Ingolf Nielsen

Renin stimulation by passive tilting: the influence of an anti-gravity suit on postural changes in plasma renin activity, plasma noradrenaline concentration and kidney function in normal man.

Plasma renin activity (PRA), plasma noradrenaline concentration, heart rate, blood pressure, and clearances of para-aminohippurate and inulin were measured in twelve normal subjects (clearances in only three subjects) before and after 40 min of 60 degrees upright tilting. The tilting experiments were repeated after inflation of an anti-gravity suit to 60 mmHg on the lower extremities. Inflation of the anti-gravity suit caused an abolition of the postural PRA increase, a marked reduction of the postural increases in plasma noradrenaline and heart rate, and elimination of the decreases in pulse pressure, inulin and para-aminohippurate clearances and sodium excretion. The results suggest a decisive role of the sympathetic nervous system for postural renin increase, probably mainly activated by stretch receptors in the low-pressure cardiopulmoanry area.

Unimpeded Plasma Renin Increase after Intravenous Furosemide during Saline Replacement

The effect on plasma renin activity of intravenous furosemide combined with saline replacement of the volume depletion was studied in twelve patients with insignificant heart disease. In ten of the patients the investigation was repeated without saline replacement. It was found that saline infusion, reducing or eliminating hemoconcentration, had no significant influence on the marked plasma renin increase. In eight of the patients the combined furosemide-saline study was performed during right-hear catheterization. Decrease in atrial pressures, known to occur within 15 min after furosemide intravenously, was virtually absent with the saline replacement. It is concluded that plasma volume reduction after intravenous furosemide is responsible for decreased filling pressures of the ventricles but not for plasma renin increase.

The relationship of urinary prostaglandins and plasma renin to sodium balance and diuresis in normal man

The significance of changes in sodium balance and urinary sodium excretion for renal PG excretion was studied in normal man. In protocol B a strongly negative sodium balance was produced in 5 healthy young subjects by a low sodium diet given for 7 days (lo mmol Na/day) with 80 mg furosemide p.o. added on the last two days. 24 hour urinary PGE2 excretion remained constant, while plasma renin increased. In protocol A the effect of i.v. furosemide (1 mg/kg bwt) on urinary PGE2 and PGF2 alpha excretion rates was examined in 5 healthy young subjects. Rapid but short-lasting increases in PG excretion rates ran in parallel with the changes in urine flow rate. The study suggests that PGE2 is not of importance for the sodium homeostasis in normal man. Renal prostaglandins may play a modifying role for the renal response to loop diuretics but are hardly instrumental for the diuretic effect.

The influence of acute blood volume changes on plasma renin activity in man

The effect of an acute 10% blood volume reduction on plasma renin activity (PRA) was examined in seven patients with minor heart diseases during haemodynamic investigation and in five healthy subjects after 3 days furosemide administration. PRA was not significantly changed. Blood pressure remained constant, atrial pressures decreased. The effect on PRA of an acute 10% blood volume expansion with albumin infusion was studied in thirteen patients with liver or heart diseases. A slight reduction of PRA after albumin did not exceed the expected decrease due to plasma dilution. Blood pressure was unchanged, atrial pressures increased. Renal blood flow increased after albumin in all of the five patients investigated. The effect of PRA of an acute 10% blood volume expansion with whole blood flow increased after albumin in all of the five patients investigated. The effect on PRA of an acute 10% blood volume expansion with whole blood was then investigated in five healthy subjects, pretreated with furosemide for 3 days. A significant decrease in PRA was found. Blood pressure remained constant. It is concluded that an acute blood loss of 10% and an acute blood volume expansion of 10% with albumin have little influence on PRA in supine man, whereas an acute blood volume expansion of 10% with whole blood induces a significant PRA suppression.

Effect of verapamil on arrhythmias and heart rate during 16 months following an acute myocardial infarction

SummaryThe present study was a prospectively planned subset of the postinfarction, double blind, randomized, multicenter, placebo controlled trial of verapamil, DAVIT II. Patients had 24 hours of Holter monitoring before randomization, i.e., second week after infarction (placebo, n=122; verapamil, n=128), after 1 month (placebo, n=108; verapamil, n=94) and after 16 months (placebo, n=75; verapamil, n = 63) of treatment. The purpose was to evaluate the effect of verapamil on the prevalence and changes over time of arrhythmias and heart rate. In patients monitored twice, a significant increase of average ventricular premature complexes (VPC) per hour from before to 1 month (p=0.0007) and 16 months (p=0.02) after was demonstrated in the placebo group, and from before to 1 months (p=0.01) after in the verapamil group. Average VPC/hr did not change from 1 to 16 months of treatment. A significant increment of >10 VPC/hr was found after 1 (p=0.03) and 16 months (p=0.05) compared to prerandomization in the placebo, but not in the verapamil group. A significant increase of supraventricular arrhythmias after 1 month compared with prerandomization was found in the placebo group (p=0.003) but not in the verapamil group. The prevalence of VPC and supraventricular tachycardia was significantly lower in the verapamil compared with the placebo group after 1 month of treatment. At 16 months no significant difference was found between the two groups. The 24 hour mean heart rate was significantly lower, 3 beats/min, in the verapamil compared with placebo after 1 and 16 months of treatment. Thus a significant increase of ventricular and supraventricular arrhythmias during the first postinfarction month, without change the following year, was seen in the placebo group. Verapamil significantly lowered heart rate, prevented supraventricular tachycardia, and reduced VPC early after an AMI. This rather limited effect of verapamil on postinfarction arrhythmias cannot explain the beneficial effect of verapamil on mortality and major events in patients without heart failure.