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Biomedical subjects

P Weidmann

Publications and source records attributed to P Weidmann.

At least 163 records · Page 9Linked to original sources
PubMed1985

Body-sodium and blood volume in a patient with licorice-induced hypertension.

A 68-year-old man a nine-year history of licorice ingestion had moderate hypertension and low plasma potassium. Exchangeable sodium and blood volume were increased to 128 and 111%, respectively of the expected values; plasma renin and aldosterone levels were suppressed. Plasma norepinephrine concentration was distinctly elevated but the pressor response to infused norepinephrine was normal. After licorice withdrawal, blood pressure, plasma potassium and blood volume reverted to normal levels within three weeks, exchangeable sodium and plasma renin within four months. Exchangeable sodium in our patient with licorice-induced hypertension was increased to a comparable extent as in primary hyperaldosteronism. Moreover, blood pressure in relation to body sodium or plasma potassium did not differ between the exogenous or the endogenous types of mineralocorticoid excess. This observation does not support the possibility that in primary hyperaldosteronism excess aldosterone secretion per se could play an important pressor role independently from sodium retention.

Aged↗
PubMed1985

Effects of human atrial natriuretic peptide on the pressor action of noradrenaline and angiotensin II in normal subjects.

The newly synthesized human alpha-atrial natriuretic peptide(alpha-hANP)(molecular weight 3082.6) was injected intravenously at stepwise increasing doses of 10, 40 and 75 micrograms into eight normal subjects (mean age +/- s.d. 24 +/- 1 years). The highest dose decreased blood pressure (BP) only slightly under basal conditions (from 118/76 +/- 8/10 to 111/71 +/- 10/13 mmHg, P < 0.005 for systolic BP) and insignificantly during angiotensin II (ANG II) pressor infusion (from 134/98 +/- 9/10 to 137/93 +/- 12/14 mmHg). In contrast, during a noradrenaline (NA) pressor infusion, BP was lowered progressively by the three alpha-hANP doses from 163/96 +/- 12/11 to 156/88 +/- 9/11 (P < 0.02), 148/78 +/- 12/7 (P < 0.001) and 148/70 +/- 10/13 mmHg (P < 0.001), respectively. Heart rate was increased similarly (P < 0.001) by a alpha-hANP during (from 51 +/- 10 to 63 +/- 12 beats/min) or ANG II infusion (from 53 +/- 5 to 64 +/- 10 beats/min). Effects were maximal from 1 to 4 min, lasting for 10 min. These observations reveal that alpha-hANP possesses vasoactive properties independent of a natriuretic action in normal subjects. Alpha-atrial natriuretic peptide may interact preferentially with noradrenergic as compared with angiotensinergic blood pressure control mechanisms.

Adult↗
PubMed1985

Cardiovascular effects of short-term selective alpha 1-adrenergic blockade with terazosin in patients with essential hypertension.

The effects of selective alpha 1-adrenergic blockade with the agent terazosin on blood pressure and cardiovascular pressor responsiveness as related to major pressor factors were assessed in 17 patients with mild to moderate essential hypertension (mean age +/- s.e.m. 48 +/- 2 years). As compared with a 2-week placebo period, terazosin, given during 8 weeks at a maximal daily dose of 10.5 +/- 1.7 mg, caused a fall of supine arterial pressure (from 153/103 +/- 3/2 to 143/96 +/- 4/2 mmHg; P < 0.05), and a marked blunting of cardiovascular pressor responsiveness to norepinephrine (NE) as judged from the pressor dose (from 0.43 +/- 0.05 to 12.74 +/- 2.93 mmol/kg per min, P < 0.05) and from the shift to the right (P < 0.01) of the correlation relating NE-induced increments of arterial pressure to the corresponding increases of plasma NE during NE infusion. Heart rate, body weight, exchangeable sodium, blood volume, NE plasma clearance, plasma epinephrine, renin, angiotensin (ANG) II and aldosterone levels, the relationships between the ANG II-induced increases in arterial pressure or plasma aldosterone and the concomitant increments of plasma ANG II during ANG II infusion as well as the heart rate responsiveness to isoproterenol did not change significantly after terazosin. The findings of the present study suggest that the fall of arterial pressure induced by selective alpha 1-adrenergic blockade in patients with essential hypertension is associated and probably explained by inhibition of alpha 1-mediated, noradrenergic-dependent vasoconstriction.

Adrenergic alpha-Antagonists↗
PubMed1985

Pathogenesis and treatment of hypertension associated with diabetes.

