Borderline Hypertensive Patients Research Articles

Improved classification of dippers by individualized analysis of ambulatory blood pressure profiles

A decrease (dip) in blood pressure during sleep occurs in normal people and in patients with uncomplicated essential hypertension. Failure to identify such a dip suggests additional pathology, which makes the identification of "nondippers" important. Rigid definitions of nocturnal time periods (eg, night is defined as lasting from 22:01 to 06:00) to identify dippers and nondippers has been used for over a decade. However, these definitions may not correspond to actual sleep patterns, and thus may lead to faulty interpretations. We investigated whether or not an analysis of ambulatory blood pressure (BP) profiles according to the patients' individual reported awake/sleep pattern would result in an improved categorization of dippers and nondippers. Four groups of patients were investigated: normotensive volunteers, borderline hypertensive patients, essential hypertensive patients, and renal transplant recipients. In all four groups, blood pressure (systolic and diastolic) decreased to a greater degree when the individual reports were employed, compared to the fixed patterns. For systolic BP this difference (individualized v fixed 06:01 to 22:00 day and 22:01 to 06:00 night) amounted to 17.6 +/- 5.0 v 13.2 +/- 5.4 mm Hg for normotensive subjects, 18.5 +/- 6.0 v 11.7 +/- 8.6 mm Hg for borderline hypertensive subjects, 17.7 +/- 10.6 v 12.9 +/- 10.4 mm Hg for essential hypertensive patients, and 8.6 +/- 11.3 v 6.5 +/- 9.8 mm Hg in renal transplant patients (all P < .05). Individualized awake/sleep reports resulted in a better classification of dippers and nondippers, since misclassifications due to divergent sleep patterns (mainly going to bed late) were avoided.

Effect of recombinant human erythropoietin therapy on ambulatory blood pressure in normotensive and in untreated borderline hypertensive hemodialysis patients

The effect of recombinant human erythropoietin (r-HuEPO) on ambulatory blood pressure (ABP) was studied in 13 anemic hemodialysis patients. Eight patients were normotensive and five patients had untreated borderline systolic hypertension. Mean hemoglobin increased from 82 +/- 3 g/L to 114 +/- 3 g/L (P < .01) after 3 to 4 months of r-HuEPO therapy (30 to 40 U/kg) administered subcutaneously three times weekly. Mean 24-h systolic and diastolic ABP measurements were significantly increased by 16 +/- 4 mm Hg and 10 +/- 2 mm Hg, respectively (P < .01 for both). Blood pressure was increased in all but one patient. In six patients, the mean 24-h systolic and diastolic ABP measurements were more than 160 mm Hg or 90 mm Hg at the end of the study. The increase in ABP was slightly but not significantly greater during the waking period as compared with the sleeping period and the circadian blood pressure pattern was not modified by r-HuEPO treatment. The blood pressure load (percentage of ABP reading exceeding 140/90 mm Hg during the waking period and 120/90 mm Hg during the sleeping period) was significantly increased (P < .05) after r-HuEPO therapy. Nine of the 13 patients failed to show the expected reduction in blood pressure during the sleeping period and were defined as "nondippers"; the others were defined as "dippers." During r-HuEPO therapy, the increase in ABP was similar in both dippers and nondippers. This suggests that the nondipper condition is not a risk factor for the development of hypertension during r-HuEPO therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased sympathetic nervous system activity in Chinese hypertensive patients with type II diabetes mellitus

To evaluate the coexistence of sympathetic overactivity and hypertension in type 2 diabetic patients, a population-based study was conducted of newly-diagnosed type 2 diabetic patients recruited from a single community located at northern Taiwan. This study included 2877 (male 1382, female 1495) middle-aged ethnic Chinese adults, aged 45–65 years. Of the 1382 males, 67 had newly-diagnosed type 2 diabetes mellitus, whereas 75 of the 1495 females had type 2 diabetes. The data showed that about 39% of diabetic patients had borderline hypertension (mean blood pressure 141/91 mmHg) whereas the average incidence in non-diabetic subjects was 15.5%. The borderline hypertensive diabetic patients had significantly higher heart rates (mean 78.8 vs. 69.3 beats/min; P < 0.001) than control subjects. However, the cardiac index was similar in both control and diabetic subjects (mean 2.48 vs. 2.53 l/min/m 2; P > 0.05). Our data show that sympathetic overactivity and increased incidence of hypertension actually existed in these type 2 diabetic patients of Chinese origin.

