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Biomedical subjects

P Weidmann

Publications and source records attributed to P Weidmann.

At least 271 records · Page 15Linked to original sources
PubMed1979

beta blockade with pindolol: differential cardiac and renal effects despite similar plasma kinetics in normal and uremic man.

Cardiac and renal effects (measured as the reduction in exercise-induced tachycardia and PRA, respectively) and circulating drug concentrations after acute beta blockade with intravenous pindolol were compared between seven normal volunteers and six patients with terminal renal failure. Kinetic parameters were similar in both groups (total body clearance, 450 mg/min), indicating enhanced extrarenal elimination in patients. For any given drug concentration, however, the uremic patients responded to beta blockade with a greater decrease in pulse rate than did normal volunteers (P less than 0.001). Moreover, in the same group, the decrease of PRA was more marked (from 13.3 to 5.7 vs. 3.3 to 1.9 ng/ml/hr) and lasted longer (8 hours and more vs. 2 hours). Plasma aldosterone remained unchanged. These data reveal an increased dependency of both heart rate and renin release on beta adrenergic-mediated mechanisms in uremic man. They also show that kinetic findings in normal subjects cannot always be extrapolated to predict kinetic behavior in disease, and that similar kinetics do not imply similar effectiveness.

Adult↗
PubMed1979

Increased ratio between changes in blood pressure and plasma norepinephrine in essential hypertension.

The pathogenic role of the sympathetic system in essential hypertension was evaluated by combined analysis of plasma catecholamine levels and the pressor sensitivity to endogenous norepinephrine. The latter was estimated indirectly by the ratio between changes in blood pressure and those in plasma norepinephrine after adrenergic neuronal blockage with debrisoquine (given orally for 6 weeks). Normal subjects and patients with borderline or established essential hypertension had comparable pretreatment levels of plasma norepinephrine and epinephrine. Debrisoquine lowered plasma norepinephrine by a similar degree (almost 50%) in these three groups; in contrast, blood pressure decreased only slightly in normal or borderline hypertensive subjects [-3.4 +/- 3.2% and -5.4 +/- 1.6% (SE), respectively] but fell significantly more (P less than 0.005) in patients with established essential hypertension (-20.7 +/- 3.9%). The ratio between percentile changes in blood pressure and those in endogenous norepinephrine levels was comparable in normal and borderline hypertensive subjects (0.03 +/- 0.08 and 0.17 +/- 0.04, respectively), but increased (P less than 0.001) in established essential hypertension (0.62 +/- 0.11). This suggests that essential hypertension may be maintained, at least partly, by the inappropriate association of normal plasma norepinephrine levels with increased norepinephrine pressor sensitivity.

Blood Pressure↗
PubMed1978

[Significance of noradrenaline in the pathogenesis of essential hypertension. Preliminary report].

The pathogenic role of the sympathetic system in essential hypertension was evaluated by combined analysis of urinary and plasma catecholamine levels and pressor sensitivity to endogenous noradrenaline. The latter was estimated indirectly by the ratio between percentile changes in blood pressure and plasma noradrenaline following adrenergic neuronal blockade with the agent debrisoquine. In normal and mildly hypertensive (141/91 to 160/105 mm Hg) subjects, supine or upright plasma levels and excretion rates of noradrenaline correlated (p less than 0.01) with age and were comparable; no correlation was present in patients with moderate to severe hypertension (greater than 160/105 mm Hg) who tended to have supernormal noradrenaline levels under the age of 40 years. Adrenaline values were normal in essential hypertension. Pressor sensitivity to noradrenaline was comparable in normal and mildly hypertensive subjects (0.03 +/- 0.08 [SE] and 0.17 +/- 0.04, respectively) but increased (p less than 0.001) in moderate to severe hypertension (0.62 +/- 0.11). These findings suggest that moderate to severe essential hypertension may be maintained, at least partly, by the inappropriate association of normal plasma noradrenaline levels with increased noradrenaline pressor sensitivity. This may also provide a rational basis for the use of pharmacologic adrenergic inhibition in the treatment of moderate to severe essential hypertension.

