摘要:

The rate of red blood cell sodium-lithium countertransport is elevated only in a subgroup of patients with essential hypertension. We have therefore compared renal and cardiac function and morphology in two groups of hypertensive patients with high (n=23) or normal (n=22) sodium-lithium countertransport (mean±SEM: 0.61±0.10 versus 0.29±0.07 mmol/l red blood cells - hr). The two groups were similar in age, sex distribution, body mass index, smoking habit, duration of hypertension, and actual levels of untreated blood pressure. Hypertensive patients with elevated sodium-lithium countertransport activity showed elevated glomenilar filtration rate (118±2 versus 109±2 ml/min • 1.73 m2;p<0.001), albumin excretion rate (23±3 versus 14±2 /ug/min; p<0.001), larger kidney volume (250±15 versus 203±13 ml • 1.73 m2;p<0.01), lower lithium clearance rate (26.7±03 versus 28.9±03 ml/min • 1.73 m2;p<0.01), and higher total body exchangeable sodium (2,716±33 versus 2,485±41 mmol • 1.73 m2;p<0.01). Left ventricular mass index (139±6 versus 119±6 g/m2;p<0.05), relative wall thickness (0J9±0.05 versus 0.29±0.04 cm;p<0.001), and left posterior wall plus intravenrricular septum thickness (2.02±0.04 versus 1.76±0.03 cm; p<0.05) were also higher in patients with high sodium-lithium countertransport Hypertensive patients with normal sodium-lithium countertransport had renal and cardiac parameters similar to those of a normotensive control group (n=21) except for a higher glomenilar filtration rate and left ventricular mass index. Finally hypertensive patients with elevated rates of sodium-lithium countertransport had significantly higher plasma triglyceride levels and lower plasma concentrations of high density lipoprotein cholesterol. Thus renal and cardiac hypertrophy, lipid abnormalities, and altered kidney function are prominent features of hypertensive patients with higher sodium-lithium countertransport

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

To characterize the normal nycterohemeral blood pressure and heart rate profiles and to delineate the relative roles of sleep and circadian rhythmidty, we performed 24-hour ambulatory blood pressure monitoring with simultaneous polygraphic sleep recording in 31 healthy young men investigated in a standardized physical and social environment Electroencephalographic sleep recordings were performed during 4 consecutive nights. Blood pressure and heart rate were measured every 10 minutes for 24 hours starting in the morning preceding the fourth night of recording. Sleep quality was not significantly altered by ambulatory blood pressure monitoring. A best-fit curve based on the periodogram method was used to quantify changes in blood pressure and heart rate over the 24-hour cycle. The typical blood pressure and heart rate patterns were bimodal with a morning acrophase (around 10:00 AM), a small afternoon nadir (around 3:00 PM), an evening acrophase (around 8:00 PM), and a profound nocturnal nadir (around 3:00 AM). The amplitude of the nycterohemeral variations was largest for heart rate, intermediate for diastolic blood pressure, and smallest for systolic blood pressure (respectively, 19.9%, 14.1%, and 10.9% of the 24-hour mean). Before awakening, a significant increase in blood pressure and heart rate was already present Recumbency and sleep accounted for 65-75% of the nocturnal decline in blood pressure, but it explained only 50% of the nocturnal decline in heart rate. Thus, the combined effects of postural changes and the wake-sleep transition are the major factors responsible for the 24-hour rhythm in blood pressure. In contrast, the 24-hour rhythm of heart rate may reflect an endogenous circadian rhythm, amplified by the effect of sleep. We conclude that modulatory factors different from those controlling nycterohemeral changes in blood pressure influence the 24-hour variation in heart rate.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Blood pressure falls after a single session of exercise. The duration for which this fall in blood pressure persists is not known. Sustained hypotension after a single session of exercise may have important implications in the treatment of patients with mild hypertension. We studied 24 subjects (12 normotensive subjects and 12 patients with mild or borderline hypertension). Blood pressure was measured in the laboratory for 30 minutes before and for an hour after graded bicycle exercise to maximal voluntary capacity. Subjects then left the hospital and measured their blood pressures at home (three measurements every 2 hours) following a strict measurement protocol for the rest of the day (usually between 8 and 12 hours). These home blood pressure measurements were compared with home blood pressure measurements recorded at the same times on a nonexercise control day. At 30 minutes after the graded maximal exercise test, the hypertensive patients experienced a fall in blood pressure from 142±3.5/93±6.5 mm Hg (mean±SEM) to 124±4.5/79±2.8 mm Hg (p<0.01). For the normotensive subjects, blood pressure after exercise fell from 117±3.1/70±2.1 mm Hg to 109±3.1/ 62±2.8 mm Hg (p<0.01). Despite these striking blood pressure reductions for the second half hour after exercise, blood pressure measurements recorded at home were not significantly different on the exercise and control days in either group. We conclude that although a single bout of exercise lowers blood pressure for a short (1-hour) period, this hypotension is not sustained.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The effect of adenosine on the forearm vasoconstrictor response to a-adrenergic and sympathetic stimulation was studied in healthy volunteers. During a predilated state achieved by infusion of sodium nitroprusside into the brachial artery, subsequent infusion of norepinephrine induced a mean increase in forearm vascular resistance of 571%, whereas this response was only 270% when an equipotent vasodilator dose of adenosine was used instead of sodium nitroprusside (nitroprusside versus adenosine,p<0.05, n=6). A comparable difference was found when the endogenous release of norepinephrine was stimulated by the local infusion of tyramine, with tyramine-induced increments in forearm vascular resistance of 438% during nitroprusside versus 93% during adenosine (n=6, p<0.05). During these tyramine infusions a similar increase in the calculated forearm norepinephrine overflow occurred in the adenosine and the nitroprusside tests. In a third experiment, we demonstrated that adenosine also reduced the vasoconstrictor response to lower body negative pressure, an endogenous stimulus, of the sympathetic nervous system. During nitroprusside, lower body negative pressure induced an increase in forearm vascular resistance of 135%, whereas this was 39% during adenosine (n=6, p<0.05). We conclude that adenosine attenuates the response to sympathetic nervous system-mediated vasoconstriction in humans, and that this effect may at least partly be explained by a postsynaptic inhibition of or-adrenergic vasoconstriction. Therefore, we think that adenosine may be an important endogenous modulator of sympathetic nervous system activity in humans.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

