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Biomedical subjects

P Weidmann

Publications and source records attributed to P Weidmann.

At least 235 records · Page 13Linked to original sources
PubMed1981

Beta-receptor-blocking agents may reverse or prevent diuretic-induced increases in serum low-density lipoprotein cholesterol.

1. The effect of treatment with a thiazide-like diuretic alone or combined with a beta-adrenoceptor blocker on serum lipoproteins was investigated in 35 patients with essential hypertension. 2. In group I (18 patients), serum low-density lipoprotein cholesterol was increased (P less than 0.001) during monotherapy with chlorthalidone (100 mg/day) but not during combined chlorthalidone--beta-blocker therapy. 3. This tendency was similar in subgroups studied with an inverse sequence of drug administration. In subgroup IA (11 men), a 22% increase (P less than 0.01) in low-density lipoprotein cholesterol after 6 weeks of chlorthalidone was reversed after use of a beta-blocker as well as chlorthalidone; in subgroup IB (five men, two post-menopausal women), low-density lipoprotein cholesterol was increased by 41% (P less than 0.05) above placebo values 6 weeks after withdrawal of the beta-blocker from combination therapy. 4. In group II (18 men), low-density lipoprotein cholesterol was increased by 13% (P less than 0.025) after 4 weeks of monotherapy with clopamide (5 mg/day) but restored to control levels 4 weeks after addition of pindolol (10 mg/day). 5. No significant changes occurred during any treatment phase in high-density lipoprotein cholesterol. 6. Certain beta-receptor blocking agents may prevent or reverse diuretic-induced increases in serum low-density lipoprotein cholesterol.

Adolescent↗
PubMed1981

Correction of altered noradrenaline reactivity in essential hypertension by indapamide.

Fourteen patients with untreated mild to moderate essential hypertension had on average an abnormally high cardiovascular reactivity to exogenous noradrenaline and angiotension II, while plasma noradrenaline, renin activity, exchangeable body sodium, and blood volume were normal. Treatment with a low dose of indapamide (2.5 mg/day) for six weeks decreased blood pressure by 10% in these hypertensive patients but not in 13 normal control subjects. Plasma or blood volume and exchangeable sodium were not changed significantly; nevertheless, the latter, and body weight, tended to be decreased slightly. Though a mild reduction in extracellular sodium in both normal and hypertensive subjects appears possible, it may not per se fully explain indapamide's blood pressure-lowering effect in essential hypertension. Indapamide induced a mild decrease in angiotensin II pressor responsiveness in normal or hypertensive subjects, but a possible depressor influence from this change was probably antagonised by a concomitant pronounced increase in plasma renin activity. In hypertensive patients, the abnormally high noradrenaline reactivity was corrected by indapamide without an accompanying increase in endogenous plasma noradrenaline levels. Indapamide-induced changes in blood pressure correlated with those in noradrenaline pressor dose. It was concluded, therefore, that indapamide may decrease blood pressure in essential hypertension at least in part by lowering an abnormally high cardiovascular noradrenaline reactivity without causing an equivalent increase in adrenergic nervous activity.

Adolescent↗
PubMed1981

Pressor factors and cardiovascular pressor reponsiveness in essential hypertension.

The sympathetic system, the body sodium-fluid volume state, the reninangiotensin system, functional and structural characteristics of the heart and blood vessels, and some other components are important complementary factors in blood pressure regulation. A deviation from the normal equilibrium among these components, with a persisting non-physiologic increase in pressor factor(s) or in the basal vascular tone and/or cardiovascular reactivity to pressor factors, leads to hypertension. This review discusses recent observations and concepts regarding the roles of various pressor factors as well as cardiovascular pressor responsiveness in the pathogenesis of essential hypertension and in the anti-hypertensive mechanism of diuretic treatment.

Angiotensin II↗
PubMed1981

[Cause and therapeutic consequence of arterial hypertension and kidney tuberculosis].

In 36 patients who underwent partial or total nephrectomy for tuberculous lesions, all 6 with preoperatively severe hypertension were cured postoperatively without any further antihypertensive treatment. The predictive values of renal vein renin determinations and the importance of renal surgery in this kind of hypertension are emphasized.

Adult↗
PubMed1980

[The therapeutic efficacy of bezafibrate in hyperlipoproteinemias of various types].

17 patients with hyperlipoproteinemia of type 11 (9 type IIa and 8 type IIb), 4 with hyperlipoproteinemia of type IV and 1 with hyperlipoproteinemia of type V were treated for 4.6 +/- 0.7 months with the new lipid lowering agent bezafibrate in a dose of 200 mg three times daily. Bezafibrate markedly lowered total serum cholesterol and triglycerides and increased HDL-cholesterol in each of these types of hyperlipoproteinemia. These data suggest that bezafibrate may be effective in reducing the possibly atherogenic LDL- and VLDL-fractions while increasing the antiatherogenic HDL-fraction.

Bezafibrate↗
PubMed1980

Norepinephrine clearance and pressor effect in normal and hypertensive man.