Platelet function and fibrinolytic activity during rest and exercise in borderline hypertensive patients

In this study we examined whether the reduced fibrinolysis and increased platelet activity that are known to occur in hypertension are already present in borderline hypertension. Twelve patients with 'borderline' hypertension (diastolic blood pressure 90-95 mmHg) were found to have substantially reduced fibrinolytic activity, both at rest and during exercise, compared with 12 normotensive controls. Euglobulin clot lysis time (ECLT) was significantly higher in hypertensive subjects (218 min vs. 145 min; P < 0.05), and this difference persisted during exercise. Resting tissue plasminogen activator activity (t-PA) did not differ in the two groups, but the brisk increase in t-PA in controls during exercise (0.64 rising to 1.44 IU mL-1; P < 0.01) did not occur to the same extent in the borderline hypertensive subjects. Levels of the fast-acting t-PA inhibitor, normally referred to as PAI-1, were considerably higher in hypertensives (9.22 vs. 4.41 IU mL-1; P < 0.02), and this difference persisted in the upright posture, indicating a decrease in fibrinolytic activity. Platelet aggregability induced by ADP in vitro was not significantly higher in the hypertensive subjects, but indices of platelet activity in vivo (B-TG and PF-4 levels) revealed enhanced platelet function in the hypertensives. These results indicate that the indicators of altered haemostatic function known to occur in hypertension, namely diminished fibrinolytic activity and increased platelet function, are already detectable during the very earliest stage of the disease.

Borderline hypertensive autosomal dominant polycystic kidney disease patients have enhanced production of renal dopamine. Normalization of renal haemodynamics by DOPA infusion

In autosomal dominant polycystic kidney disease (ADPKD) the pathophysiology of hypertension, which is frequently observed before loss of renal function, is not well understood. We investigated intrarenal dopamine, the renin-angiotensin-aldosterone system (RAAS), and plasma endothelin in relation to sodium homeostasis as potential hypertensive factors in this disease. Eight borderline hypertensive ADPKD patients with (near) normal renal function and seven matched healthy control subjects were investigated at three levels of daily dietary sodium intake: 150, 50 and 450 mmol. In the 450-mmol sodium intake period we studied the effects of renally formed dopamine by infusing its precursor DOPA (DOPAi.v., 7 micrograms kg-1 min-1). In the 50-mmol sodium intake period we studied the influence of the RAAS by administering enalaprilate (42 micrograms kg-1), followed by angiotensin II (12 ng kg-1 min-1) intravenously. GFR and ERPF were measured by continuous infusion of inulin and PAH. At all levels of sodium intake sodium balances were equal, but daily urinary excretions of dopamine and DOPA were higher (P < 0.01) in the ADPKD patients than in the controls. Renal vascular resistance, filtration fraction and blood pressure were higher in the ADPKD patients (all P < 0.05) while plasma renin activity was similar. DOPAi.v. normalized renal haemodynamics and increased plasma endothelin in ADPKD patients (all P < 0.05), while stimulation of natriuresis was equal in both groups. Enalaprilate increased plasma endothelin in the ADPKD patients and only partially normalized renal haemodynamics. In borderline hypertensive ADPKD patients: (1) urinary dopamine excretion is increased at all levels of sodium intake, suggesting that this may be needed to maintain sodium balance; (2) stimulation of renal dopamine production is able to normalize renal haemodynamics, making dopamine receptor agonism a potential therapeutic option; (3) the activity of the RAAS is not clearly enhanced; (4) renal vasodilatation increases plasma endothelin levels.

Prescription and results of physical activity.

