Hypertension is not a simple disease, and stress is a major and often overlooked component. Accordingly, therapy should be aimed at correcting all hemodynamic variables-not just the elevated resting blood pressure. Appropriate treatment that normalizes these variables promises to be more effective in treating or preventing sequelae such as myocardial infarction, sudden death, and left ventricular hypertrophy than solely lowering resting blood pressure.

Twenty young (45 years or younger) and 20 older (55 years or older) adult patients with mild hypertension were enrolled in this study to compare the hemodynamic effects of labetalol versus placebo in two age groups. Ten patients in each group were randomly assigned to receive either a single oral dose of labetalol (200 mg) or placebo. Hemodynamic parameters were recorded immediately before and two hours after ingestion. Labetalol was more effective than placebo in significantly lowering systolic blood pressure (−11 versus + 5 mm Hg, −23 versus +4 mm Hg), diastolic blood pressure (−9 versus + 2 mm Hg, −12 versus +5 mm Hg), and total systemic resistance (−259 versus +42 dynes‐sec cm−5, −390 versus + 74 dynes‐sec cm−5) in young and older hypertensive subjects, respectively. There was no signifcant changes in heart rate, stroke volume index, or cardiac index in either age group. These data indicate that labetalol lowers blood pressure in young an older hypertensives primarily by reducing peripheral resistance and that the antihypertensive effect may be somewhat greater in older patients.

In a single case study of a moderately trained, healthy man, physiologic changes during a marathon are reported. Blood was drawn prior to the race, at 1 hour and 2 hours into the race, at the end of the race, and after 1 hour of recovery. By 1 hour into the race, norepinephrine, epinephrine, and dopamine had increased nearly nine-fold, two-fold and five-fold, respectively. After 1 hour of recovery, epinephrine had returned to the pre-race value but norepinephrine and dopamine were still elevated. Cortisol increased gradually and was more than doubled by the end of the race. It was still elevated after 1 hour of recovery. White blood cells gradually increased, reaching their maximum value at the end of the race; a four-to-five-fold increase. Thromboxane B2, which had an inverse relationship to serum magnesium, was below the pre-race value for the first 2 hours but increased nine-fold by the end of the race. Serum magnesium increased from 1.44 meq/l to 1.68 meq/l at 2 hours into the marathon, dropped to 1.07 meq/l by the end of the race, and returned to its pre-race value by 1 hour of recovery. The decrease in serum magnesium at the end of the race may be associated with increased plasma free fatty acid levels.

The typical physiologic response to exercise is a rapid increase in systolic blood pressure (SBP) and heart rate (HR). Diastolic blood pressure (DBP) does not increase significantly in healthy young persons. In the literature, the blood pressure response to physical exercise tests has yielded conflicting results regarding blood pressure (BP) reactions of hypertensives or normotensive patients. Most studies show no difference in the reaction pattern of hypertensives and normotensives [10, 11, 15] unless the patients are older or already have an impaired vascular system [17]. Pickering and co-workers [14] reported last year, for example, that 20 normotensive, 19 borderline hypertensive, and 15 hypertensive outpatients showed similar increases in BP (44/0, 52/ – 1,48/ – 1 mmHg respectively).

31P n.m.r. analysis of control and diabetic hearts perfused for 1 h with a glucose buffer showed constant and normal levels of phosphocreatine and ATP. Supplementing the buffer with 0.5, 1.2 or 2.0 mM-palmitic acid had little or no effect on high-energy-phosphate levels in control hearts. In contrast, increases in palmitate concentration produced significant decreases in ATP in diabetic hearts, despite normal and constant levels of phosphocreatine. This 31P n.m.r. study suggests a defect in phosphocreatine metabolism in the perfused diabetic heart that might be related to creatine kinase kinetics.