Whether and to what extent the sympathetic nervous system participates in the development of essential hypertension has remained largely unclear. The role of the adrenergic effector - cardiovascular response axis in the pathogenesis of essential hypertension was investigated by combined analysis of blood levels, total plasma clearance and cardiovascular pressor effects of norepinephrine (NE). Measurements of plasma NE and blood pressure were performed before, during and after an intravenous infusion of NE at stepwise increasing rates in approximately age and sex-matched groups of 28 normal subjects and 35 patients with essential hypertension. The threshold of the pressor effect of NE was lower in hypertensive than in normal subjects (20 +/- 10 vs. 42 +/- 26 ng/kg min; P < 0.001); but the slope of the dose - resonse curve and basal endogenous plasma NE were in the average similar. Total plasma NE clearance estimated under steady state conditions was similar in normal and hypertensive subjects (5.3 +/- 2.5 vs. 5.4 +/- 2.31/min). NE clearance corrleated inversely with basal plasma NE in normal subjects (r = 0.57; P < 0.005). The plasma half-life of NE was about 2 min. These findings demonstrate that basal blood levels and total plasma clearance of NE during NE infusion are usually normal in essential hypertension. A low threshold of the pressor effect of NE in the presence of normal adrenergic activity may contribute to the development and/or maintenance of essential hypertension.

Adolescent↗
PubMed1980

Age-rated profile of cardiovascular reactivity to norepinephrine and angiotensin II in normal and hypertensive man.

The interrelationships among age, cardiovascular pressor reactivity to intravenously infused norepinephrine (NE) or angiotensin II, and endogenous plasma NE or renin (PRA) levels were evaluated i 31 normal subjects and 37 patients with essential hypertension. In normal subjects both angiotensin II pressor dose and PRA decreased progressively with aging. Angiotensin pressor dose correlated positively with PRA (r = 0.41, P < 0.025) and inversely with age (r = -0.46, P < 0.02). NE pressor dose and basal plasma NE were also positively correlated (r = 0.53, P < 0.005), but the two factors remained largely unchanged with aging. Findings in essential hypertension differed in certain aspects. Angiotensin II pressor dose did not correlate with either basal PRA or age; and pressor doses of NE and angiotensin II tended to be lower in some patients than in normal subjects. These findings indicate that aging is accompanied by a physiologic increase in cardiovascular reactivity to angiotensin II, probably due to a concomitant decrease in circulating renin. The dissociation between angiotensin pressor dose and PRA in essential hypertension suggests an interference from an other factor.

Adult↗
PubMed1980

Recent pathogenic aspects in essential hypertension and hypertension associated with diabetes mellitus.

The sympathetic system, the body sodium-fluid volume state, the renin-angiotensin system, functional and structural characteristics of the heart and blood vessels, and some other components are important complementary factors in blood pressure regulation. A deviation from the normal equilibrium among these components, with a persisting non-physiologic increase in pressor factor(s) or in the basal vascular tone and/or cardiovascular reactivity to pressor factors, leads to hypertension. This review discusses recent observations and concepts regarding the pathogenesis of essential hypertension and hypertension associated with diabetes mellitus. It focuses on the roles of various pressor factors as well as cardiovascular pressor responsiveness in the genesis of high blood pressure and in the antihypertensive mechanism of diuretic treatment.

Cardiovascular System↗
PubMed1980

[Comparison of oral diazoxide and minoxidil in refractory hypertension].

The efficacy and side effects of two potent vasodilatators, namely diazoxide and minoxidil given orally, were compared in 11 patients who had hypertension refractory to conventional drug treatment. The latter included diuretics, betablockers and/or sympatholytics, and either dihydralazine or prazosin. In a crossover approach, dihydralazine and prazosin were withdrawn and replaced by diazoxide or minoxidil. In nine patients the diazoxide phase preceded the minoxidil treatment, while in two it followed minoxidil treatment. Before introduction of the more potent vasodilators blood pressure averaged 181/107 mm Hg in the supine and 161/103 mm Hg in the upright position. Both, oral diazoxide (median dose 400 mg/d( and minoxidil (medium dose 17.5 mg/d) produced similar decreases (p < 0.02) in mean arterial pressure (-15%) in the supine and (-11 vs. -12%) in the upright position. They caused a comparable tendency for sodium retention and weight gain which could be satisfactorily controlled with increased diuretic therapy, except in one patient. Hypertrichosis occurred with both drugs, but tended to be somewhat milder with diazoxide. Electrocardiograms remained generally unchanged. Plasma glucose levels were increased during diazoxide treatment in six patients necessitating interruption of this therapy in four patients. It is concluded that the antihypertensive potency and most side effect of orally administered diazoxide are comparable to those of minoxidil, except for diazoxide-related hyperglycemia which may limit the use of this substance.

Blood Glucose↗
PubMed1980

[Secondary hyperlipoproteinemia induced by diuretic therapy (author's transl)].

In order to study the degree and pathogenic aspects of the secondary hyperlipoproteinemia in patients under diuretic therapy we measured serum lipids, lipoproteins and the apoproteins A1, A2 and B in 12 adults after a 4 weeks placebo period and 6 weeks of treatment with chlorthalidon. There was a significant increase in atherogenic low density lipoproteins (LDL), (18%, P less than 0.05) whereas the high density lipoprotein-cholesterol Apo A1 and A2 levels were not significantly altered. The same was true for the total serum triglyceride- and the very low density lipoprotein- and LDL-triglyceride levels. The activity of lipoprotein lipase and hepatic triglyceride lipase was slightly but not significantly increased. A delayed LDL-catabolism seems to be the most probable pathogenic mechanism underlying the Chlorthalidon-induced hyperlipoproteinemia.

Adolescent↗