In a previous haemodynamic examination, 44 young men (18-22 years) with blood pressure elevation above the 98th percentile, mean arterial blood pressure (MAP) greater than or equal to 95 +/- 6 mm Hg, showed an increased cardiac index (dye-dilution) and an enhanced resistance at maximal vasodilation of the hand (venous occlusion plethysmography during hyperaemia). This latter finding suggested arteriolar wall hypertrophy. However, the subgroup with the highest cardiac index (greater than or equal to 3.86 1 min-1 x m2) (n = 18) displayed normal vascular resistance at maximal dilation in comparison with the normotensive control group (n = 29). Consequently, functional signs of arteriolar hypertrophy were restricted to individuals with normal or low cardiac index. At the re-investigation 5 years later, a significant reduction in blood pressure was observed in the normotensive control group (MAP: from 88 +/- 7 to 85 +/- 7 mm Hg, P less than 0.05). There was no change in individuals with initially elevated blood pressure. Furthermore, cardiac index fell significantly with time in this latter group. Thus, the blood pressure elevation in the hypertensive group, previously mainly dependent on high blood flow was, 5 years later, more related to an increased total peripheral resistance, (delta total peripheral resistance = 8%). However, no definite evidence indicating development of hypertrophy of the resistance vessels of the hand was observed during the follow-up period. Since the hyperkinetic subgroup did not display a concomitant fall in blood pressure with cardiac output, our results do not support the theory that the hyperkinetic form of borderline hypertension is a temporary phenomenon, explained by the inclusion of anxious individuals afraid of the experimental situation. Hyperkinetic hypertension may be the initial phase of sustained hypertension in a subgroup of the future hypertensive population.

1.Forty-four young men with blood pressure elevation and 29 age-matched volunteer subjects were examined with invasive blood pressure and cardiac output measurements. The regional blood flow resistance of the hand during hyperaemia was calculated from blood pressure and flow data from venous occlusion plethysmography.2. In a re-examination 5 years later the same protocol was applied and an oral glucose tolerance test was performed with glucose and insulin determinations. Body composition was calculated from total body potassium data (whole body 40K counter) and body weight. 3.Patients with blood pressure elevation were characterized by a significantly higher cardiac index at rest, and a significantly increased resistance during hyperaemia of the hand in comparison with that of the controls. The patients with blood pressure elevations were also divided according to cardiac output. The hyperkinetic subgroup did not have an increased resistance during hyperaemia. Patients with blood pressure elevation had significantly increased body weight and body mass index in comparison with controls and there was a significant correlation between body wieght and regional resistance during hyperaemia. 4.In the re-examination it was found that the body weight difference between patients with blood pressure elevation and normotensive controls was explained by increased body fat. There was no difference in body weight between the normokinetic and hyperkinetic subgroups of patients with blood pressure elevation but the former group had significantly increased insulin concentrations on the glucose load. Correspondence: Dr Ove Anderson, Department of Internal Medicine, Sahlgrenska Hospital, S-413 45 Goteborg, Sweden. 5.Significant correlations were demonstrated between body weight, body fat and insulin concentration 30 min after glucose load against resistance during hyperaemia as the dependent variable. A multiple regression coefficient of 0.59 was found between the three independent variables and resistance during hyperaemia. Furthermore, the addition of the insulin concentration variable to the two independent variables body weight and body fat increased significantly the multiple regression coefficient.

Modification of carotid baroreflex heart and vascular responses during increased lung positive end-expiratory pressure (PEEP) were measured anesthetized aortic-denervated rabbits. Static carotid intrasinus pressure (ISP) was varied in increments of 12.5 mmHg over 25-140 mmHg during lung inflation conditions ranging from spontaneous breathing (SB) to positive-pressure respiration at 0.0-7.5 cmH2O PEEP. To distinguish cardiopulmonary vagally and nonvagally mediated influences, heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), and total peripheral resistance (TPR) were measured and compared before and after sequential vagotomy and beta- and alpha-receptor blockade. When compared with responses of SB animals the HR-ISP relationship was not significantly altered during controlled respiration (CR) with PEEP before or after vagotomy. With CR and then PEEP, MAP-ISP relationship curves and linear slope values (ISP range 62-113 mmHg) were significantly depressed when compared with those of SB rabbits. Before vagotomy slope values were -1.61 (SB), -1.22 (CR + 0.0 cmH2O PEEP), and -0.82 (CR + 7.5 cmH2O PEEP); respective values after vagotomy were -2.26, -0.96, and -0.64. Results of CO and TPR responses during low ISP and PEEP demonstrated components of both vagally and nonvagally mediated influences from inflation sensitive cardiopulmonary receptors.U

Reflex heart and mean arterial pressure (MAP) responses during unilateral and bilateral electrical stimulation of the central end of the cut aortic nerves were studied in 14 anesthetized closed-thorax rabbits. During control of carotid intrasinus pressure (ISP), with ISP = MAP, heart rate was 248 +/- 12 beats/min and fell -79 +/- 14, -61 +/- 16, and -117 +/- 16 beats/min during left (LAN), right (RAN), and bilateral (BAN) nerve stimulation. MAP was 79 +/- 5 mmHg and fell -57 +/- 4 (LAN), -46 +/- 6 (RAN), and -65 +/- 4 mmHg (BAN). Responses were also determined following blockade of cardiac vagal efferents (atropine) and then vagotomy (n = 4) or vagotomy alone (n = 10). Results indicated that cardiac parasympathetic effects of LAN and RAN stimulation were additive, whereas the respective summation of cardiac and arterial vascular sympathetic effects were mutually inhibitory. BAN stimulation at low (25 mmHg) and high (greater than or equal to 125 mmHg) ISP levels resulted in different magnitudes of MAP and heart rate responses before and after vagotomy and beta-receptor blockade. These results indicated that summation was mutually inhibitory for cardiac and vasomotor sympathetics when maximal stimulation of opposite influence was applied to aortic and carotid afferents. However, arterial baroreceptor afferents may summate differently at more normal blood pressure conditions.

Hemodynamic effects of loud noise before. and after central sympathetic nervous stimulation. Acta Med Scand 1987; 221: 159-64.