摘要:

SUMMARY We have investigated the changes in plasma norepinephrine and blood pressure and heart rate during a range of physical activities in eight hypertensive subjects in order to determine whether changes in plasma norepinephrine reflect changes in sympathetic activity. Blood pressure was recorded over 24 hours from an intra-arterial cannula. Plasma norepinephrine, measured by a sensitive radioenzymatic method, increased progressively with increasing levels of physical activity. In each subject a statistically significant linear relationship was observed between the logarithm of plasma norepinephrine and systolic blood pressure. Analysis of variance showed that 66% of the variance of plasma norepinephrine was associated with changes in blood pressure and heart rate. These observations support the hypothesis that plasma norepinephrine reflects short-term changes in sympathetic activity. Use of the quantitative relationship described, in conjunction with measurements of norepinephrine metabolism, may help to determine the significance of increased levels of plasma norepinephrine observed in some hypertensive patients.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY To characterize the renln-angiotensin system in the Aokl-Okamoto spontaneously hypertensive rat (SHR) more fully, serial measurements of plasma renin activity (PRA), plasma renin concentration (PRC), renin reactivity (as relative index of circulating modifiers of the renin reaction) and renin substrate concentration were made in 6- to 64-week-old SHR and in age-matched Wistar-Kyoto normotensive rats (WKY). In the evolving phase of SHR hypertension (6 and 13 weeks of age), PRA was comparable to WKY control values, whereas mature SHR with established hypertension developed, between 13 and 35 weeks of age, a high-PRA state persisting through 64 weeks of age. In 64-week-old SHR, increased plasma volume (3.54 ± 0.91 in SHR vs. 3.18 ± 0.90 ml/100 g body weight in WKY.p< 0.025), together with increased PRA (24.9 ± 3.8 in SHR vs. 13.1 2.2 ng Al/ml plasma/hr in WKY.p< 0.025), suggest that volume decrease cannot explain increased PRA. In 42-week-old SHR, PRA was incompletely suppressed by deoxycorticosterone acetate plus 1% saline orally for 4 days: 4.9 ± 1.2 in SHR vs. 0.6 ± 0.8 ng angiotensin I/ml plasma/hr in WKY,p< 0.001. Modestly increased renin reactivity of plasma was observed in SHR at all ages studied, supporting the ubiquity of increased circulating accelerators (or decreased inhibitors) of the renin reaction in hypertensive states. However, elevated renin reactivity did not account for the transition from normal to high PRA observed in mature SHR, nor did renin substrate concentration, which was consistently lower in SHR than in age-matched WKY. Temporal patterns of, and strain differences in PRA were closely paralleled by variations in PRC but not by other reaction components. Significant elevation of serum creatinine in old SHR support the presence of renal injury. We conclude that PRA and PRC are normal in evolving SHR hypertension and progress to abnormally elevated levels after hypertension is established. We postulate that “higb-renin” hypertension may develop as a consequence of the hypertensive state perse, perhaps due to nepbrosclerotic vascular disease.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Plasma renin activity is suppressed in approximately 25% of patients with essential hypertension, and the rate of in vitro angiotensin I production after addition of exogenous renin (renin reactivity) is increased in plasma of hypertensive patients. We have recently observed that blood pressure (116 ± 1.5/68 ± 1.7 mm Hg) of young women who had hypertension during a first pregnancy 3-6 years earlier (n = 63) was higher (p< 0.005) than blood pressure (109 ± 1.4/61 ± 1.7 mm Hg) of women who remained normotensive during pregnancy (n = 52). To determine if alterations of the renin-angiotensin axis observed in patients with established hypertension also occur in young adults with relatively high blood pressure, plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin substrate (PRS) and plasma renin reactivity (PRR) were compared in these two groups of subjects. Overall, PRA and PRC were Inversely related to systolic blood pressure (p< 0.02). Excluding women on oral contraceptive agents, the PRA response to standardized treadmill exercise was suppressed (< 1.0 ng/ml/hr) in 19% of women with a history of hypertension during pregnancy and in no women who remained normotensive throughout a previous pregnancy; PRR did not differ [p > 0.8) in the two groups of young mothers (27.1 ng/ml/30 min ± 1.2 SK vs 26.2 ng/ml/30 mln ± 0.9 SE). Thus, renin suppression, but not increased PRR, precedes the onset of hypertension. Oral contraceptive usage was associated with higher systolic blood pressures, increased PRS, and low PRC. Highest blood pressures and lowest PRA occurred in women with a history of hypertension during pregnancy who were taking oral contraceptive agents at the time of study.