Ingvar Aakesson

Binding of quinidine in sera with different levels of triglycerides, cholesterol, and orosomucoid protein

Abstract Serum binding of quinidine was determined in vitro by equilibrium dialysis in sera from twenty-five healthy individuals. The sera had different levels of triglycerides, cholesterol and orosomucoid ( α 1 -acid glycoprotein), but with small variations in serum albumin concentration. Binding ratio (bound/free) and per cent binding varied from 2.0 to 5.4 and from 67.1 to 84.3% respectively. Binding ratios were linearly related to serum concentration of triglycerides ( r = 0.437, P r = 0.400 P r = 0.841, P r = 0.765, P r = 0.465, P r = 0.753, P

Plasma adrenaline and noradrenaline during orthostasis in man: the importance of arterial sampling.

Plasma adrenaline and noradrenaline were measured in arterial blood and in forearm venous blood during supine rest and after 30 min standing in normotensive, healthy 50-year-old men (n = 16). After 30 min standing, venous noradrenaline had increased from 1.61 +/- 0.11 to 4.22 +/- 0.30 nmol/l and arterial from 1.43 +/- 0.06 to 2.93 +/- 0.15 nmol/l. Orthostasis induced a seven-fold increment in the forearm arterial-venous difference of noradrenaline from -0.18 +/- 0.08 to -1.29 +/- 0.25 nmol/l (p less than 0.001). Orthostasis more than doubled the forearm arterial-venous difference of adrenaline from 0.15 +/- 0.03 to 0.31 +/- 0.05 nmol/l (p less than 0.001) since arterial adrenaline increased from 0.31 +/- 0.03 to 0.53 +/- 0.05 nmol/l and venous from 0.16 +/- 0.02 to 0.22 +/- 0.02 nmol/l. Arterial adrenaline correlated significantly with venous in the supine (r = 0.64, p less than 0.01) but not in the standing position (r = 0.34, NS). The results indicate that arterial concentrations of adrenaline are a much better indicator of sympatho-adrenal activity during orthostasis than peripheral venous concentrations. For noradrenaline, measurements of arterial concentrations during the orthostatic manoeuvre seem to provide information about the total noradrenergic sympathetic reactivity, while the corresponding measurements in peripheral venous blood represent the forearm locally.

Increased arterial catecholamine concentrations in 50-year-old men with essential hypertension.

In a recent study of 50-year-old men with long-standing, untreated essential hypertension we found increased arterial and venous plasma concentrations and arterial-venous differences of adrenaline (a-v) and noradrenaline (v-a) as compared to a matching normotensive control group. The aim of the present study was to investigate whether men of this age with hypertension of shorter duration and less severity than in the first study might also have increased plasma catecholamines. Twenty-three hypertensive and 17 age-matched normotensive control men were studied. The hypertensive ones had increased supine heart rate (P less than 0.05), arterial noradrenaline (P less than 0.01) and adrenaline (P less than 0.02) whereas venous catecholamines did not differ between the two groups. The a-v differences (means +/- SE) of adrenaline (78 +/- 14 vs 42 +/- 6 ng/l, P less than 0.05) were increased in the hypertensive compared to the normotensive group. In the hypertensive, the arterial plasma concentrations of the two catecholamines correlated positively (r = 0.71, P less than 0.001) as did the a-v differences (r = 0.54, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Decreased central dopaminergic activity in essential hypertension.

Baseline serum prolactin (PRL) was found to be similar in 35 men with untreated essential hypertension (149 +/- 2/98 +/- 1 mmHg; means +/- s.e.) and 44 healthy normotensive men (126 +/- 1/80 +/- 1 mmHg), all 40 years old. A correlation between baseline PRL and aldosterone was found in the normotensive (r = 0.534, P less than 0.001), but not in the hypertensive group (r = -0.011, NS). Ten subjects from each group received intravenous metoclopramide, a competitive dopamine antagonist, while another 12 normotensive subjects were given saline only, and the effect on PRL, vasopressin (AVP) and catecholamines was followed. An exaggerated PRL response to metoclopramide was observed in the hypertensive group compared with the normotensive (P less than 0.05), and the mean normotensive peak value never exceeded the hypertensive. Plasma noradrenaline increased significantly compared with baseline (P less than 0.05) and the control group (P less than 0.001), concomitant with increased heart rate (P less than 0.05), after the administration of metoclopramide both in the hypertensive and normotensive group. After intravenous injection of metoclopramide, forearm blood flow increased significantly by 50% in the hypertensive (P less than 0.001), and 80% in the normotensive group (P less than 0.001) compared with the control group. Mean blood pressure remained unchanged as did plasma AVP, dopamine and adrenaline. The present study indicates an altered central dopaminergic activity in essential hypertension. Even at rest, endogenous dopamine exerts a modulating effect on noradrenaline release in both hypertensive and normotensive men.

Evidence of age-related variation in plasma vasopressin of normotensive men

The influence of age on plasma arginine vasopressin was examined in three groups of healthy men, 25 +/- 1 (n = 12), 40 (n = 23) and 50 years of age (n = 13), respectively. The three groups were comparable in body height, weight, blood pressure, heart rate, serum and urine osmolality, electrolytes and endogenous creatinine clearance. Compared to the 25-year olds, the 50-year old men had more than three times higher basal plasma vasopressin (7.8 +/- 1.4 vs. 2.5 +/- 0.6 ng/l, p less than 0.01), only one-third the plasma renin concentration (0.36 +/- 0.05 vs. 1.10 +/- 0.33 G.U. X 10(-4)/ml, p less than 0.01) and a significantly higher plasma noradrenaline (267 +/- 21 vs. 199 +/- 19 ng/l, p less than 0.05) while plasma adrenaline remained essentially unchanged. The 40-year olds had intermediate plasma vasopressin concentrations (4.2 +/- 0.6 ng/l). Thus, age is a variable with a substantial effect on plasma concentrations of vasopressin in addition to the well-known effect on renin and noradrenaline. Age must be taken into account in further clinical studies on vasopressin.