Showing papers by "Sverre E. Kjeldsen published in 1991"
TL;DR: The association of the hyperkinetic state with elevated norepinephrine in this study suggests that a sympathetic hyperactivity is present in a large proportion of unselected subjects with mild blood pressure elevation.
Abstract: Of 691 healthy (untreated) villagers of Tecumseh, Michigan (average age 32.6 years), 99 had a clinical blood pressure exceeding 140/90 mmHg. Thirty-seven per cent of these borderline hypertensives had increased heart rate, cardiac index, forearm blood flow and plasma norepinephrine. These subjects had elevated self-determined home blood pressure (average of 14 measurements). The present hyperkinetic borderlines had elevated blood pressure at 5, 8, 21 and 23 years of age and their parents also had higher blood pressure. The prevalence of high blood pressure in Tecumseh, its long history, elevated blood pressure readings outside the physician's office and family background of hypertension, suggests that the hyperkinetic state is a significant clinical condition. Previous studies on hospital-based populations proved that the hyperkinetic state is caused by an excessive autonomic drive. The association of the hyperkinetic state with elevated norepinephrine in this study suggests that a sympathetic hyperactivity is present in a large proportion of unselected subjects with mild blood pressure elevation.
240 citations
TL;DR: It is found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension, and the “platelet-neutral” properties of qu inapril suggest that quinAParil, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.
Abstract: The effect of various antihypertensive medications on platelet function is of increasing interest. Conflicting effects of captopril on platelet function are reported and the impact of angiotensin converting enzyme (ACE) inhibitors not containing a sulfhydryl group such as enalapril, lisinopril, and quinapril on platelet function remains unstudied. Therefore, the aim of the present study was to examine the effect of antihypertensive treatment with quinapril, a novel ACE inhibitor not containing a sulfhydryl group, on platelet function. Ten white men (age range of 32-61 years) with untreated mild-to-moderate essential hypertension (supine diastolic blood pressure greater than 95 mm Hg) were treated with 4 weeks each of placebo and quinapril in a double-blind, randomized, crossover design. Quinapril (20 mg twice a day) significantly lowered systolic (p less than 0.01) and diastolic blood pressure (p less than 0.01) without any significant effect on heart rate or plasma catecholamines. No significant change was noted for in vitro platelet aggregation induced by epinephrine, ADP, or collagen. Plasma concentrations of the platelet release factors beta-thromboglobulin and platelet factor 4 did not change, nor did the platelet content of norepinephrine, platelet weight (mg/10 ml of blood), circulating platelet count, or platelet size. Thus, as assessed by a broad spectrum of platelet parameters, we found that antihypertensive treatment with quinapril has no significant effect on platelet function in patients with mild-to-moderate essential hypertension. These "platelet-neutral" properties of quinapril suggest that quinapril, both from a thromboembolic and a hemostatic point of view, may be a rather safe agent for treatment of hypertension.
37 citations
TL;DR: In this article, it was shown by an aggregometer that epinephrine activated blood platelets, and it was proposed that platelets could be the link between stress and cardiovascular disease.
16 citations
TL;DR: The results indicate that absorption of adrenaline given by aerosol spray inhalation is more reliable when adrenaline is given by inhalation, and suggests that repeated inhalations are necessary when such adrenaline therapy is required.
Abstract: 1. The aim of the present study was to compare absorption of adrenaline given by aerosol spray inhalation with absorption after subcutaneous injection. 2. Arterial plasma adrenaline was measured in nine healthy volunteers following adrenaline administration by both methods. 3. Following inhalation of 20 puffs of adrenaline aerosol, 0.15 mg/puff, a peak arterial adrenaline concentration after 1 min and a rapid fall to baseline from this peak occurred. 4. When given by subcutaneous injection absorption was slower with a peak arterial adrenaline concentration after 4 min. The fall in arterial adrenaline from this peak level was not statistically significant within 30 min after injection. 5. There was less intersubject variation of arterial adrenaline concentration following inhalation when compared with injection. 6. Heart rate, blood pressure and finger tremor followed the changes in arterial adrenaline concentrations. 7. These results indicate that absorption is more reliable when adrenaline is given by inhalation. The rapid fall in arterial adrenaline following inhalation, suggests that repeated inhalations are necessary when such adrenaline therapy is required.
6 citations