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Clonidine is believed to reduce blood pressure by a neural action and animal experiments suggest that this consists in potentiation of baroreflexes. In 16 patients with essential hypertension we studied the effects of alterations in carotid sinus baroreceptor activity (neck chamber technique) on arterial blood pressure (catheter measurements) and heart rate, before and after Intravenous administration of 150 /ig and 300 fig of clonidine. The magnitude of the reflex responses was assessed by the slope of the linear regressions relating applied increase and decrease in tissue pressure at the carotid sinus (and therefore applied decrease and increase in carotid sinus transmural pressure) and resulting changes in mean arterial pressure and R-R interval. Clonidine caused a marked reduction in mean arterial pressure (−26 ± 3 mm Hg) and a slight but significant reduction in heart rate (− 5 ± 1 b/rain). There was no evidence for a potentiation of the baroreceptor influence on blood pressure, although a slight potentiation of the baroreceptor influence on heart rate was observed in few instances. We conclude that in man clonidine can exert a pronounced hypotensive effect without potentiating baroreceptor influence on blood pressure. Therefore this mechanism does not play a prominent role in the clinical antihypertensive action of the drug.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY It has been suggested that intrarenal levels of angiotensin II may preferentially control efferent arterlolar resistance or may influence the glomerular filtration coefficient (Kf). To examine these possibilities, micropuncture and clearance experiments were performed on nine anesthetized dogs evaluating renal and glomerular hemodynamics before and during the administration of an angiotensin converting enzyme inhibitor (SQ20,881). During the micropuncture measurements, renal arterial pressure was reduced to a range of 85 to 90 mm Hg in order to maximize renin secretion and intrarenal formation of angiotensin II. Also, this procedure minimizes potential errors In the determination of single nephron glomerular filtration rate (SNGFR) and of glomerular pressure when estimated by techniques that require complete blockade of proximal tubule fluid flow. During the administration of SQ20,881, a converting enzyme inhibitor (CEI), renal blood flow increased significantly by 13%, but GFR was not altered. There were no significant alterations in SNGFR, proximal tubule pressure, peritubular capillary pressure or estimated glomerular pressure. By using the micropressure measurements in combination with the whole kidney hemodynamic data, it was estimated that afferent resistance was reduced 23%. Although significant decreases in efferent resistance could not be documented, there was a tendency for this variable to decrease also. Neither Kr nor effective filtration pressure were altered significantly by CEI. These results do not support the contention that intrarenal effects of angiotensin II are exerted predominantly on the efferent arteriolar resistance segments; rather, they suggest that angiotensin may exert a modest tonic effect on both preand postglomeralar resistance elements in the anesthetized hydropenic dog.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Regional differences in cell size in the hearts of rats with and without cardiac hypertrophy were studied using isolated muscle cells. Isolated cardiac myocytes were prepared from left ventricular free wall inner and outer halves and the right ventricle of six male 12-week-old spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Fischer-344 rats. In SHR, blood pressure was increased to 188 ± 4 (SEM) mm Hg versus 143 ± 2 and 133 ± 10 for WKY and Fischer rats, respectively (p< 0.001). Total heart weight was increased to 1103 ± 29 mg in SHR compared to 824 ± 21 in WKY and 951 ± 23 in Fischer rats (p< 0.001). Isolated cardiac myocytes were prepared by perfusion of isolated hearts with Ca++ free Hanks' solution containing EGTA followed by collagenase-containing media. Mean length, width and volume of 150 cells stained with hematoxylin and eosin from each site were measured with a sonic digitizer. Two nuclei were present in 85 to 87% of isolated cells from all strains and regions. There was no difference among strains in right ventricular cell length, width, or volume, nor between left ventricular inner and outer halves within each strain. Left ventricular cells were larger than right ventricular cells (p< 0.05) in all strains. Left ventricular cells of SHR were larger than left ventricular cells of WKY or Fischer rats in proportion to the increase in total heart weight, indicating that cardiac enlargement in SHR is due to increased cell size rather than increased cell number.

