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Biomedical subjects

N Glorioso

Publications and source records attributed to N Glorioso.

At least 109 records · Page 6Linked to original sources
PubMed1985

High prevalence of cardiovascular diseases and enhanced activity of the renin-angiotensin system in psoriatic patients.

We have observed a significant higher prevalence of essential hypertension, cardiovascular diseases and diabetes in a group of 100 psoriatic patients compared with sex and age matched hospitalized controls. Thirty-five psoriatic patients exhibited and enhanced plasma renin activity (PRA), while urinary aldosterone excretion was raised in 27% of the group. The autonomic responsiveness of psoriatic patients, studied by cold pressure test and tilting was normal; this finding supports the hypothesis that the enhanced activity of renin-angiotensin system is not due to an increased sympathetic function in these psoriatic patients. High values of cholesterol, triglycerides and depressed HDL-cholesterol concentrations were also observed. A complete clinical and laboratory examination is very useful in psoriasis in order to initiate an appropriate treatment of the risk factors whenever present.

Aldosterone↗
PubMed1983

Trypsin-activatable inactive renin in rat plasma.

1. Activation of inactive renin in rat plasma has been studied with different trypsin concentrations and incubation times at pH 6.2 and 4 degrees C. 2. Trypsin concentrations below 2 mg/ml, lower than endogenous rat plasma anti-trypsin activity, do not activate inactive renin, whereas maximal activation is obtained with trypsin at 6 mg/ml for 1 min at 4 degrees C, pH 6.2. 3. Under these conditions trypsin can cleave dialysable fragments from renin substrate. ANG I can be generated at 37 degrees C with a pH optimum of 5.3. Nevertheless, the ANG I formation at pH 6.2 was totally unaffected. 4. Incubations longer than 2 min with trypsin at 6 mg/ml can induce a direct cleavage of dialysable ANG I-containing fragments strongly interfering with the measurements of renin activity at pH 6.2. 5. On average 40% of the total renin measured in plasma of normotensive WK rats is in the inactive form, although a wide range of variation is observed.

Angiotensin I↗
PubMed1982

Active and inactive renin after a single dose of captopril in hypertensive patients.

In 25 hypertensive patients (15 with renal artery stenosis and 10 with essential hypertension), captopril, in a single 12.5 mg dose, caused a prompt decrease in arterial pressure without changing the heart rate. Plasma active and trypsin-activated renin significantly increases, whereas inactive renin and plasma aldosterone decreased. The plasma active/inactive renin ratio was also increased, suggesting that captopril, together with a release of active renin, may induce an in vivo activation of inactive renin. No correlations were found between blood pressure changes and both pretreatment and captopril-induced variations of active, inactive and trypsin-activated renin or the active/inactive ratio. However, the percent decrease in mean arterial pressure was significantly related to the increase in the active/inactive renin ratio in a group of patients whose blood pressure was brought to normal (r = -0.78; p less than 0.001). This finding suggests the possibility that vasodilating substances, in addition to inhibiting angiotensin II formation, might play some role both in exerting a full effect of captopril on blood pressure and in triggering the in vivo mechanisms of inactive renin activation.

Blood Pressure↗
PubMed1982

In-vivo activation of circulating inactive renin by the ischemic kidney in man.

The role of the kidney as a possible source or as activator of inactive renin was studied in 22 patients with Essential Hypertension (EH) and in 20 patients with Unilateral Renal Artery Stenosis (RAS). Active and inactive renin (trypsin activation) were measured in blood samples taken simultaneously from both renal veins and from a peripheral artery during acute diuretic stimulation induced by furosemide 40 mg i.v. In EH pts active and trypsin-activated renin were significantly higher in both renal veins than in arterial blood (P less than 0.001 and P less than 0.02 respectively) whereas no difference was seen as far as inactive renin is concerned. In unilateral RAS trypsin-activated and active renin from the ischemic kidney were significantly higher (P less than 0.01 and P less than 0.005 respectively) while inactive renin was significantly lower (P less than 0.005) than in arterial blood. No significant difference was seen between arterial and renal venous blood from the contralateral kidney as far as active and inactive renin are concerned. When comparing the V-A differences for active renin to the corresponding V-A differences for inactive renin from the ischemic kidney a significant negative correlation appeared (r = -0.49 p less than 0.05) whereas no correlation was found from the contralateral kidney (r = -0.26 n.s.). These data demonstrate that the ischemic kidney, in addition to its ability to release active renin, can also activate circulating inactive renin.

Adult↗
PubMed1982

Studies on trypsin activation of inactive renin in rat plasma.

