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Biomedical subjects

A Soro

Publications and source records attributed to A Soro.

At least 55 records · Page 3Linked to original sources
PubMed1990

Ventricular inversion with truncus arteriosus.

We report clinical, angiocardiographic, and anatomic findings of an infant with ventricular inversion (atrioventricular discordance) and truncus arteriosus. The patient was in congestive heart failure and the injections into the left ventricle, right ventricle, and truncus arteriosus allowed a precise diagnosis. The autopsy confirmed this very unusual combination of anomalies and in particular it showed a truncus type 2 completely surrounded by muscular infundibulum and mainly aligned with the right ventricle. Surgical correction of this malformation is a challenge and so far, to our knowledge, has never been reported in the literature.

Abnormalities, Multiple↗
PubMed1990

[Effect of menstrual cycle hormones on cation transport in the red-cell membrane].

Erythrocyte cation transport, plasma prorenin and renin and sexual hormones were sequentially evaluated in 12 normal volunteers over the menstrual cycle. Na-K cotransport and Na-Li countertransport raised in 6 out of 12 subjects in synchronization with the ovulatory phase. When the maximal % variation (ovulatory phase) versus baseline (follicular phase) of the Na-K cotransport was plotted versus the maximal % increment of oestrogens. A direct, highly significant inverse correlation was observed (r = 0.904, p less than 0.001). Moreover, a highly significant inverse correlation between plasma prorenin and intraerythrocyte Na (r = -0.857, p less than 0.001) in the follicular phase was found. Our data suggest that erythrocyte cation transport can be influenced by sexual hormones in human.

Adult↗
PubMed1990

[Effect of chronic enalapril treatment on prorenin, renin and sex hormones during the menstrual cycle in patients with essential hypertension].

Since angiotensin II seems to be involved in the process of ovulation we studied the effect of chronic enalapril on plasma prorenin, renin, estradiol, progesterone, LH and FSH during the menstrual cycle in ten essential hypertensive women. Our data show that peripheral blockade of A I conversion does not affect the pituitary guidance and the ovarian hormonal response of the menstrual cycle and, we can speculate, that it does not interfere with the process of ovulation.

Adult↗
PubMed1990

[Protective effect of a calcium antagonist against renal vasoconstriction induced by endothelin in the normotensive rat].

We studied the effect of nifedipine, a dihydropyridine calcium antagonist, on the hemodynamic changes induced by endothelin, in awake normotensive rats. Endothelin (0.07-1.40 nmol/kg, e.v.) caused an initial hypotensive effect, followed by long lasting hypertension. Renal blood flow was reduced immediately and still remained below basal levels, at 30 minutes after endothelin injection. Nifedipine (1 mg/kg, i.p.) significantly prevented the effect of endothelin on mean blood pressure and induced a right-ward shift in the dose response curve of renal hemodynamic changes induced by endothelin. We conclude that treatment with calcium antagonist could be very useful in all those conditions in which systemic and regional vasocostriction is provoked by endothelin.

Animals↗
PubMed1990

Effects of enalapril in normotensive patients with stable effort angina: a double blind, placebo controlled study.

To assess the anti-anginal and anti-ischaemic efficacy of the ACE-inhibitor enalapril in normotensive coronary patients, a double-blind, cross-over, placebo-controlled study was performed. Eight male patients, aged 45-68 years, with stable effort angina were given enalapril (10 mg) once a day or placebo for 7 days. Maximal exercise stress tests 10w/min in the upright position were performed at the end of each period. In comparison to placebo, enalapril increased significantly 1 mm of ST depression time and decreased significantly ST depression at maximal common work. Moreover, enalapril increased significantly the angina threshold and exercise duration. Three of the eight patients ended the exercise without pain. The rate-pressure product was not significantly modified at any time. Thus, the anti-ischaemic and anti-anginal activity may be due to an increase of coronary blood flow, rather than a reduction of MVO2 consumption.

