ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Blood pressure (BP) and plasma indices of three major pressure control systems – plasma norepinephrine and epinephrine, plasma renin activity (PRA), and plasma arginine vasopressin – were measured simultaneously in 12 normal and 15 mildly essential hypertensive subjects before and after removal of 480 ml of blood by phlebotomy, to determine if there were differences in the compensatory response to acute blood loss. Responses to postural stress (change from supine to sitting position) following phlebotomy were also compared in a second group of subjects. Before phlebotomy, supine plasma hormone levels did not differ in the two groups. After phlebotomy, both groups exhibited only slight decreases (5 mm Hg) in systolic BP and a transient rise in heart rate. Only plasma norepinephrine increased significantly in both groups (35% above control in normal and 43% hi hypertensive subjects). Similar results were obtained in a second group of normal and hypertensive subjects, who were also subjected to a 10-minute postural challenge after phlebotomy. After 10 minutes in a sitting position, BP in these subjects remained unchanged but heart rate and plasma norepinephrine increased further to levels almost twice that produced by phlebotomy alone. Plasma epinephrine levels and PRA also increased with this additional stress, but plasma vasopressin remained unchanged. Changes in BP, heart rate, plasma norepinephrine and epinephrine, and PRA did not differ significantly between the two groups. These data indicate that 1) hypertensive subjects are as capable as normal subjects of maintaining BP when subjected to standard phlebotomy, 2) the sympathetic nervous system appears to be the predominant pressor mechanism activated following an acute, nonhypotensive blood loss in both groups of subjects, and 3) the addition of postural stress further accentuates the sympathetic response and increases PRA.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