The experimental conditions of trypsin activation of inactive renin in rat plasma have been studied. Our results showed that the pH optimum of trypsin-activated renin is 6.2, the same as that of rat plasma active renin. Trypsin concentration and incubation time might also interfere with the activation process. Trypsin concentration below 2 mg/ml cannot activate inactive renin. Trypsin at a concentration of 6 mg/ml for 1 min. can cleave dialyzable fragments from renin substrate which can generate Angiotensin I at 37 degrees C with a pH optimum of 5.3 but which do not affect Angiotensin generation at pH 6.2. Longer incubations (more than 2 min.), on the contrary, can produce a cleavage at 4 degrees C of Angiotensin I containing fragments directly from renin substrate strongly interfering with measurements of renin activity at pH 6.2. Trypsin concentrations lower than endogenous rat plasma anti-trypsin activity do not activate inactive renin. Much higher concentrations of trypsin, however, are needed to obtain optimum activation of inactive renin. In average, 40% of the total circulating renin in rat plasma can be activated by trypsin.

Animals↗
PubMed1982

Plasma active and inactive renin and urinary kallikrein in normal subjects in response to hydrochlorothiazide, spironolactone or aldosterone administration.

The aim of this study has been to see whether acute variations in the proportions of circulating active and inactive renin in normal subjects were related to concurrent changes in the excretion of urinary kallikrein. Hydrochlorothiazide (50 mg/day) was given to 6 normal volunteers for 6 days; another group of 6 normal subjects received spironolactone (300 mg/day) for 6 days whereas synthetic aldosterone (0.5 mg/day) was administered i.m. for three days to 3 normal subjects. Both diuretics induced a sharp rise in active and total renin and a significant transient decrease in inactive renin so that the active: total renin proportion significantly increased. Urinary kallikrein excretion did not significantly change in either group. Parenteral administration of aldosterone induced a striking fall in all renin components without changing the proportions of active and inactive renin whereas urinary kallikrein excretion increased. These results indicate that changes in active: total renin proportions can occur without parallel variations in urinary kallikrein excretion. The latter cannot be used, therefore, as a reliable index of the possible role of renal kallikrein as activator in-vivo of inactive renin in man.

Adult↗
PubMed1982

Active and inactive renin during acute reduction of renal perfusion pressure in essential hypertensives.

Arterial and renal venous active and inactive renin were studied in 5 patients with long established moderate hypertension following unilateral acute reductions of renal perfusion pressure (15% and 70% of control) by inflating a balloon catheter introduced into the right renal artery. This procedure failed to induce the expected release of active renin; total and inactive renin levels were also unchanged. On the contrary in a single normotensive patient smaller reductions of the renal perfusion pressure (-15% and -30%) were able to acutely increase the release of active renin with a concurrent conversion of inactive renin but without inducing blood pressure changes. These findings show that the renin pattern typical of unilateral renovascular hypertension, including the intrarenal activation of inactive renin, could be reproduced acutely in a normotensive subject. Moreover, a complete reversal of the above mentioned active and inactive renin pattern was observed in a recent onset renovascular hypertensive patient within 30 min from successful percutaneous transluminal dilation. The negative results observed in our hypertensive patients suggest that structural changes induced by the long duration of hypertension might have reduced the sensitivity of the baroceptors involved in renin release.

Adult↗
PubMed1982

Persistence of unilateral secretion and contralateral renin suppression after successful percutaneous transluminal dilatation in a normotensive patient.

We describe a case of a 26-year old woman with severe fibromuscular renal artery stenosis whose blood pressure was well controlled with atenolol but that remained normotensive also after discontinuation of the drug. In addition her renal vein renin pattern was typical of renovascular hypertension and an intrarenal activation of inactive renin was also present. This renin pattern remained unchanged soon after successful percutaneous transluminal dilatation whereas 15 days later both active and inactive forms of renin were found to be released by the previously stenotic kidney. This case casts doubts upon the relationships between renal artery stenosis, renin secretion and high blood pressure.

Adult↗
PubMed1981

Optimum tryptic activation of inactive renin in human plasma is independent of endogenous anti-tryptic activity.

1. Plasma samples from 31 normal subjects were treated (at 4 degrees C, pH 7.0, for 2 min) with different concentrations of trypsin (500, 1000, 2000, 3000 and 4000 microgram/ml) in order to assess which concentration yielded the maximum activation of inactive renin. 2. Endogenous antitryptic activity was also measured in all samples; the mean value +/- SD (in microgram of trypsin inhibited by 1 ml of plasma) was 953 +/- 550 microgram/ml (range 34-1800 microgram/ml). 3. In the entire group of subjects the values of trypsin-activated renin measured with trypsin at 2000 microgram/ml were significantly higher than those obtained with lower or higher trypsin concentrations. 4. With subjects divided into subgroups according to their endogenous anti-tryptic activity, the maximum yield of activation was reached with trypsin at 2000 microgram/ml. 5. No significant correlations were found between single values of active, inactive or trypsin-activated renin and the corresponding levels of endogenous anti-tryptic activity. However, a weak but significant correlation (r = 0.39, P less than 0.05) was found between single values of anti-tryptic activity and the corresponding percentage of activation of inactive renin. 6. Thus the maximum activation of inactive renin at 4 degrees C for 2 min is obtained with trypsin at 2000 microgram/ml independently of the corresponding endogenous anti-tryptic activity. It is not excluded that the content of protease inhibitors in human plasma might affect the proportion in vivo of circulating active and inactive renin.