The purpose of the present study was to determine how cigarette smoking and psychological stress combine to affect cardiovascular function. Stress was operationally defined as playing a series of difficult video games under challenging instructional conditions. Following an initial test game, 51 smokers were randomly assigned to a 2 (smoke vs. sham smoke) X 2 (stress vs. no stress) design. The results showed that the subjects who sham smoked (inhaled unlit cigarettes) under no stress evidenced minimal changes in cardiovascular parameters. Subjects who smoked under no stress evidenced approximately 12 mmHg increase in systolic blood pressure (SBP) and 9 mmHg increases in diastolic blood pressure (DBP), and a 15 beat-per-minute increase in heart rate (HR). These effects were similar in magnitude to those seen in subjects who sham smoked under stress. By contrast, subjects who smoked under stress showed markedly larger increases in all cardiovascular parameters, approximately doubling the magnitude of the observed response over that seen with either smoking or stress alone. Correlational analyses suggested the presence of stable individual differences in autonomic lability or sensitivity. Possible mechanisms are suggested whereby stress and smoking may combine to heighten the risk for coronary disease.

Male college students (n = 64) participated in a competitive "TV tennis game" while their heart rate and blood pressure were monitored. Subsequently, their health records were inspected to determine frequency of illnesses. Subjects who responded during the contest with extreme increases in heart rate and diastolic blood pressure were significantly more likely to have frequent minor illnesses than those responding with moderate or low increases.

The purpose of this chapter is to describe in some detail a proposal for a research project that, in our opinion, is a logical next step in the current efforts to understand the ways in which environmental, behavioral, and physiologic processes interact to contribute to the development of coronary-related diseases. The project described herein is actually already in the initial stage of development and has been submitted to and approved by the Western Electric Company for implementation. The research project is designed to investigate the ways in which personality characteristics, situational factors in the work environment, and individual patterns of autonomic nervous system (ANS) activity are related to stress, illness, and job productivity. The present proposal focuses primarily on the type A coronary-prone behavior pattern and associated patterns of cardiovascular and ANS reactivity. This emphasis reflects that extensive research now links the type A/B behavior dimension to increased risk of coronary heart disease (CHD), and an increasing body of evidence suggests that excessive levels of ANS reactivity shown preferentially by type A individuals may constitute one of the mechanisms for this increased risk.

In this investigation, 30 male post-myocardial infarction patients and 30 male control subjects matched according to age and occupation were given a 12-minute tape-recorded stress quiz described by Schiffer et al. Cardiovascular responses (electrocardiogram, heart rate, systolic, blood pressure, and diastolic blood pressure) to emotional stimuli were monitored in a laboratory setting at rest before the quiz and at two-minute intervals during the quiz. Heart rate and blood pressure values were significantly higher during the quiz than at rest for both patient and control groups. There was a significantly higher response for diastolic pressure and a significantly lower response for heart rate in the patient group compared with the control group. In the analysis for occupational status in the entire population, systolic pressure was significantly higher for the executives than for non-executives. Subgroup analyses of patients with angina, hypertension and/or ECG changes (N = 12) revealed a significantly higher diastolic pressure response than found in either the patients without these symptoms (N = 18) or in the controls (N = 30). In comparison to exercise test results, the emotional stress test (quiz) elicited somewhat more PVC's but less ST segment depression. These results support previous reports suggesting that emotional stress testing may be a valid tool in the diagnosis of coronary heart disease and in determining the physiological mechanisms which underlie the association between emotional stress and coronary heart disease.

This paper reviews the pathophysiologic influences of 20th century emotional stress. The physiologic consequences of cardiovascular conditioning by aerobic techniques are also reviewed. It would appear that cardiovascular conditioning has physiologic characteristics which would counterbalance those induced by such stress. Accordingly, it appears logical that cardiovascular conditioning by aerobic exercise techniques is an effective therapeutic and prophylactic tool. Future investigative efforts must take two directions. First, the extent to which exercise may be used in ameliorating the pathologic consequences of chronic stress must be scientifically documented. Secondly, in those instances where exercise is undertaken imprudently, evidence must be gathered as to the extent that physical activity precipitates maladaptive responses in humans.

Regional differences in glycogen and triglyceride metabolism were found in the ischemic dog left ventricle. Under these conditions, the subendocardium was characterized by a faster rate of glycogenolysis and the least ability to mobilize tissue triglycerides relative to subepicardial and midventricular zones.