Adolescent↗
PubMed1978

Responsiveness of plasma aldosterone: dependency upon basal secretory activity.

The responsiveness of plasma aldosterone levels to various stimuli was evaluated in 44 normal subjects, 17 patients with mild to moderate renal failure, 30 patients with terminal renal failure, and 13 anephric subjects. Plasma aldosterone, renin activity (PRA), cortisol, sodium, and potassium levels were measured before and after one hour of upright posture (N = 191); ACTH infusions (N = 76); and angiotensin II infusion (N = 36). Plasma aldosterone responses correlated (r greater than or equal to 0.53; p less than 0.02) with basal plasma aldosterone levels during upright posture in all four groups, with ACTH infusion in all groups except anephric subjects, and with angiotensin II administration in patients with mild to moderate renal failure or patients combined. These relationships were consistently closer than those between aldosterone responses and changes in PRA or basal PRA. However, postural aldosterone responsiveness at any given basal aldosterone level was significantly lower in patients with renal disease than in normal subjects, and this was associated with a parallel impairment in renin responsiveness. In contrast, when related to basal levels aldosterone responsiveness to ACTH or angiotensin II appreared to be comparable in normal subjects and patients with renal disease. Aldosterone responses to posture, ACTH, or angiotensin II did not correlate with associated changes in plasma cortisol, sodium, or potassium levels. These data suggest that basal adrenal secretory activity is a major factor conditioning aldosterone responsiveness to various stimuli in normal subjects as well as in patients with renal disease.

Acute Kidney Injury↗
PubMed1978

Increased ratio between serum beta- and alpha-lipoproteins during diuretic therapy: an adverse effect?

1. The effect of diuretic therapy on serum lipids and lipoprotein fractions was evaluated in 16 normal or labile hypertensive subjects who received in cross-over fashion chlorthalidone, frusemide or mefruside, each for 4 weeks (group A); and in 13 patients with essential hypertension treated with chlorthalidone for 6 weeks (group B). 2. All three diuretics significantly increased the ratio between serum beta- and alpha-lipoprotein fractions. This was due to an increase of the serum beta-lipoprotein fraction while the alpha-lipoprotein fraction was not changed significantly (group A) or decreased (group B). Serum cholesterol or triglycerides tended to be increased, but mean changes were often not significant. 3. The observed alterations in serum lipoproteins are consistent with the possibility of an increased risk for coronary heart disease which could offset partly the beneficial effects of a lowered blood pressure in diuretic-treated patients with hypertension.

Blood Volume↗
PubMed1977

[Increased renal prostaglandin E2 secretion in Bartter's syndrome].

In a 52-year-old patient with Bartter's syndrome, peripheral venous prostaglandin E2 (PGE2) and plasma renin activity (PRA) levels were markedly elevated and plasma aldosterone concentration (pa) was at the upper limit of normal, though inappropriately high relative to the decreased plasma and whole body potassium levels. Blood pressure, plasma volume, exchangeable body sodium, plasma cortisol and urinary catecholamines were normal. Renal venous PGE2 was two to three times higher than peripheral PGE2. Indomethacin (300 mg/day) decreased peripheral PGE2 by 50%, PRA by 84% and PA by 72%, induced a positive potassium balance (greater than 350 mEq) with normal plasma potassium levels, and returned the previously marked resistance to the pressor effect of angiotensin II to normal. During the entire study, highly significant correlations (p less than 0.001) between peripheral PGE2 and PRA (r = 0.86) or PA (r = 0.90) were found. In this patient the hyperreninemia was not related to volume depletion. These data indicate that in Bartter's syndrome renal PGE2 secretion may be increased, systemic blood levels of PGE2 may be elevated and closely related to PRA, and indomethacin ameliorates these abnormalities and improves potassium balance. These results are consistent with the ascription of an important role to excessive renal PGE2 secretion in the pathogenesis of Bartter's syndrome.

Aldosterone↗