Epidemiologic studies suggest an inverse relationship between physical activity or fitness and blood pressure. In a meta-analysis of 36 controlled intervention studies, the weighted net blood pressure response to dynamic aerobic training averaged -5.3 mm Hg for systolic and -4.8 mm Hg for diastolic pressure. The variation of the change of blood pressure among studies was mainly dependent on the initial blood pressure level and the gain in exercise capacity. The weighted net change of blood pressure with endurance training averaged -3/-3 mm Hg in normotensive patients, -6/-7 mm Hg in borderline hypertensive patients, and -10/-8 mm Hg in hypertensive patients. Reductions of blood pressure have also been observed for measurements during exercise and during ambulatory monitoring. Exercise programs can contribute to the management of hypertension. Care is needed in the choice of antihypertensive drugs for the exercising patient because some drugs may impair exercise capacity.

Dopamine D5 receptor expression is unchanged in peripheral blood lymphocytes in essential hypertension.

The present study was designed to investigate possible changes in the expression of lymphocyte dopamine receptor in essential hypertension. The expression of dopamine D5 receptor was evaluated by radioligand binding techniques using [3H]-SCH 23390 as ligand. Plasma catecholamines, aldosterone levels and plasma renin activity were also measured. Eleven borderline hypertensive patients, 15 patient with the mild essential hypertension, 7 patients with moderate essential hypertension and 5 patients with severe essential hypertension were examined. Plasma catecholamine levels were assayed by high pressure liquid chromatography with electrochemical detection. Dopamine D5 receptor was measured by radioligand binding techniques. Plasma aldosterone levels and renin activity were determined by radio immunoassay. [3H]-SCH 23390 was specifically bound to human peripheral blood lymphocytes. The binding was time-, temperature- and concentration-dependent with a dissociation constant (Kd) value of 0.59 nM and a maximum density of binding sites (Bmax) of 223 pmol/10(6) cells. Dopamine competed with [3H]-SCH 23390 binding in the submicromolar range suggesting the labelling of a dopamine D5 receptor. No changes in the density of [3H]-SCH 23390 binding sites were observed in human peripheral blood lymphocytes between essential hypertensive patients and normotensive subjects. Also catecholamines, plasma renin activity and aldosterone levels were unchanged. In spite of the availability of a sensitive technique for measuring dopamine receptors in human peripheral lymphocytes, no change in their expression was noticeable in essential hypertension. This suggests that dopamine receptor analysis in essential hypertension is not a useful marker for investigating hypertension-dependent changes of the peripheral dopaminergic system.

Vascular compliance in sodium-sensitive and sodium-resistant borderline hypertensive patients

Recently, we demonstrated a reduction in the compliance of the carotid, femoral and brachial arteries in sodium-sensitive subjects who had consumed a regular sodium intake of approximately 120 mmol per day, as compared to both sodium-resistant borderline hypertensive subjects and normotensive controls. Venous compliance was not different between the two borderline hypertensive groups and was only slightly lesser than in controls. Large artery compliance was studied using a non-invasive ultrasound vessel wall movement detector system, while venous compliance was determined by means of strain gauge plethysmography. The borderline hypertensive subjects were subsequently treated with enalapril 10 mg/day, felodipine 5 mg/day or placebo during six months. Despite similar reductions in blood pressure, enalapril induced a significant increase of the muscular femoral and brachial artery compliance, but not of the elastic carotid artery, while felodipine did not influence large artery compliance at all in the sodium-sensitive group. The effect of enalapril on muscular artery compliance was established through a dose-dependent increase in distension and not through a change in arterial diameter. Arterial compliance was not influenced by either of the drugs in the resistant group. Venous compliance was also not altered by the medication. In conclusion, femoral and brachial artery compliance in sodium-sensitive borderline hypertensive subjects, which was found to be lower than that of sodium-resistant subjects, improved with antihypertensive treatment with enalapril but not with felodipine, despite the similar reductions in blood pressure induced by both drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

