[Multiple costal eosinophilic granuloma at an unusual age].
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Eosinophilic Granuloma↗
Biomedical subjects
C Sala
Publications and source records attributed to C Sala.
Effects of angiotensin II blockade on the responses of the pituitary-adrenal axis to corticotropin-releasing factor in humans.
We investigated the possibility that angiotensin II (ANGII) augments the sensitivity of the pituitary to corticotropin releasing factor (CRF) by comparing, in patients with essential hypertension, the responses of plasma adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin activity to a bolus injection of either 0.5 or 1.0 microgram/kg of synthetic ovine CRF in control conditions and after chronic treatment with the converting enzyme inhibitor captopril to block the formation of ANGII; the effects of CRF were examined up to 4 h after its administration. In control studies, we found that the two doses of CRF induced similar increments in ACTH and cortisol, the levels of which remained elevated throughout the studies; these changes were associated with increments in plasma aldosterone that were dose dependent, less pronounced, and of shorter duration and with a slight decrease in plasma renin activity. Captopril treatment increased basal plasma renin activity and lowered plasma aldosterone while leaving basal ACTH and cortisol unchanged. During converting enzyme inhibition, the responses of ACTH and cortisol to CRF were similar to those observed in control studies, whereas the changes in plasma aldosterone and plasma renin activity were, respectively, smaller and greater. From these results, it appears that during ANGII blockade the sensitivity of ACTH to CRF stimulation is unaffected, whereas that of the adrenals to ACTH is selectively reduced at the level of the zona glomerulosa.
Angiotensin II↗
Effectiveness of Sepharose-bound trypsin versus liquid-phase trypsin plus benzamidine for activation of inactive renin in human plasma.
We compared the effectiveness of two techniques involving the use of the enzyme trypsin to activate inactive renin in human plasma. Both these methods were developed to optimize activation with trypsin by preventing the possible destruction of activated renin by trypsin itself. In one method, an antitryptic agent such as benzamidine is added to plasma, concomitantly with trypsin (liquid phase). In the other a low concentration of Sepharose-bound (immobilized) trypsin is used. In six plasma samples we have found that trypsin (1.5 mg/ml) activation, with or without benzamidine (0.8 mg/ml), yielded similar values of activated renin (11.0 +/- 2.7 vs. 11.3 +/- 2.3 ng/ml/hr). However, the addition of immobilized trypsin to pool plasma pretreated with trypsin plus benzamidine caused a further increase in plasma renin activity (PRA); in contrast, the addition of trypsin and benzamidine to pool plasma pretreated with immobilized trypsin caused a decrease in PRA. In 17 plasma samples from patients with essential hypertension we found that the inactive renin values were always higher after treatment with immobilized trypsin than with trypsin plus benzamidine (9.0 +/- 0.7 vs. 6.1 +/- 0.5 ng/ml/hr, P less than 0.01); moreover, there was a positive correlation between the differences in the values of inactive renin measured with the two methods and the values obtained with immobilized trypsin (r = 0.64, P less than 0.01). Therefore, the activation with immobilized trypsin is more effective than that with liquid-phase trypsin, alone or in combination with benzamidine, in converting inactive renin in human plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
Amidines↗
Participation of the renin-angiotensin system in the maintenance of blood pressure during changes in posture in patients with essential hypertension.
To assess whether and how the activation of the renin-angiotensin system that occurs in response to changes in posture contributes to the maintenance of blood pressure, we measured blood pressure, heart rate, plasma noradrenaline and plasma active and inactive renin in patients with essential hypertension in the supine, sitting and standing positions, (each sustained for 30 min), before and after administration of captopril. These studies were performed before and after a brief period of diuretic therapy. Both in the normal and in the sodium depleted state captopril reduced the normal adaptive response of blood pressure to changes in body position, whereas the responses of heart rate and plasma noradrenaline to these stimuli were unaffected by captopril. In contrast, the postural increases in active renin were magnified after captopril while inactive renin was unchanged throughout these acute studies. Our results indicate that during mild but rather prolonged postural stresses the generation of angiotensin by active renin supports blood pressure either through its direct vasoconstrictive effect and/or by potentiating the activity of the sympathetic nervous system. It is unlikely that the changes in active renin depend upon conversion from the inactive form.
Adult↗
Toxicity in man due to stain removers containing 1,2-dichloropropane.