Aged↗
PubMed1990

[Effects of indenolol on left ventricular mass in patients with essential arterial hypertension].

This study evaluated the effect of long-term antihypertensive therapy with indenolol, a beta blocking agent with beta 2 stimulating activity, its antihypertensive hemodynamic mechanism and its effect on hypertensive left ventricular (LV) hypertrophy. Fourteen hypertensive patients, mean age of 48 years, were serially studied during 12- month therapy with indenolol (60-120 mg daily), by recording blood pressure, electrocardiogram and echocardiogram. Blood pressure, heart rate and cardiac output significantly decreased after 1 months of therapy, LV posterior wall thickness decreased after 6 months, interventricular septum thickness and LV mass decreased after 12 months. LV fractional shortening did not change throughout the study. Blood pressure normalized (less than or equal to 140/90 mmHg) in 50% of the patients; LV mass normalized in 40% of the patients. In conclusion, indenolol was an effective antihypertensive agent, also in the long-term treatment. Its antihypertensive hemodynamic effect seems to be due mainly to a reduction in cardiac output. Indenolol caused a regression of LV hypertensive hypertrophy without impairment of LV systolic function.

Adult↗
PubMed1989

Circulating prorenin and renin in response to intravenous adrenocorticotrophic hormone in essential hypertension.

Plasma prorenin and renin changes after a bolus injection of 25 U intravenous adrenocorticotrophic hormone (ACTH, synacthen) were studied in seven untreated uncomplicated essential hypertensives over a period of 24 h. Plasma prorenin did not change significantly during the study, whereas renin after 24 h was higher than at baseline (4.3 +/- 0.6 versus 2.3 +/- 0.9 ng angiotensin I (Ang I)/ml per h, P less than 0.01). We conclude that endogenous glucocorticoid stimulation induced by exogenous ACTH and ACTH itself seem to induce a secondary or tertiary rather than a primary effect on the human renin gene.

Adrenocorticotropic Hormone↗
PubMed1989

Correlates of atrial natriuretic factor in chronic renal failure.

Plasma atrial natriuretic factor (ANF), blood pressure, age, plasma renin activity and creatinine were measured in 50 normal volunteers, 141 essential hypertensives, 35 patients with chronic renal failure who had never been dialysed and 27 patients with end-stage renal failure on constant haemodialysis. Plasma ANF was correlated positively with age in the normal group (r = 0.52, P less than 0.01) and with blood pressure in the essential hypertensives (r = 0.50, P less than 0.001), and negatively with renin in the normal and end-stage renal failure patients (r = -0.47, r = -0.34; P less than 0.01, P less than 0.05, respectively). When patients without left ventricular hypertrophy were matched for age and blood pressure, plasma ANF was significantly different between the essential hypertensives and the normal and end-stage renal failure patients (16 +/- 1, 38 +/- 6 and 148 +/- 24 pmol/l, respectively; P less than 0.001). Cardiac factors are therefore not the only determinant of circulating plasma ANF in humans with chronic renal failure.

Aging↗
PubMed1989

Effect of endothelin on regional hemodynamics and renal function in awake normotensive rats.

The effects of endothelin on regional hemodynamics and renal function were studied in awake normotensive rats. Intravenous injection of endothelin (700 pmol/kg) transiently lowered mean blood pressure (from 108 +/- 2 to 84 +/- 2 mm Hg, p less than 0.01), due to a reduction in total vascular resistance (38 +/- 1%, p less than 0.01), and increased stroke volume (29 +/- 5%, p less than 0.01) and heart rate (from 399 +/- 18 to 447 +/- 18 bpm, p less than 0.05); mesenteric and renal blood flow was reduced (37 +/- 13, p less than 0.05 and 63 +/- 5%, p less than 0.01), whereas carotid blood flow was increased (78 +/- 5%, p less than 0.01). This effect was followed by long-lasting hypertension due to increased total vascular resistance (112 +/- 19%, p less than 0.01); stroke volume, mesenteric, and renal blood flow were reduced (34 +/- 5, 41 +/- 4, and 58 +/- 4%, respectively, p less than 0.05) and carotid blood flow returned to basal levels. Bilateral nephrectomy enhanced the initial hypotensive effect. Pretreatment with nifedipine blocked the hypertensive effect, whereas bilateral nephrectomy did not. A subpressor dose of endothelin (70 pmol/kg) had no effect on stroke volume, mesenteric blood flow, glomerular filtration rate, and plasma renin activity; carotid blood flow was transiently increased (48 +/- 16%, p less than 0.05), then returned to basal levels; renal blood flow decreased (22 +/- 6 and 15 +/- 4% at 30 s and 10 min, respectively p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1989

Stimulation of plasma inactive renin by dexamethasone in the cat.

An inactive form of renin in human plasma is the biosynthetic precursor, prorenin. The cat is a good animal model for studies of inactive renin. The gene for human renin contains sequences homologous to the glucocorticoid consensus sequence. The response of cat plasma (active and inactive renin) and of angiotensinogen to administration of dexamethasone (0.5 mg/kg im, daily) was studied in ketamine-sedated cats (20 mg/kg im). Inactive renin increased by twofold after 7 days of dexamethasone (P less than 0.01). After a 7-day recovery period, it returned to base line. Active renin did not change. Angiotensinogen fell by 35% (P less than 0.01). The time course of the selective increase of plasma inactive renin showed that inactive renin began to rise after 2 days, peaking after 5 days. Ketamine alone induced inactive renin to rise slightly but significantly (P less than 0.05), although the magnitude of the increment was much less than that observed in ketamine-sedated cats receiving dexamethasone (P less than 0.01). Active renin did not change, whereas angiotensinogen was reduced by 25% (P less than 0.01). Our findings support the hypothesis that glucocorticoids might have a selective role in the synthesis and/or secretion of the precursor of renin, at least in the cat.

Angiotensinogen↗
PubMed1989

[Erythrocyte cation transport in arterial hypertension: interrelation with the renin-angiotensin-aldosterone system and the atrial natriuretic factor].

Red cell membrane Na(+)-K+ transport systems, renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic factor (ANF) were studied in a group of 50 mild essential hypertensive patients (n = 25 for each group) age, sex and blood pressure matched. Na(+)-K+ ATPase and intracellular Na+ (Na+ i) were significantly different between the two groups (p less than 0.01). A slight difference was also seen for the Na(+)-K+ cotransport (p less than 0.05) as a likely consequence of the differences in the methodology of Na+ charge to study its efflux from the red cells in vitro. A negative correlation (r = -0.47, p less than 0.01) was observed between ANF and Na(+)-K+ cotransport suggesting an interrelationship of the two systems in the homeostasis in body fluid and electrolytes.

Adult↗
PubMed1989

[Possible activation of human prorenin by contact with the cell membrane].

Semipurified human kidney prorenin was exposed in vitro to a mixture of lipids mimicking the composition of the inner leaflet of the cell membrane, in the presence of semipurified human angiotensinogen at a concentration of 1/4 Km. Prorenin was activated in a time-dependent manner over a period of 60 min. This lipid-dependent activation was completely reversed thereafter. Pre-incubation with anti-renin serum completely prevented this activated prorenin-dependent generation of angiotensin I. Our data suggest that human prorenin can be reversibly activated by contact with the cell membrane.

Angiotensin I↗
PubMed1989

[Postoperative constrictive pericarditis].

