ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The purpose of this study was to determine if any changes occurred in the basal and stimulated rates of oxygen consumption and lactate production of thoracic aortas from spontaneously hypertensive rats (SHR) and renal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats, and, if so, whether these changes were similar in these three models of hypertension. Rings of thoracic aorta were placed in an hthermic (37°C) muscle bath, and isometric tension development, oxygen consumption, and lactate production were measured. The results indicated that under basal conditions oxygen consumption, but not lactate production, was higher in aortas from all three hypertensive models; the elevation above control was greatest in the renal model (95%) and smallest in SHR (34%). On stimulation with 60 mM KCI, a significant increase in oxygen consumption above basal value occurred in all aorta samples (p< 0.05); however, lactate production was increased above basal only in aortas from hypertensive animals. Only in aortas from renal and DOCA-salt models was the rate of oxygen consumption during stimulation significantly greater than that of their normotensive controls (p< 0.05). Developed active stress in response to KCI was the same in all groups, and when the change in lactate production or oxygen consumption was expressed relative to the amount of active stress developed, no differences were observed. These results suggest that, 1) compared to values in aortas from normotensive animals, only the basal rate of oxygen consumption is higher; 2) this higher level of basal metabolic activity is not associated with an alteration in the metabolic cost of force development; and 3) there are quantitative differences between the models with regard to their metabolic characteristics.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

We have investigated the role of angiotensin II in the development of high blood pressure and in the maintenance of renal function during 2 weeks of one-kidney renal artery stenosis in conscious dogs. Responses to a fixed degree of inflation of a balloon cuff around the renal artery were compared in dogs with or without continuous enalapril (MK 421) treatment. In six untreated dogs, mean aortic pressure was increased by 17.1 ± 2.0 mm Hg, due primarily to increases in total peripheral resistance with little change in cardiac output, while glomerular filtration rate, renal blood flow, renal artery pressure, and plasma renin activity were back to prestenosis levels. In seven enalapril-treated dogs mean aortic pressure was increased by 23.0 ± 2.7 mm Hg and was not significantly different from that occurring in untreated dogs. This rise was due to increases in total peripheral resistance (10%) and cardiac output (12%). In the absence of angiotensin II, glomerular filtration rate remained low, at only 56 ± 6% of prestenosis levels. Renal blood flow returned to normal, but the renal artery pressure remained 25% lower than control values. Thus, the main role of angiotensin II in chronic one-kidney Goldblatt hypertension does not appear to be through its pressor properties but rather through its actions in the kidney to preserve glomerular filtration. This effect on renal function persisted throughout the course of the hypertension, even when the plasma renin levels returned to normal.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