Adult↗
PubMed1981

Trypsin activation of inactive renin in human plasma. An assessment of some methodological aspects.

The following methodological aspects of the use of trypsin as activator of inactive renin in human plasma have been studied: a) the effect of SBTI on renin activity and angiotensin; b) the reaction velocity of trypsin on inactive renin; c) the optimum trypsin concentration; d) the ability of human plasma to neutralize exogenous trypsin. Our results show that: 1) Some commercially available SBTI may exert an angiotensinase-like effect which can be abolished by PMSF. 2) At 4 degrees C activation of inactive renin reached a maximum within the first two minutes then no further activation could be demonstrated. 3) Trypsin 2 mg/ml yielded more inactive renin than trypsin 1 or 0.5 mg/ml. A higher concentration (3 mg/ml) gave substantially equivalent activation as (with) trypsin 2 mg/ml whereas when using a still higher concentration (4 mg/ml) a degradation of the renin system components could be noted. 4) Endogenous trypsin inhibitors can eventually inactivate exogenous trypsin up to 3 mg/ml. About 20% of renin is destroyed by trypsin 4 mg/ml within 2 min at 4 degrees C while an additional 40% is lost during the incubation at 37 degrees C if no SBTI is added.

Enzyme Activation↗
PubMed1981

[Role of renin profile and age in the choice of the therapeutic approach of arterial hypertension (author's transl)].

A group of 116 patients with grade I-II (W.H.O.) essential hypertension was studied. A diuretic treatment was instituted as a first step of therapy in 50 patients while the remaining 66 were firstly treated with beta-blockers. After 6 weeks of treatment the drugs were combined in those patients who did not achieve blood pressure control; this combination therapy was again maintained for 6 weeks and, if necessary, a vasodilating agent was added thereafter. The results show that with diuretic treatment alone diastolic blood pressure was brought to normal values (less than 95 mmHg) in 3/4 of our low renin patients, in 2/3 of normal renin and in 1/3 of high renin hypertensives. On the contrary among the group of patients treated with a beta-blocker alone more than half of the high and normal renin patients were controlled whereas this goal was achieved in only 1/4 of the low renin patients. Similar behaviour was observed subdividing the subjects in young (less than 35 yrs), middle-aged (36-49 yrs) and older (greater than 50 yrs) patients. In conclusion our data indicate that age must be taken into account in classifying hypertensive patients in renin subgroups. In addition if a renin-sodium profile is available, it can be useful in choosing between diuretics or beta-blocker as a first step treatment. Alternatively, younger patients are more likely to have better hypotensive responses with beta-blockers whereas in older patients antihypertensive treatment should preferentially be started with diuretics alone.

Adrenergic beta-Antagonists↗
PubMed1980

[Methodology of renal vein renin study: comparison between simultaneous and sequential sampling (author's transl)].

Purpose of this study has been to compare the results obtained using two different procedures in blood sampling from the renal veins for measuring renal venous renin. The first is the classical procedure which employs three catheters for simultaneous sampling from both renal veins and from the inferior vena cava, or from an artery. The other one is a simplified procedure which employs a single catheter that allows blood to be collected in the following rapid sequential manner: right renal vein, inferior vena cava, left renal vein, inferior vena cava. We have studied 13 patients (8 with essential hypertension, 5 with unilateral renal artery stenosis). Two catheters were introduced through a femoral vein and inserted into both renal veins; a third catheter was inserted into the femoral artery; then the blood sampling was performed strictly simultaneously. Soon after, the blood sampling was repeated according to the above mentioned sequential single catheter procedure. PRA was measured by Angiotensin I radioimmunoassay, then the Renal Vein Ratios (RVRR) were calculated. Even though as average of less than 20 seconds elapsed between the blood sampling in a renal vein and that in inferior vena cava, our results demonstrate that the release of renin can vary so quickly that erroneous informations may be obtained unless a strictly simultaneous sampling of blood is performed. In conclusion, our study demonstrates that the only reliable renal vein renin sampling procedure must employ the simultaneous renal venous and arterial (or inferior vena cava) blood collection.

Adult↗
PubMed1978

Effects of levodopa alone and in combination with dopa-decarboxylase inhibitors on plasma renin activity in patients with Parkinson's disease.

Plasma renin activity (PRA) of patients with Parkinson's disease was measured in recumbency, upright position, and after frusemide administration. The results show that the renin responses to both stimuli are significantly reduced as compared with those obtained in a group of normal subjects, while recumbent PRA levels of Parkinsonism patients are not significantly lower than those found in recumbent normal subjects. Levodopa treatment, alone or in combination with two different dopa-decarboxylase inhibitors, benserazide and carbidopa, does not modify the renin response to posture or to frusemide. Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release.

Adult↗