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We examined changes in P wave height in lead II of electrocardiogram during progressive exercise in patients with chronic obstructive pulmonary disease (COPD), and obtained the slope (delta P/delta VO2, %/ml/min) of the regression line calculated from the relationship between percent change of P wave height and oxygen consumption (VO2). Four COPD patients, who had a decrease over 5 mmHg in arterial oxygen tension (PaO2) at maximal exercise (group A), had significantly greater slope (0.45 +/- 0.14%/ml/min, mean +/- S.E.) than in five COPD patients (group B, 0.14 +/- 0.05), who did not have a decrease over 5 mmHg in PaO2 at maximal exercise. The increase in P wave height during exercise was inhibited by oxygen inhalation at the given VO2 in group A. These findings suggest that increase in P wave height during exercise in COPD patients may be correlated with hypoxemia during exercise.

1. To clarify whether acute changes in the properties of baroreflexes can occur in man, we evaluated the time course of baroreflex control of heart rate and cardiopulmonary baroreflex control of forearm vascular resistance (FVR) over 240 min after intravenous administration of propranolol (0.2 mg/kg) in 13 healthy young men. 2. Systolic and diastolic blood pressure remained unchanged after propranolol. Propranolol significantly decreased cardiac index and heart rate, and significantly increased total peripheral resistance. These effects remained unchanged for 240 min after propranolol. 3. Baroreflex control of heart rate was significantly augmented immediately after, and at 30, 60 min after propranolol, but partly reverted to the initial level afterwards. Cardiopulmonary baroreflex control of FVR was reduced immediately after, and at 30, 60 min after propranolol, but partly reverted to the initial level afterwards. Pressor responses to phenylephrine was reduced immediately after propranolol, but no significant differences were observed after 30 min. 4. These results suggest that acute changes in the properties of baroreflexes occur in man after propranolol.

The effect of propranolol on baroreflex control of heart rate was studied in 12 young patients with essential hypertension and was compared with that of 12 age-matched normotensive subjects. Resting heart rate and cardiac index in patients with essential hypertension were significantly higher than those of control subjects (p less than 0.001, p less than 0.01, respectively). The reduction of heart rate and cardiac index after propranolol were significantly greater in patients with essential hypertension than in control subjects (p less than 0.01, p less than 0.05, respectively). In the control state, the baroreflex slope in young patients with essential hypertension was significantly less than that of control subjects (p less than 0.01). After propranolol, the baroreflex slope was significantly increased in control subjects (p less than 0.01), but remained unchanged in patients with essential hypertension. These results suggest, first that the antihypertensive action of propranolol must be due to a mechanism other than the augmented baroreflex function and, second that increased beta-adrenergic activity is not a factor contributing to impaired baroreflex function in young patients with essential hypertension.

Baroreflex control of heart rate, pressor responses to alpha agonist (phenylephrine) and isometric exercise before and during salt loading were compared between 13 normotensive subjects with hypertensive relatives (group A) and 9 normotensive subjects with no family history of hypertension (group B). Baroreflex slope was significantly lower in group A than in group B (9.6 +/- 1.6 vs 17.6 +/- 1.9 msec/mmHg; p less than 0.01), although blood pressure, heart rate and aortic distensibility were not different between two groups. Pressor responses to phenylephrine and isometric exercise were identical for both groups. During salt loading, pressor responses to phenylephrine and isometric exercise were significantly greater in group A than in group B. Baroreflex slope was not affected by salt loading in the two groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated arterial pressure and decreased aortic distensibility. Pressor responses to alpha agonist and isometric exercise during high-sodium diet were augmented in subjects with a family history of hypertension.

Cardiopulmonary baroreflex control of forearm vascular resistance (FVR) and arterial baroreflex control of heart rate were compared between 12 normotensive subjects with hypertensive relatives (group A, 19.4 +/- 0.2 years) and 12 normotensive subjects with no family history of hypertension (group B, 19.5 +/- 0.3 years). Cardiopulmonary baroreflexes were evaluated using lower body negative pressure (LBNP) at -20 mmHg, and arterial baroreflexes were measured by Oxford phenylephrine method. Resting arterial pressure, central venous pressure, heart rate, cardiac index, total peripheral resistance, and FVR were not different between the two groups. Arterial baroreflex slope (BS) and reflex increases in FVR during LBNP were significantly lower in group A than in group B (11.4 +/- 0.9 vs. 17.1 +/- 1.1 ms/mmHg, 37.7 +/- 8.1% vs. 86.5 +/- 18.7%, respectively). There was significant correlation between %FVR and BS (r = 0.59; p less than 0.01). These results suggest that both cardiopulmonary and arterial baroreflexes are impaired in normotensive young subjects with a family history of hypertension.

1. The effects of sodium loading on cardiopulmonary baroreflex control of forearm vasoconstriction were studied using lower body negative pressure (LBNP) in 12 healthy young subjects. 2. Before and during sodium loading, there was no significant change in mean blood pressure, heart rate, central venous pressure (CVP) or forearm vascular resistance (FVR). 3. The degree of reflex increase in FVR during LBNP at -10, -20, and -40 mmHg was significantly greater during sodium loading than regular diet. 4. During sodium loading, the slope of the regression line relating percent change in FVR and change in CVP was significantly increased. 5. These results suggest that sodium loading augments cardiopulmonary baroreflex sensitivity of FVR in normotensive subjects without a family history of hypertension.