ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY In order to assess the relationship in the spontaneously hypertensive (SH) rat between the development of hypertension and the increased secretion of vasopressin which we have shown in this model, SH rats were treated with the orally effective converting enzyme inhibitor, SQ 14,225 (15 to 30 mg/kg-day in the drinking water), from ages 33 to 61 days. Systolic blood pressure (SBP) in the treated rats increased from a pretreatment level of 112 ± 6 (SE) mm Hg to only 136 ± 2 mm Hg by the fourth week of treatment. In the untreated SH rats SBP rose from 116 ± 5 mm Hg to 174 ± 4 mm Hg in this same period. Within 2 days of initiating treatment with SQ 14,225, 24-hour urinary excretion of ADH (UADHV) fell 46% and remained depressed for the duration of treatment, while in the untreated rats UADH V tended to increase. Treatment with SQ 14,225 gradually increased water intake to a level 64% higher than in the untreated rats at the end of 4 weeks. However, the fall in UADHV appeared to precede the increase in water intake. The changes in UADHV and water intake were reflected by an increased urine volume and decreased urine osmolality. All changes were reversed within 9 days after discontinuing treatment with SQ 14,225. The decreased release of vasopressin, suggested by the decreased UADHV, could have been a factor in preventing the development of hypertension in the treated rats to the extent that vasopressin acts as a pressor agent in the SH rat and that blood volume was reduced as a result of the increased urine volume.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Differences in blood pressure between blacks and whites in the United States are now well documented. The causes of these differences remain speculative. Genetic factors, personal characteristics, renal physiology, endocrine factors, autonomic nervous system function, cardiac function and various environmental factors are examined in the present review as potential determinants of racial blood pressure differences. Racial differences in renal physiology and environmental influences such as socioeconomic status seem to be likely candidates for important contributions to blood pressure differences. Further research aimed specifically at black-white blood pressure differences is of great importance to a fundamental understanding of the etiology and prevention of essential hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY We examined tbe responses to volume expansion and contraction in normals, essential hypertensives, and patients with secondary hypertension, in order to formulate a more precise method of categorizing essential hypertensives with respect to plasma renin and aldosterone responses. We studied 379 normal and 464 hypertensive patients during and after a 4 hour 2 liter intravenous saline infusion, and after 120 mg oral furosemide. The large number of normal white and black subjects permitted renin profiling according to race and age. Of 395 essential hypertensives, 12% were categorized as having low-renln, 72% normal-renln, and 16% high-renln hypertension. Our results show, when tbe renin values are adjusted for age and race, lowrenin hypertension in blacks and the elderly is less common than previously described. The most useful clinical information obtained was from measurements of plasma renin activity and aldosterone concentration following saline infusion, since that maneuver identified all patients with high-renin hypertension and also the 25 patients with primary aldosteronism. The 44 patients with renal vascular hypertension could not be identified on the basis of their renin and aldosterone responses. Tbe natriuretic and kalluretic responses during saline infusion were much greater in patients with primary aldosteronism than in other hypertensive subgroups or normal subjects. The magnitude of these responses may be of value in suggesting the diagnosis in situations where plasma aldosterone measurements are not readily available.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The abdominal aorta above the renal arteries was partially constricted or sham-constricted in rats age 6 weeks that had had adrenal demeduilation at age 4 weeks and guanethidine injections over Weeks 2-4 after birth to produce peripheral sympathectomy (S rats), and in sham-sympathectomized sbamdemedullated control rats (SS rats). Plasma noreplnephrine and epinephrine levels were reduced by 94-96% in S rats. Arterial pressures were also reduced by 30% in S rats, which, nevertheless, had hearts and aortas of normal size respective to body weight. With aortic coarctation, femoral arterial pressures did not increase but carotid pressures rose by 18-25% (p< 0.01). Expressed in terms of body weight, heart weights increased 75% and 50% (p< 0.001) and weights of eh* thoracic portion of the aorta Increased 58% and 37% (p< 0.05) with coarctation in SS and S rats, respectively. In SS rats there was also a rise in weight (26%) of the normotensive abdominal portion of the aorta (p< 0.01); in contrast, this was not true in S rats. In both SS and S rats, wall water contents of thoracic aorta, abdominal aorta, and thoracic vena cava increased by 3-8% with coarctation (p< 0.02). The normal size of heart and aorta in S rats, despite lower arterial pressures, suggests that factors other than pressure and sympathoadrenergic stimuli influence cardiovascular growth in young rats. The increased weight of the abdominal aorta in coarcted SS rats suggests that vascular wall hypertrophy in hypertension does not require elevated intravascular pressures. Increases in heart and thoracic aortic weight with coarctation in S rats suggest that cardiovascular hypertrophy may occur in the virtual absence of sympathoadrenergic stimuli. However, in the absence of both pressure and catecholamine influences, vascular hypertrophy apparently does not occur. Finally, these studies provide evidence for vascular wall “waterlogging” in coarctation