There are reports that 1,2-dichloropropane, a constituent of many commercial solvents and stain removers in Italy, has caused severe liver damage and, sometimes, acute renal failure. Between 1980 and 1983 three cases of 1,2-dichloropropane intoxication (1 by ingestion, 2 by inhalation) were observed. Clinical features included severe liver damage, acute renal failure (2 patients), haemolytic anaemia, and disseminated intravascular coagulation. The most surprising features were haemolytic anaemia and disseminated intravascular coagulation which have not been reported before. The clinical picture was similar despite different modes of exposure.
Acute Kidney Injury↗
Acute and chronic converting enzyme inhibition reduces the vasomotor response to reflex sympathetic activation in man.
Several lines of evidence indicate that angiotensin II (ANG II) may potentiate the vascular response to sympathetic stimulation. However, there are no clear signs that this action of ANG II is physiologically relevant in man. To investigate this problem, we used the lower body negative pressure technique (LBNP, -15 mmHg) to deactivate cardiopulmonary receptors and reflexly stimulate the sympathetic nervous system. The haemodynamic (changes in blood pressure, heart rate, central venous pressure, forearm blood flow) and humoral effects [changes in plasma noradrenaline (PNA) and plasma renin activity (PRA)] of this manoeuvre were examined before and after blockade of angiotensin formation achieved by the administration of the converting enzyme inhibitor, captopril. Studies were performed in patients with essential hypertension in control conditions and after acute and chronic captopril treatment. We found that the reduction in forearm blood flow induced by LBNP was significantly diminished after acute and chronic captopril in spite of the fact that the fall in central venous pressure and the increases in PNA were similar to those observed in control conditions. In contrast, the response of renin to LBNP was enhanced, at least after acute captopril administration. These findings suggest that efficiency of the reflexes originating from the cardiopulmonary receptors is impaired after captopril. Angiotensin II contributes to the vasoconstrictive ability of the sympathetic nervous system, either through a direct vascular action or by enhancing the vascular responsiveness to noradrenaline stimulation. However, this sympathetic facilitatory action of ANG II does not appear to be extended on the adrenergic mechanisms which regulate renin release.
Adult↗
The responses of adrenocorticotrophic hormone and cortisol to insulin-induced hypoglycaemic stress in man are unimpaired during chronic converting enzyme inhibition.
In vitro and animal studies indicate that circulating angiotensin II (ANG II) can stimulate adrenocorticotrophic hormone (ACTH) and cortisol secretion, but it is far from established that ANG II has a physiologically relevant influence on steroidogenesis. We studied the effects of hypoglycaemia induced with insulin injection (0.15 IU/kg) in patients with essential hypertension to answer this question. Hypoglycaemia was induced before and after a short term course of treatment with the converting enzyme inhibitor captopril to obtain a sustained blockade of ANG II formation. Alterations in serum glucose, plasma potassium, plasma ACTH, cortisol, renin activity and aldosterone were examined. In control studies there was a profound fall in serum glucose and plasma potassium after insulin, associated with increments in plasma renin activity, which correlated with those of aldosterone but not with those of ACTH and cortisol. Chronic captopril increased baseline plasma renin activity and lowered baseline aldosterone while leaving ACTH and cortisol unchanged. During converting enzyme inhibition the insulin-induced decrements in glucose and potassium, as well as the increments in ACTH, cortisol and aldosterone, were similar to those observed in control studies, whereas the increments in plasma renin activity were much greater. From these results it does not appear that ANG II has a relevant influence on ACTH and cortisol production, or on their responses to hypoglycaemic stress. Rather, these findings indicate that even under the present experimental conditions ANG II is the primary regulator of aldosterone secretion. However, this function can be taken over by ACTH when the generation of ANG II is blocked.
Adrenocorticotropic Hormone↗
[Adipose tissue metabolism in the menopause].
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Adipose Tissue↗
Effects of haemodialysis on active and inactive renin in nephric and anephric patients.
To investigate the origin, the mechanisms of regulation and the possible biological significance of inactive renin we examined the effects of haemodialysis on plasma active and inactive (cryoactivatable) renin in four anephric and in 10 nephric patients. Before haemodialysis inactive renin was similar in anephric and in the majority of nephric patients; this suggests that the source of the inactive enzyme is predominantly extrarenal. In response to haemodialysis active renin rose significantly in nephric patients whereas inactive renin showed minor and inconsistent increments in both groups. These results indicate that the response of the inactive enzyme to haemodialysis is less than that of its active counterpart and is unaffected by the presence of the kidneys. Therefore, it appears unlikely that inactive renin represents a circulating precursor of active renin.