We have previously shown that dietary NaCl supplementation increases blood pressure and sympathetic nervous system activity in association with decreased norepinephrine release and increased a2-adrenergic receptor number in the anterior hypothalamic area of salt-sensitive spontaneously hypertensive rats (SHR-S) but not in salt-resistant spontaneously hypertensive rats (SHR-R) or Wistar-Kyoto (WKY) rats. Further, acute microinjection of clonidine into the anterior hypothalamic area produced depressor responses that were augmented by high salt feeding in SHR-S but not in SHR-R or WKY rats. The current study tested the hypothesis that chronic infusion of clonidine into the anterior hypothalamic area prevents salt-sensitive hypertension in SHR-S. Beginning at age 7 weeks, immediately before initiation of 1% or 8% salt diets, clonidine (2 ng/min) or saline vehicle was infused into the anterior hypothalamic area or femoral vein of male SHR-S via osmotic minipump for 20 days. In SHR-S fed an 8% salt diet, chronic microinfusion of clonidine into the anterior hypothalamic area offset the hypertensive effect of the dietary salt supplementation and reduced the enhancing effects of dietary salt on left ventricular weight and plasma norepinephrine levels. In contrast, chronic microinfusion of clonidine into the anterior hypothalamic area did not significantly affect any of these measures in 1% salt-fed SHR-S. Intravenous infusion of clonidine at the rate used for the anterior hypothalamic area infusion did not alter any of these measures in 8% salt-fed SHR-S. These data support the hypothesis that salt-induced hypertension in SHR-S is associated with diminished sympathoinhibitory function of central o^-adrenergic receptors and that chronic microinfusion of clonidine into the anterior hypothalamic area prevents salt-sensitive hypertension in this model, at least in part, by enhancing o-adrenergic receptor-mediated sympathoinhibition.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

In both animals and humans, stimuli leading to sympathetic activation are accompanied by an impairment of the baroreceptor-heart rate reflex. To determine whether sympathetic activity normally interferes with this reflex function we examined in conscious Wistar-Kyoto (WKY) rats the effect of chemical sympathectomy by 6-hydroxydopamine on the bradycardic response to baroreceptor stimulation induced by raising blood pressure via intravenous phenylephrine boluses; control rats received vehicle. Spontaneously hypertensive rats were also studied because in these animals there is both a baroreceptor reflex impairment and a sympathetic overactivity. Baroreceptor reflex sensitivity, calculated as the ratio of the peak increase in pulse interval to the peak increase in mean arterial pressure, was 75% greater in sympathectomized WKY rats than in control WKY rats (L28±0.15 versus 0.73±0.10 msec/mm Hg, mean±SEM; p<0.0l). The sympathectomy-induced increase in sensitivity was even larger in spontaneously hypertensive rats (SHR) (1.26±0.12 versus 0.44±0.06 msec/mm Hg in sympathectomized SHR versus control SHR, +186%; p<0.01) so that the impaired baroreceptor reflex sensitivity observed in control SHR as compared with control WKY rats (-40%, p< 0.01) was no longer detectable in the sympathectomized groups. To establish whether the sympathectomy-induced potentiation of the reflex was due to an increase in cardiac responsiveness to vagal stimuli, we subjected separate groups of anesthetized, vagotomized SHR and WKY rats to graded electrical stimulation of the right efferent vagus. The bradycardic effects of vagal stimulation, however, were similar in sympathectomized and control animals. It is concluded that 1) sympathetic nerve activity normally exerts an antagonistic effect on the baroreceptor-heart rate reflex, 2) this phenomenon is much more pronounced in SHR than in WKY rats and may contribute to the baroreceptor reflex impairment typical of the former animals, and 3) the sympathectomyinduced potentiation of the reflex does not depend on an increase in cardiac vagal responsiveness.

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1991

数据来源: OVID