The pathogenesis of hypertension accompanying diabetes mellitus (DM) may involve abnormalities in at least two major blood pressure (BP)--regulating systems. Exchangeable sodium (Naex) and the cardiovascular pressor responsiveness to norepinephrine are often increased, while blood volume is normal or low, regardless of age, insulin-dependence or non-dependence, or the presence or absence of retinopathy or clinical nephropathy. In hypertensive DM, systolic BP correlated (P less than 0.001) with Naex; diuretic treatment improved norepinephrine responsiveness, Naex and BP, while calcium entry blockade improved cardiovascular responsiveness and BP without changing Naex. Plasma catecholamine, renin and aldosterone levels are usually normal or sometimes low in stable DM. Antihypertensive therapy in DM is based on 3 legs, namely antidiabetic treatment, general measured aimed at reducing BP and associated risk correlates, and if necessary BP-lowering drugs. Due to their metabolic side effects, thiazide-diuretics given in moderate to high doses are not ideal step 1 drugs in DM. Certain beta 1-blockers have fewer, although still some, unwanted side effects. Preliminary data suggest that certain calcium antagonists may often lower BP without causing relevant metabolic impairment. These agents and converting enzyme inhibitors deserve further evaluation in the treatment of DM-associated hypertension.

Angiotensin II↗
PubMed1984

[Cardiovascular risk factors: an intervention program for general practice].

A new multiple risk factor intervention program, combining a comprehensive, stepwise and health education-based approach, was tested in an outpatient setting. In the first 47 patients (aged 17-55, referred by their physicians) total cardiovascular risk (estimated by Framingham index) was reduced within the first 12 months by an average of 32.5%. This improvement derived from significant reductions in all major risk factors. These findings demonstrate the feasibility and potential, yet unexploited, benefit of a more comprehensive risk factor, approach in general medical practice.

Adolescent↗
PubMed1984

[Arterial hypertension: adenocarcinoma of the kidney or bilateral renal artery stenosis$].

In a 71-year-old female with severe hypertension, bilateral renal artery stenosis and renal adenocarcinoma, a renal vein renin study revealed suppressed renin secretion from the kidney with carcinoma and contralateral ischemia. The hypertension was not cured by surgical removal of the kidney with carcinoma. Hypertension is frequently noted in patients with renal adenocarcinoma (28% of 603 patients reported in the literature). This type of hypertension is frequently improved after removal of the tumor (83% of 36 surgically treated patients). In certain patients the pathogenesis of hypertension associated with renal adenocarcinoma may be related to renin secretion from the tumor or to renin activation due to regional ischemia caused by vascular compression. In other patients the renin-angiotensin system does not appear to play a pathogenic role in the development of hypertension associated with renal adenocarcinoma.

Adenocarcinoma↗
PubMed1984

Studies on acute glucose-induced aldosterone suppression: role of renin-angiotensin system.

Glucose loading is known to cause acute suppression of plasma aldosterone and stimulation of plasma renin activity. The relative contribution of variations in circulating angiotensin II to the regulation of aldosterone secretion following glucose loading was assessed in ten normal subjects. The effects of a standard oral glucose loading test (100 g) on plasma concentrations of glucose, insulin, potassium, aldosterone, renin activity and cortisol were studied (a) under basal conditions, and (b) after inhibition of angiotensin II with the converting enzyme inhibitor captopril (50 mg t.i.d. during 3 days). Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P less than 0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P less than 0.01); plasma potassium was decreased slightly but not significantly. Following captopril treatment preloading plasma renin activity was increased significantly, most probably reflecting an effective reduction of angiotensin II. Glucose loading caused a similar suppression of plasma aldosterone, as observed under basal conditions. This observation suggests that renin activation does not substantially contribute to the acute regulation of plasma aldosterone after an oral glucose load.

Adult↗
PubMed1984

[Orthostatic hypotension].

The practicing physician commonly encounters patients with hypotensive disturbances of orthostatic blood pressure regulation. These include the functional orthostatic syndrome as well as the true forms of orthostatic hypotension due to hypovolemia, certain cardiac, pulmonary or endocrine diseases, or (particularly in the elderly) autonomic dysfunction of varying etiology. The possible pathogenetic mechanisms are also many and varied, while various drugs may play a causative or contributory role. Careful evaluation and treatment with general measures and, if indicated, pharmacologic agents may (even in the presence of severe neurogenic orthostatic hypotension) often lead to marked improvement in blood pressure and in quality of life.