hypertension in rats not attributable to elevated levels of intravascular pressure and occurring despite the virtual absence of sympathoadrenergic influences. These findings support the hypothesis that humoral factors are involved in vascular wall “waterlogging” in hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Persons participating in a 5-day diagnostic protocol were routinely typed for ABO, Rh, MNS, Kell, Kidd, Duffy, P, Haptoglobln, phosphoglucomutase-1 (PGM-1), and add phosphatase (AcP). The study population was composed of 164 nonnotensive whites, 34 normotensive blacks, 161 whites and 43 blacks with essential hypertension, and 52 whites with secondary forms of hypertension (18 atherosclerotic reoovascular hypertensives, 17 patients with fibromuscular disease, and 17 patients with primary aldosteronism). There were no significant differences in phentotype frequencies in ABO, Rh, Kidd, Kell, Duffy, P, Haptoglobin, PGM-1 or AcP in any of the comparisons. However, there was a significantly different distribution of MNS phenotypes in comparisons of essential and atherosclerotic renovascular hypertensives with nonnotensive controls. Essential hypertensives had a lower frequency of the S gene and a higher frequency of s in whites (X3 = 12.21,p< 0.005). Atherosclerotic renovascular hypertensives differed from the normotensive population in the frequencies of both MN (X1 = 4.34,p< 0.05) and Ss (X1 = 4.21,p< 0.05). The finding of disease-blood group associations supports the hypothesis that there may be significant physiological differences between individuals of different blood types.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Daily electrical stimulation of tbe posterior hypothalamus for 12 weeks in awake rats caused persistent cardioacceleration but barely increased systolic pressure. Subsequent postmortem examination showed extensive fibrosis at sites of electrode implantation in both stimulated and unstimulated rats. Because Folkow and Rubinstein had succeeded in elevating blood pressure progressively by stimulating the “hypothalamic defence area,” chronic stimulation was repeated following their stereotaxic coordinates. Systolic pressure rose but the elevation was significant only on Weeks 8 and 10. To maintain behavioral effects during chronic stimulation, current strengths had to be increased periodically, and stimulated rats gained weight more rapidly than unstimulated controls. Both these findings indicated that electrical stimulation had damaged the brain, but since local fibrosis made histologic verification difficult, additional experiments were done to determine if functional deficits could be detected. Upon further hypothalamic stimulation, electrical thresholds were higher and pressor and sympathetic nerve responses were smaller in rats that had been stimulated chronically than in those that had not. Although our results do not disprove the hypothesis that centrally-induced sympathetic hyperactivlty initiates hypertension, they show that blood pressure cannot be elevated by hypothalamic stimulation alone when the brain has been injured.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY The bemodynamic alterations associated with the developmental phase of high blood pressure were investigated in the spontaneously hypertensive rat (SHR). All hemodynamic measurements were made in unanesthetized, unrestrained SHR and Wistar-Kyoto (WKY) rats instrumented with chronic electromagnetic flow probes on the ascending aorta and arterial pressure catheters. Rats were studied at 30-41 days, 80 days and 120 days of age. Hemodynamics of SHRs and WKYs in the 30-41 day group were monitored daily. Spontaneously hypertensive rats demonstrated a higher cardiac index than WKYs (p< 0.05) from 32 through 41 days of age. Total peripheral resistance (TPR) was not elevated in SHRs at this time. Heart rate and stroke index were elevated in SHRs (p< 0.05) from 34 through 41 days, however, stroke volume was not At 80 and 120 days SHRs had higher mean arterial pressure (MAP) and TPR than WKYs (p< 0.05), although cardiac index was not significantly different. This hemodynamic pattern of a hyperkinetic circulation prior to the development of hypertension supports the theory of total body autoregulation. A transient increase in cardiac index precedes an increase in TPR, which then normalizes cardiac index while elevating MAP.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Systemic hemodynamics, plasma volume and circulating catecholamlne levels were measured under baseline conditions in 21 patients with idiopathic mitral valve prolapse (IMVP), 13 with and eight without borderline hypertension, and compared with two control populations comprised of 34 normotensive and 15 borderline hypertensive subjects without mitral valve prolapse. The IMVP population had a faster heart rate (73 ± 2 vs 67 ± 2 beats/minute;p< 0.05) and a greater cardiac index (3.5 ± 0.1 vs 3.0 ± 0.1 liters/min/m12< 0.025) than the normotensive controls. However, heart rate and cardiac index were similar in IMVP and borderline hypertensive patients. The IMVP patients showed an increased responsiveness of heart rate and systolic arterial pressure during beta-adrenergic receptor stimulation (isoproteretiol infusion) when compared to the second control group of patients with borderline hypertension who had similar hyperdynamic circulation. Responses to upright tilt, Valsalva maneuver, and handgrip, however, did not differ between the IMVP and the two control groups. Circulating catecbolamine levels were slightly higher in IMVP patients. It is concluded that some IMVP patients (with or without hypertension) demonstrate increased betaadrenergic receptor responsiveness associated with a hyperkinetic circulation. Therefore, a hyperbetaadrenergic state could possibly account for the observed abnormal left ventricular contraction pattern and clinical symptoms in the mitral valve prolapse syndrome.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID