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Biomedical subjects

C Lechi

Publications and source records attributed to C Lechi.

At least 55 records · Page 3Linked to original sources
PubMed1983

A discrepancy between the effects of a single oral dose of captopril on blood pressure, plasma renin activity, and serum angiotensin-converting enzyme levels.

The effects of a single oral dose (100 mg) of the angiotensin-converting enzyme (ACE) inhibitor, captopril (SQ 14,224), on blood pressure (BP), plasma renin activity (PRA), plasma aldosterone (PA), and serum ACE were investigated in 18 patients with essential hypertension (EH) and in 4 with renovascular hypertension (RVH). in most patients, SQ 14,225 caused a significant reduction of BP during the subsequent 6 h, particularly in RVH patients. A significant correlation between basal PRA levels and BP reduction was observed only by considering all the patients together. After ACE blockade, a significant increase of PRA was observed in RVH and in normal-renin EH patients, but not in EH patients with lower PRA. Maximal serum ACE inhibition (over 50%) occurred after 2 h but diminished after 4 h and 6 h, whereas the BP decrease persisted for 6 h. After 3-day treatment with indomethacin (six patients) captopril's antihypertensive action was blunted, despite a reduction of baseline PRA levels and of captopril-induced PRA elevation. The antihypertensive effects of SQ 14,225 in low-renin EH patients, the lack of effect of ACE blockade on renin secretion in these patients, and the reduction of the antihypertensive effects of SQ 14,225 after indomethacin refute the interpretation of purely angiotensin-related antihypertensive mechanism.

Administration, Oral↗
PubMed1982

Contribution of four markers of tubular proteinuria in detecting upper urinary tract infections. A multivariate analysis.

The presence of tubular involvement, as a marker for the detection of urinary tract infection (UTI) site, was examined in 19 patients with pyelonephritis and in 15 patients with cystitis or asymptomatic bacteriuria. The urinary excretion of four markers of tubular proteinuria, beta 2-microglobulin (beta 2M), lysozyme (LZ), lactic dehydrogenase isoenzyme V (LAD-5) and N-acetyl-beta D-glucosaminidase (NAG), was investigated. LAD-5 appeared particularly valuable for the early detection of upper UTI. However, the overall diagnostic accuracy appeared to be further strengthened using, besides LAD-5, one additional variable. A set of simple and noninvasive biochemical tests on urine samples can reliably help to identify the site of UTI.

Acetylglucosaminidase↗
PubMed1979

Kidney 15-hydroxy-prostaglandin-dehydrogenase activity during the development of experimental hypertension in the rat.

15-hydroxy-prostaglandin-dehydrogenase (PGDH) activity was studied in rat kidney homogenates during the development of hypertension, within 20 days after left renal artery constriction by a solid silver clip. In the ischemic kidney PGDH activity increased at day 6, reached maximum at day 10, then progressively at day 15 and returned to normal levels at day 20. No difference was found between contralateral kidneys and kidneys of normotensive control rats. Variations of PGDH activity did not seem to be related to either renal perfusion pressure or renin production. Increased PGDH activity may be a consequence of an enzyme induction following increased PG-synthetase activity, or it could be viewed as a defence mechanism, according to the hypothesis of a prohypertensive effect of PG in the rat.

Animals↗
PubMed1978

Urinary kallikrein excretion and plasma renin activity in patients with essential hypertension and primary aldosteronism.

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroup: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients beta-adreno-receptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.

Adult↗
PubMed1976

Urinary and kidney kallikrein in hypertensive rats.

Urinary and kidney kallikrein were studied in rats with renal clip hypertension. The effect of protease inhibitors on urinary and kidney BAEE esterase activity was similar. Both hypertensive and not hypertensive operated rats excrete significantly less kallikrein than controls; in the ischaemic kidney kallikrein is diminished whereas is not increased in contralateral. Kallikrein is therefore related to renal functional mass but does not seem responsible for a natriuretic effect.

Animals↗
PubMed1976

Urinary kallikrein excretion in Bartter's syndrome.

Urinary excretion of kallikrein has been studied in a patient with hypokalemic alkalosis, hyperplasia of the renal juxtaglomerular apparatus and hyperreninemia, secondary aldosteronism and resistance to the pressor effect of angiotensin II (Bartter's syndrome). Urinary kallikrein was found exceedingly high in several determination, whereas it was low in patients with essential hypertension and high in patients with primary aldosteronism. Urinary kallikrein decreased after spironolactone therapy. The rise of kallikrein excretion (which is not related to plasma renin) in this case is probably caused by a direct action of the chronic excess of plasma aldosterone; it could not be accounted for as secondary to natriuresis.

Adult↗
PubMedDate not supplied

Effect of indomethacin on urinary kallikrein excretion in Bartter's syndrome of the adult.

An elevated urinary kallikrein excretion was found in 3 out of 4 adult patients with Bartter's syndrome. After prostaglandin synthesis inhibition by indomethacin, serum potassium levels rose, plasma renin activity and urinary aldosterone excretion decreased. Urinary kallikrein excretion was reduced to within normal range in all patients. The fall of urinary kallikrein excretion after indomethacin may be partly due to plasma potassium and aldosterone variations, but more likely it is dependent on the reduced prostaglandin synthesis. These results support the hypothesis that renal prostaglandins activate renal kallikrein-kinin system, hence inducing an increase of renal blood flow, diuresis and natriuresis.

Adult↗