The purpose of this study was to determine the effects of the cold pressor test on sympathetic outflow with direct measurements of nerve traffic in conscious humans and to test the strength of correlation between sympathetic nerve discharge and the changes in arterial pressure, heart rate, and plasma norepinephrine. In 25 healthy subjects, arterial pressure, heart rate, and muscle sympathetic nerve activity were measured with microelectrodes inserted percutaneously into a peroneal muscle nerve fascicle in the leg during immersion of the hand in ice water for 2 minutes. Arterial pressure rose steadily during the first and second minutes of the cold pressor test. Muscle sympathetic activity (burst frequency × amplitude) did not increase in the first 30 seconds of the test but increased from 230 ± 27 to 386 ± 52 units (mean ± SE,p< 0.05) by the end of the first minute of the test and to 574 ±73 (p< 0.01) during the second minute. In contrast, heart rate increased maximally during the first 30 seconds of the cold pressor test and returned to control during the second minute. The increases in heart rate were abolished by β-adrenergic blockade. The increases in muscle sympathetic activity during the cold pressor test were correlated with the increases in both mean arterial pressure (r = 0.86,p< 0.01) and peripheral venous norepinephrine (r = 0.72,p< 0.05); however, large changes in nerve traffic were associated with small changes in plasma norepinephrine. The major new conclusions from this study are that 1) stimulation of sympathetic neural outflow to skeletal muscle is an important component of the sympathetic response to the cold pressor test, 2) the cold pressor test appears to produce differentia] effects on sympathetic outflow to the heart and to the skeletal muscles, and 3) the arterial pressure response to the cold pressor test provides an approximate index of muscle sympathetic activity in this setting.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Alterations of cellular function of Na+, K+-edenosine triphosphatase (ATPase; Na+-K+pomp) have been implicated in the pathophyslology of essential hypertension. Therefore, this aspect of red blood cell (RBC) Na metabolism was studied in black men with newly diagnosed, untreated essential hypertension (NEH) and a normotensive control group. RBC Na content, Na+-K+pump number (ouabain binding sites), and pomp activity were measured. No statistically significant differences were found between the two groups for any of these three parameters. However, a group of previously treated essential hypertensive subjects (PEH) who had been withdrawn from therapy in the preceding 6 weeks were also studied. This group differed significantly from the NEH subjects in regard to all RBC Na+-K+pump parameters. Their RBC Na content (10.27 ± 3.23 vs 7.77 ± 2.52 mmol Na/L RBC; p = 0.006) was higher, and their Na+-K+pump activity (166 ± 50 vs 221 ± 87 nmol inorganic phosphate/mg membrane protein/hr; p = 0.03) and Na+-K+pump number (213 ± 40 vs 284 ± 85 binding sites/RBC; p = 0.001) were lower compared with those in NEH subjects. Although the PEH subjects were older and somewhat less hypertensive than their NEH counterparts, these factors were not found to influence the Na+-K+pump parameters. These results indicate that chronic diuretic therapy of patients with essential hypertension is associated with a reduced number of RBC Na+-K+pumps, Since RBCs are not considered target cells for diuretics, the effects of these drugs on RBC electrolyte metabolism may occur at the time of erythropoiesis by the production of RBCs with fewer Na+-K+pumps. Furthermore, the finding of elevated RBC Na content in PEH subjects acutely withdrawn from diuretic therapy is compatible with the renewed production of an endogenous natriuretic hormone that functions as a Na+-K+pump inhibitor.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Epidemiologies! and experimental data suggest blood pressure-lowering effects of dietary potassium. A randomized, double-blind clinical trial was used to assess blood pressure response to orally administered potassium, 120 mEq/day, and to placebo in 101 adults with mild hypertension. Blood pressure was measured with a random-zero sphygmomanometer every 2 weeks of this 8-week trial. Systolic blood pressure in the potassium-treated group decreased by 6.4 ± 13.7 (SD) mm Hg (p< 0.025) compared with 0.11 ± 13.0 mm Hg in the placebo-treated group (p = 0.96). Diastolic blood pressure in the potassium-treated group decreased by 4.1 ± 8.3 mm Hg (p< 0.05) compared with a 1.6 ± 6.5 mm Hg decrease in placebo-treated subjects (p = 0.09). Baseline blood pressure of potassium-treated subjects was unexpectedly higher than that of controls. After correcting for baseline variation, blood pressure still decreased 3.4/1.8 mm Hg more in potassium recipients than in placebo recipients (p = 0.14 and 0.24, respectively). Blood pressure decreased by 19/13 mm Hg in five blacks taking potassium vesus a 1/0 mm Hg increase in seven blacks taking placebo. Compliance with the potassium regimen was 91.5% by pill count; only one subject discontinued treatment because of side effects. In conclusion, 120 mEq/day of microencapsulated potassium chloride was well tolerated in adults with mild hypertension. An antihypertensive effect of potassium cannot be ruled out despite the fact that there was no statistically significant difference between potassium-treated and placebo-treated subjects after adjustment for differences in baseline blood pressure. Systolic blood pressure was affected more than diastolic blood pressure. Blacks may be particularly sensitive to blood pressure-lowering effects of potassium chloride. A larger clinical trial stratified by baseline blood pressure and race is required.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Radloisotope renography was performed in 21 patients with hypertension and unilateral renal artery stenosis with and without premeditation with 25 mg of captopril, and the results were compared with the effect of percutaneous transluminal angioplasty on the blood pressure, assessed 6 weeks after angioplasty. Angioplasty caused a considerable decrease in blood pressure in 15 of the 21 patients. In 12 of these 15 patients, captopril induced changes in the time-activity curves of the affected kidney only, suggesting deterioration of the excretory function of that kidney, while the function of the contralateral kidney remained normal. After angioplasty the asymmetry in the time-activity curves diminished despite identical pretreatment with captopril. Such captopril-induced unilateral impairment of the renal function was not seen in the six patients with unilateral renal artery stenosis whose blood pressure did not change after percutaneous transluminal angioplasty or hi 13 patients with hypertension and normal renal arteries. The functional impairment of the affected kidneys was characterized by a decrease of Tc-diethylenetriamine pentaacetic acid uptake and a delay of BIIhippurate excretion, while the ulI-hippurate uptake remained unaffected. These data are in agreement with a reduced glomerular filtration rate and diuresis during preservation of the renal blood flow, changes that can be expected after converting enzyme inhibition in a kidney with low perfusion and an active, renin-mediated autoregulation of the glomerular filtration rate. These data suggest that functional captopril-induced unilateral changes, shown by split renal function studies with noninvasive gnmma camera scintigraphy, can be used as a diagnostic test for renovascular hypertension caused by unilateral renal artery stenosis. With the criteria used, a sensitivity of 80% and a specificity of 100% were obtained.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

