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Biomedical subjects

G Keusch

Publications and source records attributed to G Keusch.

At least 91 records · Page 5Linked to original sources
PubMed1982

Catecholamines, sodium and renin in unilateral renal hypertension in man.

The relative roles of plasma or urinary norepinephrine (NE) and epinephrine (E), exchangeable sodium, blood volume, and plasma renin (PRA) or aldosterone in the pathogenesis of unilateral renal hypertension was evaluated. 99 normal subjects and 33 age-matched untreated hypertensive patients with unilateral renal parenchymal disease (RPD) (n = 18) or unilateral renal artery stenosis (RAS) (n = 15) were compared. Measurements were repeated following operative treatment in 23 patients. Plasma and urinary NE or E, exchangeable sodium and blood volume did not differ significantly between normal and untreated subjects with RPD or RAS. Both patient subgroups had increased blood pressure and supine PRA (p less than 0.001); these abnormalities were milder with RPD. Plasma aldosterone and upright PRA were significantly elevated (p less than 0.05) in RAS only. Operative treatment of RPD and RAS caused decreases in blood pressure (-18 and -28%) and PRA; they correlated in RPD (r = 0.56; p less than 0.05). In RPD and RAS, exchangeable sodium, blood volume, and NE or E values were not significantly changed following operation, except for mildly increased upright PNE in RAS. These observations suggest that the sympathetic system plays no major role in the maintenance of unilateral renal hypertension in man. However, the 'normal' body sodium-volume state in RPD or RAS may be inappropriate relative to coexisting hypertension. In addition to its established role in RAS, mild activation of the renin-angiotensin system may also be important for the pathogenesis of hypertension caused by unilateral RPD.

Adult↗
PubMed1981

[Cardiovascular diseases after kidney transplantation: an analysis of predisposing factors].

Out of 512 recipients of kidney allotransplants 36 patients exhibiting cardiovascular complications (coronary artery disease, cerebrovascular accident, aneurysm of aorta, peripheral arterial occlusions) were compared with an age and sex matched group of recipients without cardiovascular problems. The following significant differences were observed in the study group versus the controls: high systolic and diastolic blood pressure, longer duration of hypertension before renal allografting, higher serum concentrations of cholesterol, triglycerides and uric acid, and an increased incidence of left ventricular hypertrophy and preexisting cardiovascular disease. No differences were found between the two groups as regards smoking habits, overweight, hyperparathyroidism, duration of hemodialysis treatment and type of kidney disease. Diabetes mellitus, family history of cardiovascular complications and hypertonic alterations of the eye fundus were more frequent, but not to a statistically significant extent, in the study group as compared to control patients. These findings show the need for regulation of blood pressure, hyperlipemia and hyperuricemia to ensure successful longterm rehabilitation after kidney allografting.

Cardiomegaly↗
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↗
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

[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↗
PubMed1980

Effects of chronic alpha and beta adrenoceptor blockade with labetalol on plasma catecholamines and renal function in hypertension.

Plasma catecholamines and renal function were evaluated in 18 patients with essential hypertension treated with the alpha and beta adrenoceptor blocking agent, labetalol. Following 6 weeks of labetalol therapy, blood levels of epinephrine and norepinephrine remained unaltered. Glomerular filtration rate and renal plasma flow were decreased similarly by about 20% (P less than 0.025). Tubular rejection fraction of sodium was increased by 36% (P less than 0.001) while sodium excretion was comparable to control conditions. Labetalol's potential to cause a mild reduction in kidney function should be considered, but may have no clinical consequences in most hypertensive patients receiving such treatment. The lack of increased plasma catecholamine levels during therapy supports the concept that labetalol's alpha-blocking potential is limited to post-junctional receptors, leaving the prejunctional feedback control of catecholamine release intact. Moreover, labetalol's blood pressure-lowering mechanism may be largely independent of changes in sympathetic nervous activity.

Adult↗
PubMed1980

Increased serum low-density lipoprotein cholesterol in men treated short-term with the diuretic chlorthalidone.

The effect of the diuretic chlorthalidone (100 mg/day for 6 weeks) on serum lipoproteins was evaluated in 37 subjects. In 19 men with essential hypertension (aged 41 +/- 3 yr), 8 normal men (26 +/- 3 yr), or all of these men considered together, chlorthalidone significantly increased serum low density lipoprotein--cholesterol (LDL-C) by 20% (p less than 0.05 to less than 0.01). There was also a tendency for increased LDL-C in seven postmenopausal women (+/- 15%) but not in three premenopausal women with essential hypertension. High density lipoprotein--cholesterol was not significantly changed in hypertensive women or normal men and decreased slightly (p less than 0.05) in hypertensive men. Apolipoproteins A-I, A-II, and B were not changed significantly in women or men. Diuretic-induced lipoprotein alterations were not associated with altered plasma volume and unrelated to variations in serum potassium, glucose, insulin levels, blood pressure, and body weight. Short-term diuretic therapy with chlorthalidone may increase serum LDL-C in young or middle-aged men with normal or high blood pressure.

Adolescent↗