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1

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Acute and chronic effects of nifedipine in arterial hypertension (1978)

Pedersen, O. Lederballe ; Mikkelsen, E.

Springer

European journal of clinical pharmacology 14 (1978), S. 375-381

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ISSN: 1432-1041

Keywords: Arterial hypertension ; antihypertensive therapy ; calcium antagonists ; nifedipine ; forearm hemodynamics

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary Sublingual administration of nifedipine 10 mg to 11 patients and 20 mg to 6 patients with arterial hypertension caused a rapid and significant decrease in blood pressure in both groups. The average maximal reductions in the two groups were 21/16 mm Hg and 27/21 mm Hg. A concomitant rise in heart rate was found. Forearm blood flow showed a significant increase and the calculated vascular resistance a significant decrease 15–60 min after administration of both the 10 mg and the 20 mg doses. There was a negative correlation between basal vascular resistance and the maximal change of this parameter (r=−0.72, p〈0.01). Plasma concentrations of nifedipine showed considerable individual variation, with slow absorption in some patients, which indicated failure of sublingual absorption in them. The difference between the mean plasma concentration in the two dose groups was statistically significant after 45 min. A negative correlation was present between the plasma concentration of nifedipine and the observed change in calculated vascular resistance (r=−0.74 at t=30 min). Treatment of 10 hypertensive patients with nifedipine 30–60 mg daily for 6 weeks reduced mean blood pressure from 175/115 mm Hg to 151/96 mm Hg (p〈0.001). Heart rate and forearm blood flow rose, whereas the forearm vascular resistance showed a significant decrease. Side effects of a sensation of heat and reddening of face were noted in some patients. It is suggested that nifedipine may be useful both in the acute and chronic treatment of arterial hypertension.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00716377

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2

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Renal effects of pinacidil in hypertensive patients on chronic beta-blocker therapy (1986)

Krusell, L. R. ; Christensen, C. K. ; Pedersen, O. Lederballe

Springer

European journal of clinical pharmacology 30 (1986), S. 641-647

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ISSN: 1432-1041

Keywords: pinacidil ; hypertension ; vasodilators ; renal function and — haemodynamics ; beta-blockers ; guanidines ; pharmacokinetics

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary The acute and chronic effects of pinacidil on blood pressure (BP) and renal function were investigated in 10 patients with moderate arterial hypertension insufficiently controlled by chronic beta-blockade. Acute i. v. administration of pinacidil caused a significant fall in BP of 29.9/18.3 mm Hg and, despite beta-blockade, a concomitant rise in heart rate (HR) of 21%. Renal vascular resistance (RVR) showed a marked reduction as a consequence of the fall in BP, and a transient rise in renal plasma flow (RPF). Diuresis and renal clearance of sodium and uric acid showed a parallel fall. The excretion rates of albumin and β2-microglobulin were also significantly reduced. Pharmacokinetic studies indicated that glomerular filtration was responsible for elimination of the parent drug, and that proximal tubular secretion was the pathway of excretion of the main metabolite, pinacidil pyridine-N-oxide. During therapy for 4 months there was no further significant reduction in BP, despite increases in the daily dose of pinacidil. The effects on HR were less conspicious after 4 months; renal haemodynamic parameters and body weight were not significantly changed. The initial level of RVR and the initial acute reduction in this parameter appeared to be major determinants of the long-term BP response. The drug was well tolerated apart from one patient who developed slight fluid retention. However, concomitant administration of a diuretic will probably be necessary during routine use of this therapeutic combination.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00608209

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3

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Does verapamil have a clinically significant antihypertensive effect? (1978)

Pedersen, O. Lederballe

Springer

European journal of clinical pharmacology 13 (1978), S. 21-24

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ISSN: 1432-1041

Keywords: Arterial hypertension ; calcium antagonist ; verapamil ; hypotensive action

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary Verapamil was evaluated as an antihypertensive agent in a pilot study. Intravenous administration of 0.1 mg/kg, followed by constant infusion of 0.0035 mg/kg/min, reduced both systolic and diastolic blood pressure significantly; the maximal average decrease of 23/16 mm Hg occurred after 5 min. The resting pulse rate rose during infusion and prolongation of the atrio-ventricular conduction time was a constant finding. After the initial drop in blood pressure, a rise toward control levels was observed, despite an increase in the infusion rate. Five patients received oral treatment with verapamil 320–640 mg daily for 7 weeks. In four of the five patients a blood pressure reduction was obtained (mean: 14/12 mm Hg), but normotension was not achieved in any of them. In contrast to the acute studies, the atrio-ventricular conduction time showed no change and a decrease in resting pulse rate was noted. Two patients experienced sensations of heat and reddening of face during treatment. It is concluded that verapamil has a rather modest antihypertensive effect and it is not suitable for the treatment of arterial hypertension.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00606677

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4

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Distribution, elimination and natriuretic effect of furosemide in patients with severe arterial hypertension (1978)

Andreasen, F. ; Pedersen, O. Lederballe ; Mikkelsen, E.

