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An exaggerated, early prolactin response (p less than 0.01) was observed in ten patients with untreated essential hypertension (148 +/- 4/97 +/- 1 mmHg, means +/- SE) compared with ten healthy normotensive men of the same age (124 +/- 3/78 +/- 2 mmHg) after administration of metoclopramide, a competitive dopamine antagonist. The normotensive peak value of prolactin never exceeded that of the hypertensive (p less than 0.05). Since prolactin is considered an indicator of central dopaminergic activity, these findings suggest an altered central dopaminergic activity in mild essential hypertension.

Seventeen 50-year-old hypertensive men (157 +/- 4/110 +/- 2 mmHg, mean +/- SE) were given low sodium diet for one week, which was supplemented with potassium the following week. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:5 and 1:12, respectively, during dietary intervention. Arterial plasma vasopressin decreased by 3.4 +/- 1.7 ng/l (0.05 less than p less than 0.10) and urinary excretion of vasopressin was reduced by nearly 50% (p less than 0.001) during sodium depletion, while plasma noradrenaline increased by 38% (p less than 0.001) and plasma dopamine showed an increase by 58% (p less than 0.001). Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). With combined salt depletion and potassium supplementation, arterial plasma vasopressin decreased by 9.5 +/- 4.0 ng/l (p less than 0.05) compared to control. Urinary excretion of vasopressin together with plasma noradrenaline and dopamine were unchanged during the second week. The reduction of blood pressure was most marked during the first week (143 +/- 3/103 +/- 2 mmHg, p less than 0.05), but continued to fall also during the second week. Thus, during sodium restriction in middle-aged hypertensive men, blood pressure reduction occurs concomitantly with inhibited vasopressin release, despite enhanced renin and catecholamine release. Potassium supplementation during sodium restriction induces only minor changes in these variables.

Hypertensive men aged 42 (n = 35) were compared to normotensive men of similar age (n = 44). Platelet numbers were similar in the two groups, but hypertensive men had larger venous platelets than the normotensive (7.46 versus 7.12 femtoliter, p = 0.01). Plasma concentration of beta-thromboglobulin (BTG), a marker of platelet release reaction, was increased in arterial blood in hypertension (40 versus 21 micrograms/l, p = 0.02). The normotensive subjects had markedly higher BTG concentration in venous compared to arterial blood (p less than 0.01), but this arterio-venous difference was not present in the hypertensive group. Twelve normotensive subjects received infused saline, which did not induce changes in platelet variables. Adrenaline was infused to 13 hypertensive and 12 normotensive subjects, with dose gradually increasing to 0.04 microgram/kg/min. Platelet count increased in both groups, but significantly more in the hypertensive group. Platelet volume and BTG both increased markedly in the hypertensive group, but not in the normotensive men. Thus, young men with hypertension have increased platelet activity and increased sensitivity to exogenous adrenaline.

The long-term effects of prazosin in chronic congestive heart failure were studied in 10 patients (New York Heart Association class III-IV) in a double-blind cross-over study. Patients with systolic blood pressure greater than 120 mmHg and left ventricular filling pressure greater than 15 mmHg were included. Prazosin lowered the arteriovenous oxygen difference both at rest and during exercise (p less than 0.05), increased cardiac index (p less than 0.01) and reduced right atrial pressure and systemic vascular resistance (p less than 0.05) during exercise. Left ventricular filling pressure was also reduced, but not significantly, during exercise. Our data show that prazosin has beneficial long-term effects during exercise in patients with chronic congestive heart failure.

Background: B-type natriuretic peptide (BNP) measurements are useful for diagnosing congestive heart failure (CHF) in patients presenting to the Emergency Department with acute dyspnoe. Whether the diagnostic accuracy of BNP is affected by the age and gender of the patients remains unknown. Aims: To evaluate the accuracy of BNP testing for diagnosing CHF in an unselected group of patients admitted to the emergency department of a Norwegian teaching hospital with a principal complaint of shortness of breath and to assess whether the diagnostic accuracy of the test differs according to age and gender. Methods: BNP levels in plasma were determined by a point-of-care device upon arrival in 155 patients presenting with acute dyspnoe. The diagnostic ‘gold’ standard for CHF was adjudicated by two independent cardiologists who were blinded to the BNP data. Results: By univariate logistic regression analysis, BNP was strongly related to a diagnosis of CHF. In a multivariate model BNP provided additional prognostic information to patient age and gender, radiographic evidence of pulmonary congestion and cardiomegaly, and the presence of pulmonary rales and jugular vein distention by physical examination. There was no significant interaction between age and BNP or between gender and BNP with regard to the accuracy of diagnosing CHF. The area under the receiver–operating characteristics-curve was 0.86 (95% confidence interval 0.78–0.93) in women and 0.90 (0.82–0.97) in men. The area under the curves were 0.82 (0.73–0.92) and 0.88 (0.80–0.97) for patients (both genders) aged ≥76 and

