Reports of elevated plasma catecholamine levels and augmented responses to autonomic blockade suggest increased sympathetic tone in borderline hypertension. It is not known if this reflects greater sympathetic neural outflow. We directly recorded muscle sympathetic nerve activity (microneurography) in 15 normotensive and 12 borderline hypertensive age-matched men to determine whether borderline hypertensive individuals have elevated sympathetic nerve activity. Supine heart rate, blood pressure, plasma norepinephrine, and efferent muscle sympathetic nerve activity (peroneal nerve) were measured after 6 days of both low and high dietary sodium intake (10 and 400 meq sodium/24 hr). Sympathetic nerve activity was elevated significantly in borderline hypertensive individuals on both low (37 ±1 in borderline hypertensive individuals vs. 29±1 bursts/min in normotensive individuals; p<0.01) and high (25+1 in borderline hypertensive individuals vs. 16±1 bursts/min in normotensive individuals; p<0.01) sodium diets. The borderline hypertensive group had higher systolic (p<0.01) and diastolic (/?<0.05) blood pressures independent of sodium intake. Across both groups, high sodium intake reduced muscle sympathetic nerve activity (p<0.001), plasma norepinephrine (/»<0.001), diastolic blood pressure (p<0.02), heart rate (/?< 0.002), and increased weight (p<0.005). A significant (p<0.05) group-by-diet interaction was observed for plasma norepinephrine levels. Specifically, compared with the normotensive group, plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet (p=0.08) and lower on high sodium diet (/?=0.23). High sodium intake increased diastolic pressure by over 5 mm Hg in six of 27 subjects (four borderline hypertensive and two normotensive). Sympathetic activity in sodium-sensitive subjects was not elevated compared with sodium-resistant subjects and also declined during high sodium intake. This study supports the hypothesis of elevated central sympathetic neural outflow in borderline hypertension. (Hypertension 1989;14:177-183) I ncreasing evidence suggests that mild or borderline hypertension is characterized by augmented sympathetic activity both at rest and in response to physical and psychological stressors.1 -5 For example, Esler et al 6 found elevated plasma norepinephrine levels (compared with This manuscript from the University of Iowa was sent to Randall M. Zusman, Consulting Editor, for review by expert referees, for editorial decision, and final disposition.Address for correspondence: Dr. Erling A. Anderson, Department of Anesthesia, University of Iowa, College of Medicine, Iowa City, IA 52242.Received August 12, 1988; accepted March 22, 1989. normotensive persons) in younger, but not older, hypertensive humans. Goldstein 7 reviewed studies of plasma catecholamine levels in hypertension and noted that significant elevations were reported in 11 of 16 studies comparing young (less than 40 years) hypertensive individuals with normotensive individuals but in...

The present study examined the role of personality as a predictor of mortality among patients with chronic renal insufficiency. A prospective evaluation of the influence of personality on patient survival was conducted over an average 49-month period. Cox regression was used to evaluate the effects of 5 dimensions of personality in a sample of 174 patients (100 male and 74 female). At follow-up, 49 patients had died. Significant demographic and clinical predictors of survival included age, diabetic status, and hemoglobin level. After these predictors were controlled for, 2 personality traits, conscientiousness and neuroticism, predicted patient mortality. Patients with high neuroticism scores had a 37.5% higher estimated mortality rate. Patients with low conscientiousness scores had a 36.4% increased mortality rate.

Among end-stage renal disease (ESRD) patients on hemodialysis, death from withdrawal from life-sustaining dialysis is increasingly common. The present study's objective was to examine depression as a potential risk factor for hemodialysis withdrawal. Two hundred forty ESRD hemodialysis (133 male and 107 female) patients were followed for an average of 4 years after depression symptom assessment. Of these, 18% withdrew from dialysis. Using multivariate survival analysis and after controlling for the effects of age (p < .001) and clinical variables, the authors found that level of depression symptoms was a unique and significant predictive risk factor for the subsequent decision to withdraw from dialysis (p < .05). The potential impact that depression may have on the decision to withdraw from hemodialysis should be considered by health care providers, patient families, and patients.

