摘要:

No. Abstract

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

No. Abstract

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

No. Abstract

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

To dissociate the effects of an elevated blood pressure on the cardiovascular regulatory functions from those of aging in the hypertensive elderly individual, resting hemodynamic measurements and circulatory autonomic functions in 30 elderly (mean age, 66 years) hypertensive (World Health Organization stages I and II) patients were compared with those in 30 healthy elderly (mean age, 65 years) normotensive volunteers. The elderly hypertensive group showed a significantly lower cardiac index and higher total peripheral resistance. β-Receptor sensitivity, as determined by chronotropic dose of infused isoproterenol, and baroreceptor reflex sensitivity index, derived from phase II, but not phase IV, of Valsalva's maneuver, were only slightly but significantly reduced in the hypertensive group. The variability of heart rate at rest as an index of parasympathetic control of heart was similar between these two groups. Plasma norepinephrine level was significantly inversely related to resting mean blood pressure (r=−0.31,p< 0.05) when analyzed as a whole group. Plasma renin activity, but not plasma aldosterone, was significantly decreased in the hypertensive group. To define the effects of age itself, these parameters in normotensive elderly subjects were also compared with those in 12 young normotensive subjects (mean age, 23 years). Although resting hemodynamic measurements did not differ, various circulatory autonomic functions were significantly different between these two age groups. The variability of heart rate in 24-hour ambulatory monitoring, β-receptor responsiveness, resting vagal cardiac activity, and baroreceptor reflex sensitivity derived from phase IV of Valsalva's maneuver were significantly depressed in the elderly. Resting plasma norepinephrine level was elevated and renin-aldosterone system decreased in the elderly. Thus, the hemodynamic pattern of elderly hypertensive patients with mild essential hypertension is of the low-output, high peripheral resistance type. Neither the sympathetic nervous nor the renin-angiotensin system is likely to be responsible for this increase in peripheral resistance. Furthermore, in contrast to the currently prevailing belief, high blood pressure, although an important modulating factor in the younger patients, has very limited, if any, influence on the cardiovascular regulatory functions in older subjects whose autonomic functions have already been substantially altered by advancing age.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