Red blood cell Li+-Na+countertransport and Na+-K+cotransport activities, home blood pressure, invasive systemic hemodynamics, and limb venous compliance were measured in 65 white men (23 normotensive, 22 borderline hypertensive, and 20 mild essential hypertensive subjects). Li+-Na+countertransport activity was positively and significantly correlated with subject-determined home systolic blood pressure (r = 0.31,p< 0.02) and with directly measured systolic (r = 0.29,p< 0.02) and diastolic (r = 0.27,p< 0.03) blood pressures in the hemodynamic laboratory, independent of potential confounding variables. Analysis of the hemodynamic determinants of blood pressure revealed a significant positive correlation of countertransport with vascular resistance (r = 0.30,p< 0.02) but not with cardiac output or cardiac index. High red blood cell Na+-K+cotransport activity was not independently associated with hypertension or with a characteristic hemodynamic pattern but was related to decreased venous compliance. Red blood cell Li + -Na+countertransport deserves further study as a marker for the genetic substrate of human essential hypertension. Red cell Na+-K+cotransport may be altered secondarily by factors related to high blood pressure and seems to be a valid marker for abnormalities of the venous system in hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

To determine the mechanism of blunted sympathetic reflex responses in early renovascular hypertension, we measured inotropic and chronotropic responses of the heart to β-adrenergic stimulation in vivo and myocardial β-adrenergic receptor number and adenylate cyclase activity in 10 dogs during an early stage of one-kidney renal hypertension. Mean aortic pressure was higher hi the hypertensive dogs (152 ± 4 mm Hg) than in eight sham-operated dogs (122 ± 1 mm Hg;p< 0.001), but heart rate, cardiac output,' and left atrial pressure did not differ between the two groups. Blood pressure reduction with a direct-acting vasodilator, pinacidil, resulted in marked increases in heart rate (+97 ± 12 beats/mm) and rate of change of left ventricular pressure (dP/dt; +1447 ± 367 mm' Hg/sec) in normotensive dogs but only blunted heart rate (+54 ± 12 beats/min) and minimal left ventricular dP/dt (+376 ± 264 mm Hg/sec) responses in hypertensive dogs. In contrast, intravenously administered isoproterenol produced similar increases in heart rate and left ventricular dP/dt in the two groups. These two groups also did not differ in either left ventricular β-adrenergic receptor number and affinity or basal, isoproterenol-stimulated, and fluoride-stimulated adenylate cyclase activity. Thus, despite blunted reflex responses to blood pressure reduction, hypertensive dogs showed neither reduction in chronotropic and inotropic responses to direct β-adrenergic stimulation nor β-adrenergic desensitization of the myocardium, as assessed by β-adrenergic receptor number and adenylate cyclase activity. Blunted reflex responses in this model of early hypertension must be due to factors operating at some locus other than the β-adrenergic receptor-adenylate cyclase complex.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

We recently reported that the vagal cardiopulmonary baroreceptor reflex inhibition of renal nerve traffic is impaired in rabbits with renal hypertension. The purpose of this study was to determine if the locus of the abnormality is mainly in the brain or in the afferent limb of the reflex. Experiments were done in α-chloralose-anesthetized rabbits with (a = 10) or without (a = 10) hypertension induced 6 to 8 weeks before study by wrapping the left kidney in cellophane followed by removal of the right kidney. The left side of the chest was opened, and a pericardia! cradle was made. Nicotine was applied tp the epicardial surface of the heart in concentrations of 10 to 500 μg/ml, and changes in arterial pressure and renal nerve traffic were measured. Dose-dependent decreases in traffic and arterial pressure resulted that were significantly smaller in hypertensive than in normotensive rabbits. After sinoaortic baroreceptor denervation, a similar impairment in the responses of hypertensive rabbits was observed. Vagotomy nearly abolished the responses of the renal nerves to epicardial nicotine. The responses of the lumbar sympathetic nerves to epicardial nicotine also were impaired in renal hypertensive (n = 8) compared with normotenslve rabbits (n = 8). If the behavior and number of chemically sensitive endings are assumed to be unaltered in hypertension, then these findings are explained best by an abnormality in the central nervous system. These results support the view that the previously reported impairment in the vagal cardiopulmonary baroreceptor reflex control of renal nerve traffic is due mainly to a central abnormality, although they do not exclude an abnormality in the afferent limb of the reflex.

ISSN:0194-911X    

出版商:OVID    

年代:1987

数据来源: OVID