Showing papers by "Sverre E. Kjeldsen published in 1988"

Increased platelet and vascular smooth muscle reactivity to low-dose adrenaline infusion in mild essential hypertension.

Abstract: During low-dose adrenaline infusion, platelet count, platelet size, plasma beta-thromboglobulin (BTG) and forearm vascular resistance (FVR) were measured in twelve 40-year-old men with mild, untreated hypertension. The average platelet count increased from 195 to 226 X 10(9)/l (P less than 0.001), platelet size from 7.31 to 7.53 X 10(-15)/l (P less than 0.01), BTG from 0.61 to 1.08 nmol/l (P less than 0.02) and FVR decreased from 97 to 58 (arbitrary units; P less than 0.001) during the infusion. The change in platelet count reflects splenic release of platelets, the change in plasma BTG reflects platelet release reaction, while the reduced FVR reflects vascular smooth muscle cell relaxation. In 11 normotensive men aged 40 years, platelet count increased from 187 to 201 X 10 g/l (P less than 0.01) during an equal low-dose adrenaline infusion. This increase in platelet count is significantly less than in the hypertensive group (P less than 0.01). There was statistically no significant change in platelet size, BTG or FVR in the normotensive group. Arterial adrenaline rose from 0.5 to 2.5 nmol/l in the hypertensive and from 0.5 to 2.4 nmol/l in the normotensive group. A third group of 12 normotensive men received saline infusion: neither platelet parameters nor FVR changed in this group. Thus, a small and equal dose of adrenaline elicited a greater increase in platelet count, an enhanced platelet release reaction and a more pronounced forearm vasodilation in hypertensive than in normotensive subjects.

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

Abstract: The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 +/- 11 (SE) to 24 +/- 5 and 19 +/- 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 +/- 2.9 to 39.6 +/- 4.7 pg/mg (p less than 0.005) and venous plasma norepinephrine increased from 3.7 +/- 0.4 to 5.6 +/- 0.5 pg/ml (p less than 0.005), and venous plasma dopamine increased from 26 +/- 4 to 41 +/- 5 pg/ml (p less than 0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p less than 0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion.

Decreased platelet-free dopamine and unchanged noradrenaline and adrenaline in essential hypertension.

Abstract: The content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 +/- 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 +/- 0.9 pg/mg found in the normotensive (p less than 0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.

Hyper-responsiveness to low-dose epinephrine infusion in mild essential hypertension.

Abstract: The present study was undertaken to evaluate the effects of intravenous infusion of small amounts of epinephrine on haemodynamics, renal electrolyte excretion and blood platelets in essential hypertension. Arterial plasma epinephrine concentrations were increased during the infusion to approximately 2.5 nmol/l both in a group of 40-year-old men with untreated mild essential hypertension (blood pressure 154 +/- 3/100 +/- 3 mmHg, n = 12) and in a group of age-matched male controls (124 +/- 3/78 +/- 2 mmHg, n = 11). In the hypertensive group only, mean blood pressure decreased, forearm blood flow increased, forearm vascular resistance decreased (P less than 0.001 for all) and the urinary excretion of sodium and potassium increased (P less than 0.01 for both). The hypertensive group also responded with an increase in plasma beta-thromboglobulin (P less than 0.05), blood platelet size (P less than 0.05) and a higher increase in platelet counts than in the normotensive group (P less than 0.05). Thus, in several ways the hypertensive patients showed a hyper-responsiveness to amounts of epinephrine which corresponds well to the plasma concentration achieved during psychological and physical activity.

Plasma Adrenaline: Relations to Blood Pressure, Blood Platelet Function and Blood Lipids in Essential Hypertension

Abstract: For various reasons plasma catecholamines should be measured in arterial blood when comparing hypertensive and normotensive groups (1, 2). Measurements of plasma catecholamines in peripheral venous blood may conceal important hypertensive-normotensive differences (2). Plasma catecholamines seem to be subjected to a peripheral arterialvenous fractional extraction of approximately 50%. Thus, arterial adrenaline represents the effective adrenaline concentration to which the tissues are exposed. Besides, plasma noradrenaline in peripheral venous blood mainly represents local release related to skeletal muscle sympathetic tone which seems unchanged in essential hypertension ( 3 ) .

Long-term pacing in VVI-modes elicit similar sympathetic drive.

Abstract: Ventricular inhibited (VVI] pacing in patients with atrioventricular (AV) hlock may increase sympathetic nervous tone compared to the hemodynamically superior AV synchronous mode even if symptoms of cardiac decompensation are lacking. Thus, short-term VVI pacing induces a higher release of norepinephrine into coronary sinus blood than does atrial pacing.^ However, this difference may subside due to adaptation during long-term pacing. A general increase in the adrenergic drive should be reflected in systemic catecholamine concentrations. We examined seven symptom-free patients, aged 32-74 years, treated with dual chamber pacemakers for high degree AV block: Cordis Sequicor 233 (Cordis Corp., Miami, FL, USA) in four and Intermedics 483-01 (Intermedics, Inc., Freeport, TX, USA) in three patients. Holter monitoring during VVI pacing demonstrated continuous pacing with the atria in stable sinus rhythm in all patients. In random succession the pacemakers were programmed either to VVI 70 ppm or to optimal DDD program. Each period lasted 7-21 days, and the patient was not informed of the pacing mode used. At the end of each period the patient was examined at 8 A.M. after at overnight fast and an abstension from drugs, coffee, tea, and tobacco. A plastic cannula was inserted into a forearm artery under local anaesthesia without epinephrine. After supine rest for 30 minutes in a quiet and dimly lit room, 5 mL of aterial blood was collected for catechoiamine assay. The patient was then exercised on a tricycle ergometer, and blood sampling was repeated at maximal work. The blood samples were immediately placed on ice with a preservative and centrifuged. The plaisma was stored at —70° until analysis. Plasma epinephrine and norepinephrine concentrations were measured by the method of Peuler and Johnson^ as previously reported.^ The resting plasma norepinephrine concentrations in VVI and DDD were 253 ± 28 pg/mL (mean ± SEM) and 226 ± 54 pg/mL, respectively, increasing during exercise to 2,962 ± 768 pg/mL and 2,848 ± 768 pg/mL. The corresponding plasma epinephrine concentrations were 60 ± 10 pg/mL and 58 ±C 10 pg/mL at rest and 353 ± 74 pg/mL and 338 ± 62 pg/mL during exercise.* None of the differences between VVI and DDD was statistically significant. Atrial rates were identical in both pacing modes, and Holter monitoring revealed that during the last 24 hours before blood sampling all patients had close to 100% paced rhythm. Thus, the preset study cannot demonstrate any difference between VVI and DDD long-term pacing with respect to arterial catecholamine concentrations. Arterial catecholamine concentrations reflect the total sympathetic stimulation, whereas, venous samples are influenced by organ secretion or extraction of catecholamines. Thus, during VVI and DDD pacing, any difference in myocardial catecholamine release or uptake, if present, was not large enough to appear in systemic circulation.