PubMed Health⌕ Search

Biomedical subjects

A Rappelli

Publications and source records attributed to A Rappelli.

At least 73 records · Page 4Linked to original sources
PubMed1987

Angiotensin converting enzyme inhibition reduces ACTH release due to hypoglycaemia.

To investigate the role of Angiotensin II in the release of ACTH, the response of adrenocorticotrophic hormone to hypoglycaemia was studied before and during treatment with an angiotensin converting enzyme inhibitor, enalapril, in 15 male patients with essential hypertension. Plasma levels of ACTH were measured before and 60, 90 and 120 min after an i.v. bolus of normal saline, as placebo, and, 3 days later, after an i.v. bolus of regular insulin (0.15 U/Kg b.w.). Enalapril treatment was then started and both placebo and hypoglycaemic tests were repeated 15 days thereafter. No changes in ACTH plasma levels were observed after acute normal saline either before or during enalapril treatment. On the contrary, hypoglycaemia induced a sharp increase of ACTH before enalapril (from 19.5 +/- 4.1 to 74.4 +/- 13.0 pg/ml, p less than 0.01 60 min after insulin) but not during ACE inhibition (from 26.1 +/- 6.2 to 34.6 +/- 5.9 pg/ml, NS, at min 60 of the study). The present data confirm our previous observation on the reduction of the hypoglycaemic-induced ACTH release during ACE inhibition with captopril and support the hypothesis that circulating Ang II may exert a facilitating role on adrenocorticotrophic hormone release.

Adrenocorticotropic Hormone↗
PubMed1987

The effects of aprotinin, a glandular kallikrein inhibitor, on renin release and urinary sodium excretion in mild essential hypertensives.

The effects of aprotinin on renin release and renal function were evaluated in 24 male essential hypertensive patients, on unrestricted (N = 17) and on chronic low as well as on high Na intake. Aprotinin (1 x 10(6) KIU) or Saline (200 ml) were infused in all patients for 6 hrs. Blood samples were taken for plasma renin activity (PRA) and 6-hr urine collections were obtained for active and inactive kallikrein, Na+, K+, Cl-, Ca++ excretion measurements. In patients on unrestricted sodium diet aprotinin had no effect on BP, glomerular filtration rate, renal plasma flow, urinary sodium and potassium excretion. However an inverse relationship was found between pretreatment urinary sodium excretion and the percent reduction of the latter after aprotinin. A significant reduction in urinary sodium excretion was induced by aprotinin in patients on high sodium intake, whereas no change was observed in the same patients when on low sodium diet. Aprotinin reduced the urinary excretion of active kallikrein by 81% and the active to total kallikrein ratio from 24% to 6%, suggesting that it could interfere with the in-vivo activation of inactive kallikrein. Infusion of aprotinin induced a significant decline in active renin but did not modify inactive renin levels in patients on unrestricted sodium diet as well as in patients on low or high sodium intake. Our data suggest that the inhibition of kallikrein and/or other serine proteases by aprotinin can interfere with renal release of active renin and also support the hypothesis that the renal kallikrein system exerts a regulatory control on sodium excretion in salt replete hypertensives.

Adult↗
PubMed1987

Effect of nifedipine and verapamil on carbohydrate metabolism in hypertensive patients with impaired glucose tolerance.