Adult↗
Dissociation of the effects of alpha 1-adrenergic blockade on blood pressure and renin release in patients with essential hypertension.
Prazosin, a selective antagonist of postsynaptic alpha-adrenoreceptors, was used to investigate the influence mediated by the juxtaglomerular alpha-adrenoreceptors on renin release in man. We studied, in seven patients with essential hypertension, the acute effects of 0.25 mg prazosin, given intravenously, on blood pressure and plasma renin activity, the degree of alpha-blockade induced by the drug being assessed by comparing the increments in blood pressure following a test dose of phenylephrine before and after prazosin administration. We also measured the increments in plasma renin activity in response to beta-adrenergic stimulus consisting of an isoproterenol challenge, before and during the prazosin induced alpha blockade. Prazosin infusion caused, within 20 min, a marked reduction of the pressor response to phenylephrine, a significant increment in plasma renin activity, and no change in blood pressure. The increments in renin in response to isoproterenol were significantly greater, both in absolute and percent values, after rather than before prazosin. These results indicate that the increase in renin during systemic alpha 1-adrenoreceptor blockade may be independent of the fall in blood pressure and support the view that the juxtaglomerular alpha 1-adrenoreceptors participate in the regulation of renin release with an inhibitory action, which antagonizes the stimulating influence of the beta-adrenoreceptors.
Adolescent↗
Time course of the changes in active and cryoactivatable renin in response to acute stimuli before and after diuretic therapy in man.
In order to elucidate whether inactive renin may represent a precursor of the active enzyme we examined the short-term effects of ambulation and of Captopril administration on active and cryoactivatable renin in patients with essential hypertension before and after 5 days of diuretic therapy. We have found that in the large majority of patients before diuretic the increments in active renin in response to these stimuli were moderate and associated with unchanged levels of cryoactivatable renin; significant decrements in cryoactivatable renin were observed only in a small group of patients in whom the increments in active renin induced by ambulation were unusually rapid and marked. Diuretic therapy caused parallel increments in baseline values of active and of cryoactivatable renin and potentiated the response of the active enzyme to ambulation and to Captopril; however, cryoactivatable renin was still unmodified during both the acute stimuli. Thus, it appears that, normally, the rise in active renin induced by ambulation and Captopril administration is associated, both before and after diuretic therapy, with unchanged levels of the inactive enzyme; however, before diuretic, abrupt increments in the demand for active renin can determine changes in opposite direction of inactive renin as if the latter were a precursor of the former.
Adolescent↗
[Dyshomogeneity of the response of cryoactive renin to orthostatism in normotensive and essential hypertensive patients].
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Adult↗
[Dyshomogeneity of responses of cryo-activated renin to orthostatism in normotensive subjects and those with essential hypertension].
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Adult↗
Alpha 1-Adrenoceptor blockade: dissociation of its effects on renin release and arterial blood pressure in man.
1. The possibility that the juxtaglomerular alpha 1-adrenoceptors mediate an inhibitory action on renin release in man was examined in seven patients with essential hypertension, by measuring (i) the acute effects of prazosin (0.25 mg intravenously), a selective alpha 1-adrenoceptor-blocking agent, on arterial pressure and plasma renin activity, the degree of alpha-blockade induced by the drug being assessed by comparing the pressor response with that to a test dose of phenylephrine before and after prazosin administration, and (ii) the increases in plasma renin activity in response to isoprenaline before and during the prazosin-induced alpha-blockade. 2. Twenty minutes after the infusion of prazosin, when the pressor response to phenylephrine was reduced by 80% with respect to control, (i) mean arterial pressure was practically unchanged, (ii) plasma renin activity was almost doubled and (iii) the increases in plasma renin activity in response to isoprenaline were significantly greater, both in absolute and percentage values, than those observed before prazosin. 3. The increments in baseline plasma renin activity induced by prazosin in the absence of decrease in arterial pressure and the enhancement in renin responsiveness to the beta-adrenoceptor stimulus suggest that, in man, the juxtaglomerular alpha 1-adrenoceptors exert a direct, suppressive action on renin release.