To investigate renal tubular handling of sodium in various types of experimental hypertension, sodium, lithium, and inulin clearances were measured simultaneously in unanesthetized rats. Fractional excretion of lithium was used as an index of proximal sodium reabsorption. Eight groups of animals, all of the Wistar-Kyoto strain, were studied. Three were hypertensive: spontaneously hypertensive rats (SHR), rats with two-kidney, one clip renal hypertension, and uninephrectomized rats with deoxycorticosterone-salthypertension. The five normotensive control groups included animals given normal, low, or high dietary sodium loads and rats with reduced renal mass. Fractional excretion of lithium was not influenced by moderate changes of glomerular filtration rate, but was sharply enhanced by sodium loading. Increased blood pressure was associated with enhanced urinary sodium excretion in uninephrectomized deoxycorticosterone-salt hypertensive and two-kidney, one clip hypertensive rats, as a result of decreased distal tubular reabsorption (“pressure natriuresis”). In contrast, SHR showed reduced sodium excretion and decreased fractional excretion of lithium, which suggests that increased sodium reabsorption in the proximal tubule may contribute significantly to the maintenance of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The tissue content of norepinephrine, dopamine1and epinephrine was determined in different zones of the kidney in normotensive Sprague-Dawley and Otago Wistar rats and in genetically hypertensive Otago Wistar rats. One kidney in each animal was chronically denervated to allow estimation of the neuronal contribution to renal catecholamine content. In all strains, the renal cortex contained negligible amounts of nonneuronal norepinephrine and dopamine1while outer and inner medullary layers contained progressively larger amounts. Nonneuronal epinephrine was distributed fairly evenly through cortex and medulla. Neuronal norepinephrine content was similar in inner and outer cortex, substantially less in outer medulla, and not discernible in inner medulla. The amounts of neuronal dopamine were consistent with its localization predominantly in noradrenergic nerves. The renal cortices of normotensive Wistar rats contained more neuronal norepinephrine and less neuronal dopamine than those of Sprague-Dawley rats, and the cortices of hypertensive Wistar rats contained slightly more norepinephrine than thw of normotensive Wistar rats. In both normotensive strains, long-term salt loading decreased selectively the neuronal norepinephrine in renal cortex. By contrast, in hypertensive animals, cortical norepinephrine was not reduced by salt loading. These results indicate that the genetically hypertensive rat may have an abnormal sympathetic reflex response to increased bld volume.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The isomyosin composition in left and right ventricles from aldosterone-salt-treated hypertensive rats and from vehicle-infused and aldosterone-infused normotensive control rats was compared. A significant incremental increase (20%) in the percentage of V1isomyosin and parallel decrease in the percentage of V3isomyosin occurred in both left and right ventricles from aldosterone-salt-treated animals compared with those in normotensive vehicle-infused controls. No change in the ventricular isomyosin distribution was observed in animals infused with aldosterone without salt, which indicates that aldosterone does not directly affect the ventricular isomyosin composition. The changes in left ventricular isomyosin composition were accompanied by significant left ventricular hypertrophy (38%;p< 0.05), whereas no hypertrophy was observed in the right ventricle. Plasma thyroxine levels were significantly lower in aldosterone-salt-treated rats (3.7 ± 0.6 μg/dl;p< 0.05) than in normotensive vehicle-infused (6.0 ± 0.7 μg/dl) or aldosterone-infused (6.7 ± 0.3 μg/dl) controls. These results indicate that factors such as alterations in thyroid status or a volume overload component of this hypertensive model, in addition to increased systolic blood pressure, may contribute to a biventricular shift in isomyosin cornposition in the aldosterone-salt model of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The role of central nervous system α-adrenergic and β-adrenergic receptors in the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress (air stress) in conscious spontaneously hypertensive rats (SHR) was examined. Intracerebroventrlcular administration of the α2-adrenergic receptor agonist clonidine (1, 5, and 15 μg) prevented the effects of air stress on renal sympathetic nerve activity and urinary sodium excretion. Clonidine, 5 and 15 μg, lowered baseline mean arterial pressure and renal sympathetic nerve activity and increased baseline urine flow rate and urinary sodium excretion; clonidine, 1 μg, had no effect on these baseline levels. Intravenous administration of 5 μg, but not 1 μg of clonidine, abolished the renal responses to air stress. Intracerebroventricular administration of α2-adrenergic receptor antagonists (yohimbine, rauwolscine) reversed the effects of clonidine. α2-adrenergic receptor blockade alone, α1-adrenergic receptor blockade (20 μg prazosin), or combined α1-adrenergic and α2-adrenergic receptor blockade (30 μg phenoxybenzamine) had no effect on the renal sympathetic nerve activity or antinatriuretic responses to air stress. Intracerebroventricular, but not Intravenous, administration of the β2-adrenergic receptor antagonist ICI 118551 (30 μg) prevented the Increased renal sympathetic nerve activity and antinatriuretic responses to air stress. In contrast, intracerebroventricular administration of the β1-adrenergic receptor antagonist atenolol (30 μg) had no effect on the renal responses to air stress. These results indicate that the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious SHR can be prevented by pharmacological stimulation of central α1-adrenergic receptors or by blockade of central β2-adrenergic receptors.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