Os I, Hofstad AE, Brekke M, Abdelnoor M, Nesheim BI, Jacobsen AF, Birkeland K, Larsen A, Midtbo K, Westheim A (Ullevaal University Hospital and Aker University Hospital, Oslo, Norway). The EWA (Estrogen in Women with Atherosclerosis) Study: a randomized study of the use of hormone replacement therapy in women with angiographically verified coronary artery disease. Characteristics of the study population. Effects on lipids and lipoproteins. J Intern Med 2000; 247: 433–441. Objectives. To evaluate the effects of hormone replacement therapy (HRT) on lipids and lipoproteins in postmenopausal women with coronary artery disease. Setting. In this single-centre, controlled and randomized study taking place in a tertiary referral clinic, patients were examined at baseline, and after 3 and 12 months. All analyses were performed examiner-blind. Subjects. Postmenopausal women (n = 118) with angiographically verified coronary artery disease were recruited consecutively from patients referred for investigational procedures due to coronary artery disease. Interventions. The women were randomized to HRT, i.e. transdermal application of continuous 17-β oestradiol with cyclic medroxyprogesterone actetate tablets every 3rd month for 14 days, or to a control group. Main outcomes. Effects on lipids and lipoproteins. Results. After 3 months of unopposed oestradiol, triglycerides decreased significantly compared to the control group (P = 0.006). Sequential administration of medroxyprogesterone caused a decrease in HDL cholesterol (P = 0.01), concomitantly with a decrease in ApoA1 lipoproteins (P = 0.007). No other changes in lipids or lipoproteins were observed. After 12 months of therapy, no significant differences were observed between the two groups in lipid or lipoprotein levels. Concomitant statin treatment did not alter the main findings. Conclusions. In postmenopausal women with established coronary artery disease in whom the majority is treated with statins, no additional effect of HRT on lipids or lipoproteins could be observed except for a transient decrease in triglycerides in the initial unopposed oestradiol phase. No deleterious effect could be observed during medroxyprogesterone administration except for a small transient decrease in HDL cholesterol and ApoA1 lipoproteins.

The effect of a cold pressor test (CPT) on haemodynamics in relation to general and regional sympathetic activity and arginin vasopressin (AVP), was studied in eleven patients with severe congestive heart failure (CHF). Compared to an age-matched control group (C), resting arterial plasma noradrenaline (NA) (419 +/- 77 vs. 182 +/- 15 pg ml-1), and adrenaline (A) (142 +/- 28 vs 54 +/- 10 pg ml-1) were higher (P less than 0.05) in CHF. AVP showed no significant difference (14 +/- 4 vs. 9 +/- 4 pg ml-1). During CPT systolic and diastolic blood pressure and systemic vascular resistance increased (P less than 0.01), as did NA (delta 114 +/- 39 pg ml-1, P less than 0.01), A (delta 33 +/- 10 pg ml-1, P less than 0.01) and heart rate (delta 10 beats min-1, P less than 0.01). The myocardial v-a difference of NA decreased (P less than 0.05), but was unchanged across the renal vascular bed during CPT. The a-v difference of NA in the hepatic vascular bed, and fractional extraction of A in the coronary sinus, renal and hepatic vascular beds remained unchanged during CPT. AVP did not change significantly and no change in cardiac index or left ventricular filling pressure was observed during CPT. These data suggest that despite an increased activation of the sympathetic nervous system at rest, a further increase in blood pressure and catecholamines took place during CPT. Thus, the effect of a CPT which activates the central sympathetic system seems not to be altered in patients with severe CHF.

Seventeen 50-year-old men, previously untreated and all with mild to moderate essential hypertension, were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. Urinary excretion of Na+ decreased from 201 +/- 11 to 24 +/- 5 and 19 +/- 4 mmol 24 h-1, respectively, after 1 and 2 weeks (means +/- SE) while the urinary Na+: K+ ratio changed from 2:1 to 1:4 and 1:11. Despite significant changes in blood pressure, body weight, serum electrolytes, sympathetic noradrenergic tone, haemoglobin concentration and haematocrit, no significant change appeared in serum total cholesterol, HDL-cholesterol or triglycerides. Thus, low sodium diet alone and combined with potassium supplementation seems neutral to blood lipoproteins in the treatment of essential hypertension.

To elucidate the myocardial metabolic and haemodynamic effects of an inotropic drug in patients with coronary artery disease (CAD) without evident congestive heart failure (CHF), the acute effects of prenalterol were studied in nine patients. Patients with documented CAD by leftsided cardioangiography and end-diastolic pressure greater than 15 mm Hg were included in the study. They were examined at rest and during supine exercise at a level just below their anginal threshold before and after prenalterol. At rest, rate pressure product (RPP) increased by 40% (P less than 0.01), cardiac index rose 20% (P less than 0.01), cardiac venous flow (CVF) increased by 18% (P less than 0.05), and myocardial oxygen consumption (MVO2) increased by 20% (P less than 0.05) after prenalterol administration. Despite a decrease in mean pulmonary capillary venous pressure (PCV) of 40% (P less than 0.01), myocardial lactate extraction fell significantly (P less than 0.01) and lactate production was observed in three of nine patients compared to before prenalterol administration. During exercise, RPP increased by 20% (P less than 0.01), cardiac index remained unchanged, CVF increased by 25% (NS) and MVO2 showed a tendency to an increase (NS) after prenalterol administration. Mean PCV pressure decreased by 30% (P less than 0.01). Myocardial lactate extraction was markedly reduced during exercise (P less than 0.01) and five of nine patients showed lactate production compared to that before prenalterol administration. Thus, despite a decrease in left ventricular filling pressure, increased myocardial oxygen demand occurred after acute administration of prenalterol. Prenalterol and probably similar inotropic drugs should be used cautiously in patients with CAD without clinical evidence of congestive heart failure.

Summary. The haemodynamic effect of two successive supine exercise tests 20 min apart was examined in 12 patients with angina pectoris. All the patients had coronary artery disease verified by angiography and were accepted for coronary bypass surgery. They exercised 20–40 W and all of them had angina during the first exercise test. Half the patients did not experience angina during the second of the two exercise tests (‘warm-up’ responders). In these patients left ventricular filling pressure (LVFP) was reduced by 40% (P