REACTIVITY OF CEREBRAL BLOOD FLOW TO CARBON DIOXIDE IN HYPERTENSIVE PATIENTS

To evaluate hypertensive cerebral involvement before cerebrovascular accidents. Cerebral microvascular responses to changes in the arterial partial pressure of CO2 (pCO2; the CO2 reactivity) were compared among patients with different stages and severity of hypertensive disease. Fifty-eight patients with hypertension, 11 with borderline hypertension, 15 hypertensives with cerebral infarction and 58 normotensive controls were studied. The cerebrovascular CO2 reactivity was determined by measuring simultaneously the end-tidal pCO2 and the blood flow velocity in the middle cerebral artery using transcranial Doppler sonography under hypocapnic, normocapnic and hypercapnic conditions. CO2 reactivity was impaired in the hypertensive patients compared with in the normotensive controls, but less so than in the symptomatic hemisphere of the hypertensive patients with cerebral infarction. The CO2 reactivity in the borderline hypertensive patients was greater than that in both the symptomatic and asymptomatic hemispheres of the hypertensive patients with cerebral infarction. In the subjects without cerebral infarction, two risk factors for cerebral atherosclerosis (age and hypertension) were negatively correlated with cerebrovascular CO2 reactivity. In the hypertensive patients age and the estimated duration of hypertension were negatively correlated with cerebrovascular CO2 reactivity. CO2 reactivity in the patients with hypertensive or arteriosclerotic retinopathy or ST-T changes on their electrocardiogram was impaired compared with that in the patients without such changes. Hypertension affected the microvascular reactivity of the brain before the development of cerebrovascular accidents, and its effect varied dependently on the extent of involvement of other target organs.

Extreme changes in dietary sodium effect daily variability and level of blood pressure in borderline hypertensive patients.

This study examined the effect of large changes in dietary sodium on the average ambulatory blood pressure and its variability in 19 patients with uncomplicated borderline hypertension. Each patient participated in a 16-week protocol that consisted of four 4-week periods of different sodium intake (medium (120-160 mEq/day) during periods 1 and 3 and low (< 40 mEq/day) or high (> 225 mEq/day) during either period 2 or 4. The 24-hour urine sodium during the low and high periods averaged 18 and 327 mEq/day, respectively. Ambulatory blood pressure monitoring was done at the end of the fourth week of the low and high diet periods. During monitoring, pressures were recorded every 15 minutes while awake; in addition, patients kept diaries noting activities, posture, and situation at each measurement. The results show that there was a decline of 16/7 mmHg in the average ambulatory awake systolic and diastolic pressures from the high sodium to low sodium diets. Corresponding casual pressures decreased an average of 15 and 8 mmHg, respectively. In examining the factors associated with ambulatory pressure variability, systolic pressure showed greater variation by activity on a low sodium diet than on the high. The findings suggest that sodium restriction has a variable, but in some cases marked, effect on lowering the ambulatory blood pressure in borderline mildly hypertensive patients and that sodium balance may be important to consider when examining ambulatory blood pressure variability. © 1994 Wiley-Liss, Inc.

Differential Effects of Antihypertensive Drugs on Hypertension: Associated Risk Factors

The primary aim of the management of hypertension should be to prevent coronary heart disease. Antihypertensive treatment should have a beneficial effect on the risk factors associated with coronary heart disease, particularly hypertension, dyslipidemia, hyperinsulinemia, and/or glucose intolerance. Other important risk factors include central obesity, left ventricular hypertrophy, hypokalemia, and smoking. In patients genetically predisposed to essential hypertension, metabolic alterations characterized by insulin resistance, hyperinsulinemia, and dyslipidemia tend to occur already before the development of hypertension, obesity, or redistribution of body fat. In the treatment of normotensive or borderline hypertensive diabetic patients, angiotensin-converting enzyme (ACE) inhibitors have shown superiority to other agents due to their antiproteinuric effect and their beneficial influence on the glomerular filtration rate. ACE inhibitor treatment of patients with overt diabetic nephropathy has been reported to reduce the risk of mortality and the need for dialysis or transplantation. Beta blockers and thiazide diuretics are still the 'gold standard' of antihypertensive therapy in non-diabetic patients, as they offer at least some prognostic benefit, while the influence of the newer antihypertensive drugs on morbidity and mortality in these patients is not yet known. Nevertheless, since practicing physicians have to treat patients rather than statistical numbers, the current trend towards a more individualized selection, including the newer antihypertensive drugs with consideration of their metabolic, cardiac, and renal action profile, is also difficult to rebut. ACE inhibitors and most calcium antagonists have already evolved as the preferred drugs for the treatment of hypertension in diabetics due to their favorable effects on some of the cardiovascular and renal risk factors.