Maximal vasodilator capacity of resistance vessels has been shown to be reduced in normotensive young men with a family history of hypertension. The present study attempted to examine whether venous distensibility is decreased in normotensive men with hypertensive relatives. The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph in 17 normotensive young men with hypertensive relatives (mean blood pressure, 85 ± 2 [SE] mm Hg; age, 22 ± 1 years) and 18 young men with no family history of hypertension (mean blood pressure, 81 ± 2 mm Hg; age, 22 ± 1 years). The venous pressure-volume curve in men with hypertensive relatives as compared to that in men with no famUy history of hypertension was shined toward the pressure axis (p< 0.001). This finding suggests that venous distensibility is decreased in normotensive young men with hypertensive relatives. Administration of phentolamine, 1 mg/min i.v. for 5 minutes, did not alter venous distensibility, and venous distensibility after phentolamine administration was less in men with hypertensive relatives than in men with no family history (p< 0.001), which suggests that decreased venous distensibility found in normotensive young men with hypertensive relatives was unlikely to be related to α-adrenergic mechanisms. These results suggest that aormotensive young men with a family history of hypertension have vascular abnormalities that involve veins as well as arteries.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The factors responsible for 24-hour blood pressure and heart rate variabilities have never been clarified; however, studies performed in unanesthetized animals have shown an increase in blood pressure variability after sinoaortic denervation, and a negative relationship has been reported occasionally between blood pressure variability and baroreflex control of heart rate in humans. We have systematically investigated this issue in 82 ambulant hypertensive subjects using 24-hour intraarterial blood pressure recording (Oxford method) in which blood pressure and heart rate variabilities were measured by calculating the standard deviations of the values obtained throughout the 24 hours or during separate daytime and nighttime periods. Baroreflex sensitivity was assessed by the bradycardic or tachycardic responses to intravenous injections of phenylephrine or nitroglycerin and by the blood pressure response to changes in carotid transmural pressure obtained with a neck chamber. The sensitivity of the baroreceptor-heart rate reflex as Bssessed by the vasoactive drug technique showed a negative relationship with 24-hour blood pressure variability as well as with daytime and nighttime blood pressure variabilities measured separately (r = −0.28 to −0.50,p< 0.05). These Variabilities also correlated negatively with the sensitivity of the baroreceptor-blood pressure reflex as assessed by the neck chamber technique. By contrast, baroreflex sensitivity showed a positive correlation with heart rate variabilities (r= 0.32 to 0.47,p< 0.05). The relationship between baroreflex sensitivity and blood pressure and heart rate variabilities was confirmed when the data were analyzed by multiple regression to adjust for blood pressure and age differences among the 82 subjects. These results suggest that 1) arterial baroreflexes exert a buffering influence on the magnitude of daytime and nighttime blood pressure variabilities in humans; 2) these reflexes favor heart rate variability, which may represent one of the means by which baroreflex stabilization of blood pressure is accomplished; and 3) because of the low correlation indices between baroreflex sensitivity and blood pressure and heart rate variabilities, other factors (probably central in nature) are important in determining the size of these variations.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID

摘要:

The present study undertook to examine aldosterone excretion during sleep as an integrated measurement of aldoderone production. A 24-hour urine collection was divided into awake and sleep fractions. Urinary aldosterone and electrolyte excretion were measured in 26 healthy children (mean age, 8.9 ± 1.9 [SD] years) and 28 adults (mean age, 29.9 ± 9.5 years). Aldmterone excretion in children was 5.6 ± 3.9 (SD) μg/g creatinine during the awake period, which was significantly different from the 3.9 ± 4.1 μg/g creatinine value recorded during sleep (p< 0.002). In adults, awake aldosterone excretion was significantly greater than that during sleep; 4.9 ± 2.7 versus 3.2 ± 1.6 μg/g creatinine (p< 0.001). Sleep aldosterone excretion values were highly correlated with the corresponding 24-hour aldosterone excretion values (r= 0.85,p< 0.001) in children and in adults (r= 0.64,p< 0.001). Sleep aldosterone excretion was correlated with 24-hour potassium excretion (p C0.02) only in children. Sleep aldosterone excretion correlated with neither sleep nor 24-hour sodium excretion in children or adults. Sleep electrolyte excretion rates were highly correlated with 24-hour excretion rates in both children and adults. Dexamethasone, 1 mg, administered the night before to suppress the normally high morning levels of endogenous adrenocorticotropic hormone, had no discernible effect on sleep aldosterone excretion. These results indicate that measurement of aldosterone excretion in an easily collected sleep urine sample provides a reliable index of aldcwterone production in children and adults.

ISSN:0194-911X    

出版商:OVID    

年代:1986

数据来源: OVID