Springer

European journal of clinical pharmacology 14 (1978), S. 237-244

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ISSN: 1432-1041

Keywords: Furosemide ; arterial hypertension ; protein binding ; sodium excretion ; renal function ; pharmacokinetics

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary Furosemide 40 mg was injected intravenously in 7 patients with severe hypertension and vascular complications. A two compartment, open model was used to describe the disappearance of the drug from serum. The mean serum clearance (Cls=1.83 ml/min · kg) was significantly reduced compared to the mean Cls-value of a group of normals (2.96 ml/min · kg). A significant correlation was found between Cls and mean blood pressure, as well as between Cls and renal clearance (mean Clr=0.83 ml/min · kg); extrapolation of the regression line yielded a Cls-value of 50 ml/min for Clr=0. The Clr was also significantly negatively correlated with mean blood pressure. Protein binding of furosemide was normal, except in one patient, who had considerable impairment of renal function. Apparently more than 90% of unchanged furosemide passed in urine was excreted by tubular transport. A highly significant negative correlation was found between Cls and the fraction of furosemide excreted as a glucuronide. During the first two hours, significantly less sodium was excreted by the patients than by a comparable group of normal subjects. The correlation between serum concentration of furosemide and the amount excreted of sodium was not significant, but highly significant correlations were found between the amounts of furosemide and sodium excreted by the kidney in 0–30 and 0–60 min. In all the individual patients an approximately linear relationship with wide variation in the slope was found between the cumulative excretion of furosemide and sodium from 0–30 min to 0–60 and to 0–120 min. After 120 min deviations were observed in the curves from 4 of the patients, which indicated that smaller and smaller additional amounts of sodium were excreted with constant additional amounts of furosemide.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00560456

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5

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Renal uric acid handling is not affected by beta-adrenoceptor blockade in normotensive subjects (1985)

Pedersen, O. Lederballe ; Jacobsen, F. K. ; Stengaard-Pedersen, K.

Springer

European journal of clinical pharmacology 28 (1985), S. 223-224

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ISSN: 1432-1041

Keywords: uric acid ; beta-adrenoceptor blockade ; blood pressure ; timolol

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary Nine normotensive healthy females received timolol 5 mg daily for a 4-day period and subsequently 20 mg daily for another 4-day period. None of the two dosages of timolol caused significant changes in serum uric acid or 24-h urinary fractional excretion of uric acid. Thus the increments of serum uric acid previously found in hypertensive patients is not likely to be caused by beta-adrenoceptor blockade per se.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00609696

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6

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Effect of nifedipine on plasma renin, aldosterone and catecholamines in arterial hypertension (1979)

Pedersen, O. Lederballe ; Mikkelsen, E. ; Christensen, N. J. ; [et al.]

Springer

European journal of clinical pharmacology 15 (1979), S. 235-240

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ISSN: 1432-1041

Keywords: nifedipine ; arterial hypertension ; calcium antagonist ; renin ; aldosterone ; catecholamines ; autonomic activity

Source: Springer Online Journal Archives 1860-2000

Topics: Chemistry and Pharmacology , Medicine

Notes: Summary Acute sublingual administration of nifedipine 10–20 mg to 13 hypertensive patients caused a rapid decrease in blood pressure (BP) and a concomitant increase in heart rate (HR), plasma noradrenaline (NA) and plasma renin activity (PRA); there was no significant change in plasma adrenaline (A) or aldosterone (ALDO). Basal PRA was the major determinant of the rise in PRA, as a close correlation was present between the basal value and the increase caused by nifedipine (r=0.92, p〈0.001). The rise in PRA was also correlated with the plasma concentration of nifedipine after 60 min (r=0.80, p〈0.01), but it was not correlated with the decrease in BP, the rise in HR or the increase in NA. Nifedipine 30–60 mg daily for 6 weeks caused a reduction in mean BP from 133 to 113 mmHg (p〈0.001). Body weight and serum potassium decreased but no consistent change was noted in NA, PRA, ALDO or 24 h-excretion of catecholamines. A significant correlation was present between the change in NA and that in PRA (r=0.74, p〈0.01). The alterations in the various parameters in the acute and chronic studies were not correlated. The findings indicate that different regulatory mechanisms are activated during acute and chronic administration of nifedipine. It is suggested that an initial rise in sympathetic activity gradually decreases during prolonged therapy, but it still remains a determinant of PRA.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00618511

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