Effects of Intravenous Fructose Infusion on Sodium Handling and Peripheral Vascular Tone in Pre-Hypertensive Subjects.

The hemodynamic and humoral effects of i.v. fructose infusion and a control infusion were studied in 12 borderline hypertensive patients according to a single-blind, cross-over, randomized protocol. Fructose infusion decreased urinary sodium excretion and significantly increased plasma insulin, plasma Na+/K+ ATPase inhibitory activity, and forearm arterial and venous tone (+13%), the last of which was not observed during the control infusion (-2.5%). Levels of ANF and PRA in plasma were not altered by either infusion. We conclude that the sodium retention caused by acute i.v. fructose loading could be related to the increase in plasma insulin levels, which may directly affect individual susceptibility to sodium by enhancing sodium reabsorption at renal tubules. This sodium retention could contribute to the release of a plasma Na+-pump inhibitor apparently unrelated to extracellular volume expansion and potentially responsible for the early peripheral vascular involvement found in hypertension-prone men. (Hypertens Res 1994; 17: 239-242)

Borderline hypertension, daily stress and psychological variables

AbstractBorderline hypertensive patients (N = 33) were studied in order to ascertain if they showed a specific psychological profile and a greater emotional and cardiovascular reactivity than normotensive controls (N = 21). Borderline hypertensive patients scored significantly higher in type A behaviour (JAS), total hostility (BDI), anxiety, physical symptoms and general psychopathology (GHQ), but did not differ from controls in the frequency and intensity of stressful daily events, the quality and magnitude of emotional response (daily evaluated through visual analogue scales) and the degree of blood pressure variability. Taken in general, results did not confirm the psychological and psychophysiological profile repeatedly proposed for hypertensive patients.

Reversal of diastolic dysfunction in borderline hypertension by long-term medical treatment. Longitudinal evaluation by pulsed Doppler echocardiography.

This study aimed to assess the left ventricular diastolic function of borderline hypertensive patients (BHT) and to determine the effect of long-term blood pressure control by an angiotensin converting enzyme inhibitor on the left ventricular filling profile. Pulsed Doppler echocardiograms were obtained from 18 BHT (14 men, 4 women; mean age: 55 years) and 20 age-sex matched normotensive controls. Studies were done at rest and immediately after exercise on a supine ergometer bicycle. Of the 18 patients, 11 were treated with delapril (30 mg/day) and followed up with longitudinal studies for 24 weeks. At baseline, BHT had a normal left ventricular structure. They showed a decreased peak velocity of early filling (E) (43 +/- 7 v 56 +/- 13 cm/sec, P < .01) and E/A ratio (0.83 +/- 0.2 v 1.08 +/- 0.3, P < .01), whereas peak velocity of late filling (A) and deceleration time (Dec T) were similar in the two groups. Exercise-enhanced filling indices were observed in both groups. Following blood pressure control, no change was observed in the left ventricular morphology. In contrast, progressive improvement of resting and after exercise peak velocity of early filling and E/A ratio were achieved. This indicates that long-term angiotensin converting enzyme inhibition ameliorates cardiac function in borderline hypertension.

Factors associated with acute salt-sensitivity in borderline hypertensive patients.

The acute sensitivity to sodium loading has been investigated in 26 borderline hypertensive patients (BHT) undergoing acute i.v. NaCl infusion. Measurements included blood pressure (BP), forearm vascular resistance (FVR) and venous distensibility (VV30), plasma renin activity (PRA), plasma aldosterone, plasma atrial natriuretic factor (ANF), and plasma levels of endogenous Na+/K+ATPase inhibitor. Sodium loading was associated with a greater than 8% increase in mean BP in 12 patients defined as salt-sensitive (NaCl-SENS) in comparison to salt-insensitive (NaCl-INSENS) subset. NaCl-SENS patients in comparison to NaCl-INSENS exhibited 1) a greater baseline VV30 (2.1 vs 1.4 ml/100 ml; p less than .005), and a response to saline characterized by 2) increased FVR (21.4 vs -6.5%; p less than .005), 3) blunted PRA suppression (-42 vs -67%; p less than .05), 4) delayed ANF response and 5) release of a Na+/K+ATPase inhibitor. Post-loading cumulative urinary sodium excretion was reduced in NaCl-SENS borderline hypertensives compared to NaCl-INSENS (2.6 vs 3.8 mumol/min/Kg; p less than .05). We conclude that acute salt-sensitivity in BHT is characterized by a blunted hormonal response to sodium loading which could be responsible of the activation of hemodynamic as well as humoral mechanisms leading to progressive blood pressure increase.

