (0.13 +/- 0.03 mEq/min) after 3 h from O2 removal. The basal fractional excretion of filtered Na+ was significant lower in hypoxemic patients than in normal subjects (0.72 +/- 0.3% in patients with COPD vs. 0.95 +/- 0.7% in normal subjects, p < 0.05), while, at the end of O2 administration, it became higher in patients with COPD than in controls (1.62 +/- 0.4% in patients with COPD vs. 0.89 +/- 0.5 in control subjects, p < 0.001). In conclusion, our findings showed an oxygen-related increase of both the urinary Na+ excretion and the fractional excretion of filtered sodium in patients affected by COPD.

Carbon Dioxide↗

Effects of short-time insulin suppression on renal sodium excretion in type II diabetic hypertensives.

The effects of a short-time insulin suppression on Na+ excretion were evaluated in 9 type II diabetic hypertensive males. All patients had a body mass index < 26 and normal plasma lipid levels. After 2 weeks under constant NaCl intake (120 mEq of NaCl daily) either octreotide, a somatostatin analogue, or its vehicle were infused in a forearm vein during acute volume expansion (0.20 ml/kg/min isotonic saline given intravenously over a period of 30 min). A double blind randomized cross-over design was followed, and each patient was given both infusions at one week interval. Blood and urine samples for the evaluation of plasma insulin and serum and urine Na+ were taken at time-30, 0, 30, 60, 90, 120, and 240 min. Our data showed that octreotide completely suppressed insulin levels (from time 0 to 60 min). During acute volume expansion+octreotide, Na+ excretion was 0.20 +/- 0.15 mEq/min at time 0, 0.23 +/- 0.21 mEq/min at time 30, 0.64 +/- 0.24 mEq/min at 60 (p < 0.05 vs time 0), 0.71 +/- 0.35 mEq/min at 90 (p < 0.05 vs time 0), 0.78 +/- 0.10 mEq/min at 120 (p < 0.01 vs time 0) and 0.71 +/- 0.12 mEq/min at 240 min (p < 0.05 vs time 0). As compared to acute volume expansion alone, octreotide induced a significant increase of Na+ excretion at 60 and 90 min (p < 0.05). In conclusion, a short-time insulin suppression, as obtained by the somatostatin analogue octreotide, enhances the natriuretic response to intravenous saline load in lean type II diabetic hypertensives.

Adult↗

Amlodipine in ambulatory hypertensive patients: humoral and haemodynamic effects.

In order to evaluate the mid-term effects of amlodipine, a 1,4-dihydropyridine calcium antagonist, as well as its effects on the renin-angiotensin-aldosterone system (RAAS), on water and electrolyte balance, on urinary excretion of albumin (UAE) and on lipid metabolism, thirteen hypertensive patients (2 M, 11 F, mean age 54 years) were studied in the course of 24 weeks of therapy with amlodipine at 5-10 mg/day. Pre-therapy and periodically during therapy, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded in the sitting orthostatic positions (2 measurements). Laboratory tests were performed at times O and at 24 wks with the patients fasting for at least 12 h in the recumbent position. The tests included: plasma renin activity (PRA), plasma aldosterone (PA), serum angiotensin converting enzyme (SACE), blood urea nitrogen (BUN), blood creatinine, plasma electrolytes (Na, K, Cl), triglycerides, total cholesterol (TC) and HDL-cholesterol (HDLC), along with 24-h urine samples (with sterile urine) to determine UAE. The results of this study demonstrate that SBP, DBP and HR were significantly reduced during the 24 wks of therapy. The water and electrolyte and renal function were not modified. After treatment the levels of TC were significantly reduced. No change was observed in the RAAS, while the mean levels of UAE were reduced though not significantly. In conclusion, amlodipine was shown to be effective for the therapy of hypertension; it does not cause reflex tachycardia even in mid-term therapy and was effective in reducing TC levels.

Adult↗

[The behavior of serum angiotensin-converting enzyme in normotensive subjects, in subjects with essential hypertension and in subjects with primary hyperaldosteronism on the orthostatic test].

The results of this study demonstrate that only in healthy normotensive subjects during extended orthostatism that the renin-angiotensin-aldosterone system remains integral and is characterized by a significant increase in serum angiotensin-converting enzyme (SACE), plasma renin activity (PRA) and plasma aldosterone (PA). SACE modification do not seems to directly follow that of PRA (as shown by the absence of a direct correlation between SACE and PRA). In essential hypertension, the behavior of SACE seems to change, without demonstrating a significant increase in the mean levels of this enzyme. Finally in hypertension of known origin, such as primary hyperaldosteronism, the low levels of SACE in the recumbent position (not stimulated by orthostatism) seem to depend (by mechanism of negative biofeedback) on the increased serum levels of PA, which is moreover verified in the same group for PRA.

Adult↗

[Behavior of plasma levels of endothelin 1 and noradrenaline in patients with stable angina during the cold pressor test].

The aim of this study was to evaluate the behaviour of plasma endothelin-1 (ET-1) and norepinephrine (NE) levels in patients with stable angina during a sympathetic stimulation test as the cold pressor test. We enrolled in the study 29 subjects: 14 patients with stable angina (all men, mean age 58.3 +/- 7.3 years) and 15 healthy subjects (all men, mean age 54 +/- 5 years). All patients with stable angina had a stenosis of the coronary arteries (at least 70% of the stenosis in one of the coronary arteries) confirmed by angiography. Before (-15 min; 0 min) during (+2 min) and after the cold pressor test (+5 min, +10 min, +20 min, +30 min) were measured the blood pressure and the heart rate. At the same time were collected venous samples for the ET-1 and NE determination. ET-1 levels increased only in the patients with stable angina (ET-1: O' = 9.8 +/- 3.7 pg/ml; +2' = 11.1 +/- 4.5 pg/ml; +10' = 14.8 +/- 7.1 pg/ml; +20' = 11.6 +/- 5.1 pg/ml; p < 0.05 vs 0', +2'; +20'). The NE levels increased in both groups (NE stable angina: 0' = 105 +/- 31 pg/ml; +2' = 206 +/- 127 pg/ml; +5' = 223 +/- 135 pg/ml; p < .05 vs +2', +5'); (NE healthy subjects 0' = 85 +/- 10 pg/ml; +2' 165 +/- 49 pg/ml; p < 0.05 vs + 2'). In conclusion, our study showed that cold pressor test is a stimulus for the sympathetic system in both groups. The increased levels of ET-1 detected only in the patients with stable angina suggest that this peptide can take part to the pathogenesis of the coronary artery disease.

Aged↗