The present study found that participation in a behavioral self-regulation intervention resulted in no unique intervention effect on a key indicator of adherence for those with severe chronic kidney disease. There was, however, modest within-subjects improvement in interdialytic weight gain for the intervention group which meshes with other evidence showing the utility of behavioral interventions in this patient population. ClinicalTrials.gov Identifier: NCT01066949.

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With a modified version of the Ways of Coping Checklist, the relation of coping to adherence among 57 hemodialysis patients was examined. The association of a particular type of coping to adherence was predicted to depend on the specific type of stressful encounter being considered. As predicted, coping efforts involving planful problem solving were associated with more favorable adherence when used in response to stressors involving a relatively controllable aspect of the hemodialysis context. For less controllable stressors, coping efforts involving emotional self-control were associated with more favorable adherence. The seeking of informational support in response to an uncontrollable encounter was associated with poorer fluid-intake adherence. Confrontive coping was associated with poorer adherence for both high- and low-control situations.

The renal and adrenal responses to a continuous infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril were studied in 27 chronically catheterized sheep fetuses (less than 120 days gestation, n = 15, and greater than 130 days gestation, n = 12; term being 145 days) and in 12 newborn lambs between 8 and 21 days of age. Total renal blood flow did not change during ACE inhibition. However, the renal vascular resistance decreased significantly in newborn lambs (-21.8 +/- 5.7%) and in fetuses greater than 130 days (-21.7 +/- 4.7%) but not in fetuses less than 120 days. A significant decrease in filtration fraction (-19.2 +/- 6.5%) was observed in newborn lambs. No changes in urinary kallikrein and prostaglandin excretion rate were observed during ACE inhibition in any group of animals. ACE inhibition produced similar declines in blood pressure in both groups of fetuses (-10.2 +/- 3% in fetuses less than 120 days and -9.5 +/- 4.6% in fetuses greater than 130 days) and in newborn lambs (-13.4 +/- 2.1%). The percent changes in plasma renin activity were similar in all groups of animals. However, a significant decline in plasma aldosterone concentration was observed only in newborn lambs (from 130 +/- 31 to 64 +/- 9 pg/ml). These results suggest that the renin-angiotensin system might have physiological significance during maturation, but that this role seems to be more important in near-term fetuses (greater than 130 days) and postnatally than early in gestation.

The purpose of this study was to evaluate effects of high and low sodium intake on arterial pressure and forearm vascular resistance in subjects with borderline hypertension and to compare responses to sodium excess in these subjects with responses in a recent study in normotensive subjects. Six subjects with borderline hypertension were studied after ten days of high (410 mEq/24hr) and low (10mEq/24hr) sodium intake. Potassium intake was constant. In five of six subjects, high sodium intake decreased forearm blood flow and increased forearm vascular resistance and arterial pressure. During low and high sodium intake forearm blood flow averaged 7.8 plus or minus 1.2 (SE) and 5.9 plus or minus 0.8 ml/min x 100 ml, respectively; forearm vascular resistance averaged 13.5 plus or minus 2.2 and 19.1 plus or minus 3.0 units, respectively; and mean arterial pressure averaged 89 plus or minus 3 and 98 plus or minus 2 mm Hg, respectively. High sodium intake augmented forearm vasoconstrictor responses to lower body negative pressure, a stimulus to neurogenic vasoconstriction. The results contrast with our earlier results in normotensive subjects in whom sodium excess produced forearm vasodilatation and failed to increase arterial pressure significantly. Decreases in renin and aldosterone with high sodium intake were similar in the two groups. The results suggest that excessive sodium intake in subjects with borderline hypertension produces abnormal increases in forearm vascular resistance, neurogenic vasoconstriction, and arterial pressure. The reasons for the contrast between the borderline hypertensives and normotensives are unknown, but they do not seem to be related to the renin-angiotensin-aldosterone system.