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 The purpose of this study was twofold: 1) to determine whether the failure of rats with chronic renovascular hypertension to respond to the angiotensin II antagonist (AHA) with a decrease in mean blood pressure (BP) was due to the agonistic effect of the antagonist; and, 2) if this was not the case, to examine whether a positive sodium balance impaired the reversal of the hypertension, after unclamping, in the rats that did not respond to angiotensin inhibitors. For this purpose, rats with chronic, two-kidney Goldblatt hypertension (one renal artery clamped and contraJateral untouched) were tested for their BP response to the AHA (1- Sar-8-Ala-angiotensin II) and to the converting enzyme inhibitor (CEI) SQ20,881, which is devoid of agonistic effect. Approximately 50% of the rats responded to both inhibitors either with no change or with a decrease in BP of less than 20 mm Hg (nonresponders). The other 50% had a decrease in BP of 20 mm Hg or greater (responders). The decrease in BP produced by the AHA and the CEI correlated significantly (r= 0.76). Nonresponders to both inhibitors were undamped or sham undamped. A positive sodium balance was produced before surgery by injecting either 400 or 1000 /iEq of sodium and was maintained for 12 hours. Direct BP significantly decreased 12 hours after surgery in the undamped rats despite a continuous positive sodium balance. In the sham undamped rats, BP did not change. These data indicate that the failure to respond to the AHA is not due to the agonistic effect of this peptide. Furthermore, these data suggest that a positive sodium balance is not a major patbogenetic factor in maintaining the high BP in the nonresponder rats, since a positive sodium balance failed to maintain the hypertension after unclamping.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Captopril inhibits angiotensin II formation and bradyklnin degradation in vivo. Eleren patients with essential hypertension (EH) and four patients with renovascular hypertension (RVH) were treated with captopril for periods ranging from 3 days to 12 months. All patients had a diastolic blood pressure (DBP) over 95 ram Hg after receiving a placebo for 3 days. Captopril given in ascending doses (10-1000 mg/day) caused normalization of blood pressure in all but three patients, one with serere RVH whose pressure fell 11%, one patient with severe EH, whose pressure fell 27%, and one with EH whose Mood pressure fell 8.5%. The average control DBP in patients with EH was 113.7 ± 5.5 (SE) mm Hg and feU to 89.9 ± 3.6 mm Hg (< 0.001), while DBP in patients with RVH fell from 110.7 ± 7.6 mm Hg to 943 ± 8.2 (p< 0.005). All patients were studied in balance on a 100 mEq sodium (Na) diet Plasma renln activity (PRA) versus 24-bour urinary Na excretion increased sevenfold during therapy while converting enzyme activity fell by about one half. The magnitude of the blood pressure response was not related to control PRA. Cardiac output was estimated by ecnocardiography during placebo administration and during maintenance therapy with captopril. A significant change was not observed. Total peripheral resistance fell an average of 18.9% (p< 0.05) in 11 of the 13 patients in whom the measurement could be made. It is concluded that captopril effectively lowers Mood pressure in patients with EH or RVH by reducing total peripheral resistance.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

SUMMARY Sodium depletion was induced in dogs to raise plasma renln activity (PRA) from 1.11 to 26.48 ng/ml/hr. Little overall change in blood pressure (BP) occurred, but cardiac output (CO) and central venous pressure fell, while total peripheral resistance and heart rate (HR) increased.A nonapeptide converting enzyme inhibitor (CEI) produced a fall in BP which was linearly related to log. PRA; the intercept with PRA was at 1.05 ng/ml/hr, dose to the average value for dogs on a normal diet. The fall in BP with this agent was not accompanied by an increase in HR or CO.When Sar'-Ala' angiotensin II was used to antagonize the action of angiotensin, the fall in BP was also linearly related to log. PRA. However, for a given level of PRA this fall in BP was less than that achieved with CEI and the intercept of BP fall with PRA was 2.6 ng/ml/hr. Again with this agent there was little change in HR or CO as BP was reduced.Thus, both antagonists lowered peripheral resistance without exciting the bomeostatic reflexes indicating that, as PRA rose above the normal resting level, the angiotensin generated had both a direct and indirect effect in maintaining BP.

ISSN:0194-911X    

出版商:OVID    

年代:1979

数据来源: OVID