Intracellular Ca2+ influx is an essential step in insulin (I) release. Calcium antagonists are reported to reduce I release in vitro and in patients with impaired glucose tolerance (IGT) during acute administration. Their effects during long-term therapy are still controversial. To evaluate the effects of chronic verapamil (V) and nifedipine (N) on carbohydrate metabolism, 12 hypertensive patients (WHO II; aged 37-64 years) with IGT underwent intravenous glucose tolerance tests (IVGTT) (0.33 g/kg body weight in 3 min), arginine (A) infusion (30 g/30 min), and hypoglycemic stress (regular insulin 0.15 U/kg body weight) during which blood levels of glucose (G), I, growth hormone (GH), glucagon (IRG), and cortisol (C) were measured. The patients were then randomized to V (120 mg b.i.d.) or N (20 mg b.i.d.) treatment and, 1 month later, both IVGTT and A infusion were repeated. Hormone determinations were performed by the radioimmunoassay (RIA) and G by the enzymatic method. The patients were maintained on their usual diet for the duration of the study. The rate of decline of G during IVGTT was expressed as Conard's K coefficient (K; normal values greater than 1.3). I and GH during IVGTT were evaluated as the differences between basal and peak values. I, IRG, and GH during A infusion were analyzed as incremental areas. Our results show that neither V nor N impaired carbohydrate metabolism in hypertensive patients with IGT.

Adult↗
PubMed1986

Captopril-induced proteinuria in hypertensive psoriatic patients.

We have previously reported on a high prevalence of high renin essential hypertension in psoriasis. Since angiotensin-converting enzyme (ACE) was also reported to be increased in some psoriatics, we found it rational to treat 10 patients with hypertension and diffuse psoriasis with captopril at a dose of 25 mg t.i.d. Five patients had high PRA levels and in 1 of them serum ACE was also increased. Serum creatinine, BUN and urinalysis were normal in all of them. SPB fell from 163 +/- 3 to 138 +/- 3 and DBP from 107 +/- 3 to 86 +/- 2 mm Hg after 1 month of captopril treatment. A surprising clinical improvement of the cutaneous lesions occurred in 3 patients previously resistant to every local or systemic treatment. Unfortunately, however, 3 patients developed heavy proteinuria (greater than 2 g/day) which disappeared after captopril discontinuation. The unexpected incidence of reversible proteinuria induced by low doses of captopril in our patients recommends a careful monitoring of the renal function every time this drug is employed in the treatment of hypertension in a psoriatic.

Adult↗
PubMed1986

Renal vein renin in renovascular hypertension: the experience of two Italian centers.

A retrospective analysis of renal vein renin results has been done in 96 patients with renal artery stenosis and hypertension studied in two Italian centers (Sassari and Pisa) with respect to the outcome of either surgery or percutaneous transluminal angioplasty (PTA). In all patients the renal vein renin ratio and the V-A/A ratios for the affected and unaffected kidney were calculated. Each patient underwent surgery (75) of PTA (21): 71 subjects were cured, 17 improved whereas the arterial pressure did not vary after revascularisation procedure in 8 patients. In the Pisa series all 54 patients showed a lateralisation with contralateral renin suppression and 95% of them benefitted from surgery. In the Sassari series 42 patients were submitted to PTA or surgery, not only on the basis of a positive renal vein renin study but taking into account a complete clinical evaluation: 8 of them were cured or improved in spite of negative renal vein renin criteria. In the two series, the better predictive index appeared to be the suppression of the renin secretion from the contralateral kidney while the high/low renin ratio showed a consistent amount of false-positive and false-negative results. Our retrospective study demonstrates that the renal vein test in hypertensive patients with renal artery stenosis is highly predictive of the curability of the disease, particularly when contralateral suppression of renin secretion is present. On the other hand, since patients with negative renin indexes can also take benefit from surgery of PTA, the renin parameters cannot be adopted as the sole criterion in making the decision to operate.

Adult↗
PubMed1986

Acute response to captopril as a predictive test for surgery in renovascular hypertension.