The relation of red blood cell sodium-stimulated lithium countertransport to blood pressure (BP) and prevalence of hypertension was assessed in univariate and multivariate analyses for 2,748 men and women aged 25–74 years who participated in the baseline examination of the Gubbio Population Study in north central Italy. Since age-specific countertransport values were consistently higher for men than women, all analyses were done for men and women separately. In simple correlation analyses, countertransport was significantly related to systolic and diastolk BP in both sexes (r values 0.107–0.163). In age-adjusted analyses, countertransport was significantly related to BP level of both men and women not receiving antihypertensive treatment; mean levels were high for hypertensive persons receiving antihypertensive therapy compared with normotensive persons. Age-adjusted prevalence rates of hypertension were progressively higher for both sexes in successively higher quintiles of countertransport, almost twice as high for those in the highest quintile compared with those in the lowest quintile. Correspondingly, age-adjusted logistic regression analyses showed countertransport to be related significantly to prevalence of hypertension for both men and women (p< 0.001). Since age, body mass index, plasma total cholesterol, uric acid, glucose, urinary sodium/potassium excretion, pulse, and (for men) daily alcohol intake also were significantly correlated with BP, and in some instances with countertransport, relation of countertransport to BP was also assessed in multivariate analyses with control for these variables. For men and women, multiple logistic coefficients for the relation of countertransport to prevalence of hypertension were significant (p< 0.05) or borderline significant (0.05<p< 0.10); a person with a high countertransport value was 1.3–1.9 times more likely to be hypertensive than a person with a low value. These findings indicate that the cross-sectional relation between countertransport and hypertension generally remains significant with control for other traits known to be related to hypertension. However, prospective data are lacking as to whether countertransport is an independent risk factor for incidence of hypertension. Such data are needed for further clarification of the relation of high countertransport to the etiology of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Oral hydrocortisone increases blood pressure and enhances pressor responsiveness in normal human subjects. We studied the effects of 1 week of oral hydrocortisone (200 mg/day) on blood pressure, cardiac output, total peripheral resistance, forearm vascular resistance, and norepinephrine spillover to plasma in eight healthy male volunteers. Although diastolic blood pressure remained unchanged, systolic blood pressure increased from 119 to 135 mm Hg (SED±3.4,p< 0.0l), associated with an increased cardiac output (5.85–7.73 l/min, SED±0.46,p< 0.01). Total peripheral vascular resistance fell from 15.1 to 12.2 mm Hg/l/min (SED±1.03,p< 0.05). Restmg forearm vascular resistance remained unchanged, but the reflex response to the cold pressor test was accentuated, the rise in resistance increasing from 10.5 mm Hg/ml/100 ml/min (R units) before treatment to 32.6 R units after treatment (SED±6.4,p< 0.025). The rise in forearm vascular resistance accompanying intra-arterial norepinephrine (25, 50, and 100 ng/ min) was also significantly greater after hydrocortisone, increasing from an average of 14.9±2.4 R units before treatment to 35.1±5.5 R units after hydrocortisone (SED±6.0,p< 0.05). A shift to the left in the dose-response relation and fall in threshold suggested increased sensitivity to norepinephrine after treatment. Measurement of resting norepinephrine spillover rate to plasma and norepinephrine uptake indicated that overall resting sympathetic nervous system activity was not increased. The rise in resting blood pressure with hydrocortisone is associated with an increased cardiac output (presumably due to increased blood volume). The increased responsiveness of the peripheral vasculature to reflex pressor stimuli appears to be due to changes in end-organ responsiveness since similar changes occurred with local administration of norepinephrine.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Repeated neurogenic pressor episodes by hindquarter compression were elicited in nine experimental dogs. Conscious dogs underwent 6 hours of compression every day over a period of 9 weeks. The average mean blood pressure increase during the compression periods was 25 mm Hg, but after decompression the blood pressure promptly returned to baseline values. This blood pressure response was constant and did not change over the 9-week period. The blood pressure increase was associated with a significant increase of plasma norepinephrine values. After validity of the model was established, echocardiographic measurements were performed at baseline and after 3, 6, and 9 weeks of compression in six experimental and six time-control dogs. Concentric left ventricular hypertrophy was already detectable at 3 weeks, and at the ninth week, the left ventricular mass was 28% above the baseline value. The left ventricular mass in time-control dogs remained unchanged over the same period of time. The time-left ventricular mass curves in experimental dogs were significantly different (by profile analysis), had different means (p< 0.005), were not parallel (p< 0.0006), and the overall group difference was highly significant (p< 0.00001). Since left ventricular hypertrophy, a poor prognostic sign in clinical situations, can evolve before established hypertension, present therapeutic recommendations based on permanently elevated blood pressure values may not be entirely justified.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