Seven cases of postoperative constrictive pericarditis (PCP) were discovered in a retrospective study of patients given heart surgery in a hospital receiving patients from all over Italy in 1970-85. Five of those patients had received surgery for chronic rheumatic heart disease, 2 for congenital heart defects. Four had received a second heart operation before the pericardial condition was recognised. All were females and all presented systemic venous hypertension (one of them only after acute doses of physiological solution) with thickening of the pericardial layers revealed by sonography. In six cases the electrocardiographic ventricular complexes were normal or increased in amplitude and the heart/chest ratio was greater than 0.55. Pericardial knock was masked by natural or artificial atrioventricular valve opening noises in 6 cases. In one case only there were pericardial calcifications or signs of an earlier postpericardiotomy syndrome. The haemodynamic investigation revealed signs of ventricular diastolic constriction in 6 patients. Three patients died from complications of cardiac cirrhosis: 2 of them had previously received partial pericardiectomy. Another two, given the same operation, preserved a reasonable functional capacity 5 and 10 years after the pericardiectomy. One patient in NYHA functional class III has so far refused haemodynamic assessment (and surgical treatment) of the pericardial disease. Finally, the last patient complains only of attacks of heart palpitation caused by atrial flutter and controlled by antiarrhythmic treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effects of nitrendipine on blood pressure, renin-angiotensin system, and kidney function in essential hypertension.

The effects of nitrendipine (10 mg b.i.d.) on blood pressure, renin-angiotensin-aldosterone system, and kidney function (by means of glomerular and tubular function) were studied in comparison to captopril (50 mg b.i.d.) and to nitrendipine (10 mg q.d.) + captopril (25 mg b.i.d.) in 30 untreated essential mild-to-moderate hypertensives. The blood pressure lowering effect was similar with either regimen. Nitrendipine showed an acute and chronic natriuretic effect not accompanied by modifications of kidney function. All regimens were well tolerated by the patients without any appreciable side effects over the 4-week study period.

Adult↗
PubMed1988

Plasma clearance and effects of alpha-hANP infused in patients with end-stage renal failure.

The effects and clearance of synthetic atrial natriuretic peptide (alpha-hANP) were investigated in eight patients with end-stage renal failure and six normal volunteers. ANP or vehicle was infused for 1 h at 10 pmol.kg-1.min-1 in random order on two separate occasions. During ANP infusions in end-stage renal patients, microhematocrit rose by 9.8 +/- 2% (P less than 0.005, n = 8), from base-line values of 0.24 +/- 0.02. Serum protein and albumin rose consistently. In contrast, during placebo infusions, no significant changes were seen. Blood pressure, heart rate, plasma renin concentration, serum creatinine, and electrolytes did not change significantly during either study phase. In end-stage renal failure patients, metabolic clearance rate of infused ANP was 1.04 +/- 0.095 l/min and its plasma half-life was 4 min 34 s. In normal volunteers, metabolic clearance rate was 2.6 l/min and its plasma half-life 3 min 30 s. The data suggest that ANP promotes contraction of plasma volume via a mechanism independent of renal function and also indicate that the kidney is not the only organ involved in the ANP metabolism.

Adult↗
PubMed1987

Urinary kallikrein excretion can predict the blood pressure response to a single oral dose of captopril.

The antihypertensive efficacy of ACE inhibitors depends in theory from the blockade of the angiotensin II formation but also from the inhibition of kinin breakdown. To test whether a blunted activity of the kallikrein-kinin system might account for the failure of ACE inhibitors in lowering BP in patients in whom the renin-angiotensin system is not enhanced, thirty-one essential hypertensives with normal or low PRA were evaluated before and after a single oral dose (50 mg) of captopril. A significant fall both in systolic and diastolic blood pressure (BP) was obtained in the subgroup of patients who were classified as "normal kallikrein hypertensives" according to whether their pretreatment urinary kallikrein excretion was within the normal range, while no significant change in BP was observed in "low kallikrein hypertensives". Furthermore the mean percentage fall in mean BP, throughout the 2 hours following captopril administration, was significantly related to the basal value of urinary kallikrein excretion (r = 0.47, p less than 0.05) in the entire group of patients. Our results suggest that a blunted activity of the kallikrein system might be responsible for failure of captopril in lowering BP in patients in whom the renin-angiotensin system is not pathogenetically implicated.

Administration, Oral↗