Brain natriuretic peptide as a cardiac hormone in essential hypertension

purpose: A natriuretic peptide, brain natriuretic peptide (BNP), has been isolated from porcine hearts. We performed this study to determine if BNP is secreted from the heart and to identify changes, if any, in the plasma BNP concentration in essential hypertension. patients and methods: We measured the immunoreactive (ir) BNP concentration at intracardiac sites including the coronary sinus of five patients with heart disease during cardiac catheterization. We examined plasma ir-BNP in 48 hypertensive patients, 15 borderline hypertensive patients, and 25 normotensive subjects. results: Plasma ir-BNP in the coronary sinus was greater than at other cardiac sites. The concentration was significantly higher in hypertensive subjects than in borderline hypertensive or normotensive subjects. Hypertensive patients with left ventricular hypertrophy (LVH) established by echocardiography had higher plasma ir-BNP levels than those without LVH. In the hypertensive group, plasma ir-BNP was closely correlated with the LV mass index. In these patients, BNP levels were correlated with mean arterial pressure and inversely correlated with the LV ejection fraction, although these correlations were weak. Reverse-phase high-pressure liquid chromatography showed that the major component of circulating ir-BNP in the hypertensive and normotensive subjects corresponded to authentic human BNP-32. conclusions: Human BNP-32 was secreted through the coronary sinus from the heart and may act as a cardiac hormone. Plasma BNP was increased in many of the hypertensive subjects with LVH The increase in BNP seemed to be related to LVH or the cardiac overload associated with LVH.

Atrial natriuretic factor modulates the plasma levels of a Na+/K+ATPase inhibitor in volume expanded borderline hypertensives.

To evaluate the existence of a relationship between atrial natriuretic factor (ANF) and plasma Na+/K+ATPase inhibitory activity in humans, we examined the hemodynamic and humoral response to volume expansion in 41 borderline hypertensive patients (BHT) with either normal (n = 33) or low plasma renin activity (n = 8). The study was carried out by measuring blood pressure, forearm circulation, plasma renin activity (PRA), ANF, and plasma levels of an endogenous Na+/K+ATPase inhibitor before and after 2 h of acute intravenous NaCl infusion (0.22 mL/min/kg bodyweight). The early (45 min) changes of ANF and those of Na+/K+ATPase inhibitory activity attained at the end of saline infusion were inversely related in BHT with normal PRA and directly related in the low-PRA population (r = 0.64). The time-course of ANF response to sodium loading was significantly delayed in BHT characterized by normal venous distensibility. They also showed a greater increase in plasma Na+/K+ATPase inhibitory activity occurring with an hypertensive, vasoconstrictive, and sodium retaining response as well. We conclude that in normal PRA borderline hypertensives, ANF may modulate the release of a plasma Na+/K+ATPase inhibitor in a setting where extracellular volume is acutely expanded. Our findings also suggest that dissimilarities in peripheral venous distensibility are able to influence the time-course of ANF response. The blunted ANF increase observed in response to NaCl loading in a subset of BHT could represent an early marker of the attitude of such patients to develop high blood pressure leading to the release of a Na(+)-pump inhibitor and influencing individual salt-sensitivity.

Dopaminergic abnormalities in borderline essential hypertensive patients.