In normotensive Sprague-Dawley rats and Wistar-Kyoto (WKY) rats stimulation of renal mechanoreceptors or chemoreceptors by increasing ureteral pressure or renal pelvic perfusion with 0.9 M NaCl results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis. However, in 14–15-week-old spontaneously hypertensive rats (SHR) renal sensory receptor stimulation failed to elicit a contralateral inhibitory renorenal reflex response. The present study was performed to examine whether the lack of a renorenal reflex response in SHR was related to elevated arterial pressure by studying the responses to renal sensory receptor stimulation in 5–6-week-old SHR and in 12–16-week-old SHR that had been treated with captopril from 3 weeks of age to prevent the development of hypertension. In 5–6-week-old SHR, mean arterial pressure was 113±3 mm Hg. Graded increases of ureteral pressure of 15 and 29 mm Hg resulted in graded increases in ipsilateral afferent renal nerve activity of 57±22% and 120±38%. Contralateral urinary sodium excretion increased from 0.26±0.06 to 0.35±0.07 μmol/min/g and from 0.36±0.08 to 0.46±0.11 μmol/min/g, respectively. In captopril-treated SHR, mean arterial pressure was 109±3 mm Hg. Increasing ureteral pressure by 34 mm Hg increased ipsilateral afferent renal nerve activity 65±21% and contralateral urinary sodium excretion from 1.28±0.24 to 1.53±0.30 μmol/min/g. Similar results were produced by renal chemoreceptor stimulation. It is concluded that renal sensory receptor stimulation results in a contralateral inhibitory renorenal reflex response in 5–6-week-old SHR and in SHR treated with captopril to prevent the development of hypertension. These results suggest that the previously demonstrated lack of a renorenal reflex response to renal sensory receptor stimulation hi hypertensive SHR is related to the maintenance of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Studies were carried out to determine if the release of atrial natriuretic factor (ANF) is altered in the inbred Dahl salt-sensitive (SS/Jr) rat. Isolated heart-lung preparations of prehypertensive young SS/Jr rats (6–8 weeks of age) and age-matched inbred Dahl salt-resistant (SR/Jr) rats were used. At this relatively young age the blood pressure difference between strains (SS/Jr, 108±3 mm Hg; SR/Jr, 103±2 mm Hg) was minor. ANF release was stimulated with preload-induced or afterload-induced atrial stretch. Increased preload produced increases in right and left atrial pressures that were equivalent between young SS/Jr and SR/Jr rats; increased afterload produced increases only in left atrial pressures, which again were equivalent for young rats of the two strains. At any preload-induced change in atrial pressure SS/Jr rat hearts released less ANF than those of SR/Jr rats. Similarly, at any afterioad-induced increase in left atrial pressure, SS/Jr rat hearts released less ANF than those of SR/Jr rats. In contrast to the above results in young rats, the strain differences were dramatically reversed when older rats (5–6 months of age) were used; at this age SS/Jr rats were markedly hypertensive (SS/Jr, 211±8 mm Hg; SR/Jr 130±4 mm Hg). Hearts from adult hypertensive SS/Jr rats released more ANF than hearts from adult normotensive SR/Jr rats at any left atrial pressure as afterload was increased. This reversal of SS/Jr rats from hyposecreters to hypersecreters of ANF is probably a consequence of hypertension-induced changes such as cardiac hypertrophy and recruitment of the ventricles to produce ANF. It is concluded that the hyposecretion of ANF by prehypertensive SS/Jr rats may represent a genetic trait relevant to the pathogenesis of genetic hypertension and that this is obscured by adaptive changes in the heart as hypertension progresses.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID

摘要:

Properties of human atrial natriuretic factor (ANF) binding to the crude membrane fraction of rat kidney were studied using the ANF-radiolabeled receptor assay; the developmental change of renal ANF receptors in three age groups of spontaneously hypertensive rats (SHR) was also investigated with the methods of radiolabeled receptor assay and the quantitative approach of in vitro macro-autoradiography. Temperature and incubation time greatly influenced ANF binding capacities because of the degradation of radiolabeled ligand. Addition of 5 mM MgCl2to assay buffer was useful for the stabilization of ANF specific binding. Scatchard analysis suggested that the crude membrane fraction of rat's kidney had a single binding site with the apparent dissociation constant of 0.55 nM. In the study of the developmental change of renal ANF receptor in SHR, systolic blood pressure of the SHR at the age of 5 weeks and 12 weeks was significantly higher than that of age-matched Wistar-Kyoto (WKY) rats, but there was no significant difference in blood pressure between SHR and WKY rats at the age of 3 weeks. Concerning the radiolabeled receptor assay of ANF, the apparent dissociation constant and maximum binding capacity in SHR were low in all age groups when compared with those of WKY rats. In the in vitro macro-autoradiographic observation, the specific binding of ANF was localized mainly in the renal cortex, and these binding patterns of SHR and WKY rats were the same in all age groups. The specific binding in the kidney of SHR was proved to be quantitatively smaller than that in WKY rats using the research analysis system (RAS 1,000) as investigated in radiolabeled receptor assay. These findings suggest that the kidneys of SHR have a higher affinity and lower capacity binding sites (possibly genetic in origin) for ANF from a young age, and these changes in the renal ANF receptor may affect the progression of the hypertensive state in SHR.

ISSN:0194-911X    

出版商:OVID    

年代:1989

数据来源: OVID