Adolescent↗
[Assessment of the zinc risk in thermal zincification factories: environmental monitoring].
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Air Pollutants↗
Time-course of the anti-hypertensive action of atenolol: comparison of response to first dose and to maintained oral administration.
To show whether repeated administration of atenolol for several days would influence its pharmacokinetic parameters and the extent and duration of the pharmacologic responses, the plasma level of atenolol and changes in heart rate, blood pressure and plasma renin activity were measured in 12 hypertensive patients at various times of day (9 a. m., 12 noon, 3 p. m. and 7 p. m.) after oral administration of the first dose of atenolol 100 mg, again during the 7th and 14th days of continued once-daily administration of the same dose, and finally during the three days following withdrawal of the drug. The peak plasma concentration of atenolol (about 600 ng/ml) was found 3 h after administration of the first dose, and measurable amounts (50-70 ng/ml) were found after 24 h. None of the pharmacokinetic characteristics were changed by administration of a single daily dose for two weeks. After withdrawal of the drug, detectable amounts of atenolol were found in plasma for at least 48 h. The first dose of atenolol caused prompt (3 h) and prolonged (up to 24 h) lowering of supine and standing systolic and diastolic blood pressures, slowing of supine and standing heart rate, reduction of the blood pressure and heart rate responses to dynamic exercise, and a decrease in plasma renin activity. The extent and time-course of all these responses were not influenced by repeated once-daily administration of the 100 mg dose for two weeks. Most of the effects continued during the withdrawal days, the lowering of blood pressure being somewhat more prolonged than the slowing of heart rate. It is concluded that a once-daily dose of atenolol 100 mg decreases blood pressure and heart rate throughout the following 24 h, without excessive daily fluctuation in its effects, and without signs of tolerance or accumulation.
Administration, Oral↗
Antihypertensive and renal effects of orally administered verapamil.
In 12 in-patients with moderate uncomplicated hypertension, maintained on constant sodium intake for 15 days, single-blind oral administration of verapamil 80-160 mg t.i.d. for 10 days had a significant antihypertensive effect: in the supine position systolic blood pressure decreased from 177 +/- 5 to 150 +/- 3 mmHg, and diastolic pressure from 111 +/- 3 to 96 +/- 2 mmHg; standing values were similarly lowered from 171 +/- 7 to 143 +/- 4 mmHg, systolic, and from 118 +/- 4 to 97 +/- 2 mmHg, diastolic. The heart rate did not show any significant change (from 79 +/- 3 to 77 +/- 2 beats/min, supine, and from 92 +/- 3 to 87 +/- 3 beats/min, upright). The antihypertensive effect was uniform throughout the day, being similar 2, 3, 6 and 8 h after administration of a dose. Dynamic exercise (75-100 watts on a cycle-ergometer) caused identical increases in arterial pressure and heart rate on the last day of placebo and again on the last day with verapamil, but the peak levels of systolic pressure reached during exercise were lower after verapamil than with placebo, because of the lower blood pressure before exercise. Reduction of arterial pressure by verapamil was not accompanied by increased plasma renin activity, or by renal retention of sodium and water: there was a small increase in sodium excretion, at least during the first days of verapamil administration (from 107 +/- 15 to 113 +/- 15 mEq Na+/day), and a slight significant reduction in body weight (from 74.2 +/- 3.7 to 73.5 +/- 3.7 kg). It is concluded that oral administration of verapamil significantly lowers blood pressure without simultaneously inducing cardiac stimulation, renin secretion or salt and water retention.
Adult↗
Dose-response curve and time course of the antihypertensive effect of SKF 92 657, a beta-receptor-blocking and vasodilating compound.
1. The antihypertensive effect of the new drug, SKF 92 657, a hydrazinopyridazine derivative, possessing both beta-adrenoreceptor-blocking and vasodilating properties, was investigated in essential hypertension. 2. Single oral doses of 1.0 or 2.0 mg/kg did not produce any consistent decrease in blood pressure; 4.0 mg/kg was the threshold dose for a mild but not significant blood pressure reduction, whereas 8.0 mg/kg caused a significant and marked blood pressure decrease without clinically relevant changes in heart rate. 3. Continued administration of the drug for 7 days induced a significant and uniform reduction in blood pressure without tachycardia. The increase in systolic blood pressure and in heart rate caused by dynamic exercise was left unaffected by the drug.
Adrenergic beta-Antagonists↗