To explore whether an altered metabolic pathway of dihydroxyphenylalanine (DOPA) may be related to some previously observed dopamine abnormalities in borderline hypertension, we measured basal and DOPA-induced (500 mg orally) changes in blood pressure and pulse rate as well as in three hourly plasma and urine samples. We found that borderline hypertensive patients compared with controls 1) showed a higher baseline urinary excretion of methoxytyramine, a marker of exocytotic dopamine release, with a greater DOPA-induced decrease of systolic blood pressure without reflex tachycardia; 2) had in response to DOPA a blunted plasma DOPA and free dopamine increase but an accentuated plasma dopamine sulfate and urinary DOPAC excretion; and 3) eliminated comparable quantities of dopamine in urine despite a lower rise in the glomerular DOPA load. Furthermore, although DOPA elicited natriuresis in both groups, its effect was greater in borderline hypertensive patients, who lacked the urinary sodium correlation with urinary dopamine excretion seen in control subjects. These data are compatible with increased basal exocytotic dopamine release and accelerated neuronal and renal (extraneuronal) dopamine generation from administered DOPA in borderline hypertension. The DOPA-induced hypernatriuresis exceeding augmented dopamine in borderline hypertensive patients, contrasting with the urinary sodium and dopamine correlation in control subjects, suggests that DOPA induced an additional natriuresis in borderline hypertensive patients by a decrease in renal sympathetic tone because of its central inhibition of sympathetic outflow, which also may account for the absence of reflex tachycardia.

Effects of endurance training on baroreflex sensitivity and blood pressure in borderline hypertension

Physical training offers a potential nonpharmacological strategy for control of mild and borderline hypertension, but its effect on blood pressure is controversial. We investigated the effects of endurance training on waking and sleeping blood pressure and on baroreflex sensitivity in 16 borderline hypertensive patients. First, 8 patients were assessed before and after a 6-month endurance training programme. Then, when it was clear that blood pressures were lower after training, a further 8 patients were studied not only at the end of the training programme but also after 4 months' abstention from exercise (detraining). Measurements were taken of baroreflex sensitivity (response to iv phenylephrine), blood pressure, R-R interval, and blood pressure and R-R variability. Ambulatory blood pressures were measured in 13 patients (7 trained, 6 detrained) and sleep blood pressures in 6 patients (3 trained, 3 detrained). Increased fitness was associated with a decline in resting arterial blood pressure of 9.7 (SE 2.0) mm Hg systolic and 6.8 (1.2) mm Hg diastolic, and with a decline in ambulatory blood pressure of 4.8 (1.4) mm Hg and 7.5 (2.1) mm Hg, respectively; both p less than 0.05. Baroreflex sensitivity was 14.0 (1.8) ms/mm Hg in the unfit and 17.5 (2.0) ms/mm Hg in the fit; p less than 0.05. Sleep blood pressures were not lower in the fit despite longer sleep R-R intervals. These findings indicate that, in some subjects with borderline or mild hypertension, a physical training programme is sufficient to bring the blood pressure within normal limits.

Abnormal cardiovascular reactivity in borderline and mild essential hypertension.

Cardiovascular and hemodynamic reactivity was evaluated with M-mode echocardiography, phonocardiography, and carotidography in correlation with circulating catecholamine levels in 25 normotensive subjects, 15 borderline hypertensive patients, and 42 mildly hypertensive patients during isometric exercise at 30% of the maximum force for 3 minutes. At rest, norepinephrine and epinephrine levels were significantly higher, and the cardiac index was similarly increased in both groups of hypertensive patients, but the cardiac mass index was significantly increased only in the mildly hypertensive group. During isometric exercise, the sympathoadrenal reactivity as well as the pressor and chronotropic responses were similar in normotensive subjects and both groups of hypertensive patients. However, the variations in blood pressure were achieved through totally different hemodynamic mechanisms in normotensive subjects and hypertensive patients. In normotensive subjects, the increase in blood pressure could be linked mainly to an increase in cardiac contractility and performance, whereas in either group of hypertensive patients, the increase in blood pressure was mainly associated with an increase in peripheral resistance. These observations are consistent with the hypothesis of a blunted beta-adrenergic reactivity and a predominance of alpha-adrenergic vascular reactivity in borderline and mildly hypertensive patients. This phenomenon, which appears to be unrelated to age or severity of hypertension, could be an important mechanism underlying the development of hypertension in humans.