Autonomic Nervous System Diseases↗
PubMed1984

Increased serum high-density lipoprotein cholesterol in hypertensive men treated with the potent vasodilator carprazidil.

The effects of the potent arteriolar vasodilator carprazidil on serum lipoproteins and various clinical, biochemical and endocrine parameters were assessed in 15 men with mild to moderate essential hypertension. Following a carprazidil monotherapy (average dose 50 to 60 mg/d) of 8 weeks (N = 15) or 16 weeks (N = 12) duration, blood pressure was decreased significantly (P less than 0.01), while serum high-density lipoprotein cholesterol (+ 26% and + 24%, respectively; P less than 0.01) and the alpha-lipoprotein fraction (+ 26% and + 41%) were increased. Low- and very low-density lipoprotein cholesterol, triglycerides, as well as mean body weight, blood and plasma volume, heart rate, and plasma renin, aldosterone, norepinephrine, and epinephrine were not consistently altered. These results indicate that treatment of hypertensive men with carprazidil in modest dosage may have a favorable influence both on blood pressure and serum lipoproteins.

Adult↗
PubMed1984

Effects of treatment with diuretics on serum lipoproteins.

Diuretics, when used for antihypertensive therapy, may also affect lipoprotein metabolism. The following observations were made after 1-12 months of treatment. Various thiazide-type diuretics significantly increased the potentially atherogenic serum low-density lipoprotein cholesterol (LDL-C) and/or very-LDL-C (V-LDL-C) fractions, while the antiatherogenic high-density lipoprotein cholesterol (HDL-C) level was largely unchanged. Certain loop diuretics also increased the LDL-C/HDL-C ratio. Both types of diuretics elevated serum triglyceride (Tg) levels in some, but not all, studies. Levels of LDL-C were increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women, but not in chlorthalidone-treated premenopausal women. Only two diuretics evaluated, indapamide and spironolactone, had no apparent influence on lipoproteins. A tendency for increased Tg levels and lower HDL-C concentrations was apparent during combined thiazide-type diuretic-beta-blocker treatment; these changes resembled those observed during beta-blocker monotherapy. Diuretic-induced increases in LDL-C were prevented or reversed by concomitant beta-blockade, but not by combination treatment with sympatholytics such as reserpine, methyldopa, and clonidine. Prospective studies are needed to clarify the long-term course and the pathogenic and prognostic relevance of lipoprotein changes induced by various diuretics. In the meantime, it is of clinical interest that premenopausal women may be protected from thiazide-induced increases in LDL-C, certain diuretic agents have no significant effect on serum lipoproteins, and beta-blockers may prevent or reverse increases in LDL-C in men and postmenopausal women during diuretic treatment.

Adolescent↗
PubMed1984

Disturbed noradrenergic blood pressure control in normotensive members of hypertensive families.

The possible influence of a family history of hypertension on some variables of adrenergic blood pressure regulation was assessed. Blood pressure, heart rate, plasma renin activity, adrenaline and noradrenaline concentrations, and plasma or urinary electrolyte estimations did not differ significantly between two groups of normotensive subjects matched for age and sex with and without a family history of hypertension. Compared with subjects without a family history, however, an appreciably decreased pressor dose of infused noradrenaline, a distinct shift to the left in the relation between noradrenaline induced changes in mean arterial pressure and concomitant plasma noradrenaline concentrations, and an enhanced pressor response to given increases in plasma noradrenaline concentrations occurred in the group with a family history. These findings suggest that an imbalance between cardiovascular noradrenaline responsiveness and circulating noradrenaline is a common familial disturbance which could possibly predispose to the development of essential hypertension.

Adult↗
PubMed1984

Pathogenesis and treatment of hypertension in renal tuberculosis.

39 patients underwent partial or total unilateral nephrectomy for treatment of renal tuberculosis. Before surgery, blood pressure was increased in 12 cases (30%). 5 patients had only mild hypertension which was not modified following surgery. 7 patients had moderate to severe hypertension, and in 5 of them blood pressure was normalized following nephrectomy, indicating a renal pressure mechanism. Special investigations in some of these patients revealed no evidence of a pathogenic role of the adrenergic system, but support the participation of the renin-angiotensin system in at least some patients with hypertension associated with renal tuberculosis.

Adult↗
PubMed1984

Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.

The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg X min was assessed in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P less than 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angiotensin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.

Adult↗