To test the hypothesis that acute angiotensin-converting enzyme (ACE) inhibition might predict the postoperative blood pressure outcome, a single oral dose of captopril ranging from 12.5 to 100 mg, was given to 26 patients with renovascular disease and its hypotensive effect was compared with that of surgery (21 patients) or of percutaneous transluminal angioplasty (PTA) (5 patients). Both systolic and diastolic blood pressure fell significantly (p less than 0.001) from 179.9 +/- 5.4/114.1 +/- 2.1 to 148.4 +/- 3.8/94.1 +/- 1.9 after captopril and to 141.1 +/- 3.7/88.9 +/- 2.0 at least 3 months after operation. Postoperative pressure values were directly related to those after captopril (SBP: r = 0.65, p less than 0.001; DBP: r = 0.45, p less than 0.05) as were their absolute decrements (SBP: r = 0.70, p less than 0.001; DBP: r = 0.64, p less than 0.001). However, after captopril, individual pressure tended to be higher (and their decrements to be lower) than after operation. 12 out of 19 patients cured by surgery were considered cured by captopril, while 5 out of the remaining 7 were improved and 2 not cured. The 6 patients improved by surgery or PTA were also improved by captopril and the only patient not cured by surgery was not cured by captopril. Therefore, if we consider both cure and improvement as a positive result, the captopril test gave 23 true-positive, 1 true-negative and 2 false-negative responses. Taken together, these data suggest that acute ACE inhibition may be an useful tool in predicting postoperative blood pressure of patients with renovascular disease.

Adolescent↗
PubMed1985

Prokallikrein and kallikrein inhibitors in human urine.

Kallikrein activity (KA) and kallikrein inhibitors (KI) were evaluated in urine from normal subjects and essential hypertensives. Kallikrein inhibitors were almost completely removed by dialysis against water, confirming previous reports of their low molecular size. The negative relationship found between KA and KI in urine samples from 12 normal subjects suggests that KI might play a role in the modulation of KA excreted by the kidney. Heating (85 degrees C for 20 min) partially reduced (-52%) KI, indicating thermostable substances other than peptides as KI. When cations were evaluated as possible KI, by adding different salts to dialysed salt-free urine, only sodium was able to inhibit KA by 20% at a concentration not far from the physiological range. Trypsin added to dialysed urine produced a striking increase in KA without significant changes in Km and pH optimum. These findings, together with the observation that acid dialysis did not increase KA, strongly support the hypothesis that trypsin-activatable kallikrein might be a pro-enzyme. A lower urinary excretion of active kallikrein was found in 48 essential hypertensives when compared with 31 normotensive controls. However, trypsin-activatable kallikrein excretion was similar in the two groups, suggesting that low KA in hypertensives might not reflect a defective conversion of the pro-enzyme into the active form.

Adult↗
PubMed1985

Blunted adrenocorticotrophic hormone release during captopril treatment.

High tissue levels of angiotensin II have been reported in the median eminence suggesting a possible role in the regulation of adrenocorticotrophic hormone (ACTH) secretion. To verify this hypothesis in man, the pituitary-adrenal axis response to hypoglycaemia was studied before and during captopril treatment in eight male essential hypertensive patients (stage I WHO; aged 35-52 years). Plasma levels of ACTH, cortisol and glucose were measured before and 60, 90 and 120 min after an intravenous bolus of normal saline as placebo an, 3 days later, after an intravenous bolus of rapidly acting insulin (0.1 IU/kg body weight). Captopril treatment was then started and both placebo and hypoglycaemic tests were repeated 15 days thereafter. No changes in ACTH, cortisol or glucose plasma levels were observed after acute normal saline, either before or during captopril administration. On the contrary, hypoglycaemia induced a sharp increase of ACTH plasma before captopril (from 27.7 +/- 11 to 131.30 +/- 26 pg/ml, P less than 0.01, 60 min after insulin) but not during angiotensin converting enzyme (ACE) inhibition (from 28.9 +/- 9 to 42.9 +/- 11 pg/ml, NS, at min 60 of the study). Our present data, showing a blunted ACTH response to hypoglycaemia during ACE inhibition, suggest that circulating angiotensin II may participate in the regulation of the release of the ACTH, possibly by a stimulation of angiotensin II receptors localized in the brain but outside the blood-brain barrier.

Adrenocorticotropic Hormone↗
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↗