ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Relatively few studies of hypertension have been carried out in Mexican-Americans, a population characterized by high rates of obesity and non-insulin-dependent diabetes mellitus. We therefore compared the prevalence of hypertension according to four different definitions in 3,297 Mexican-Americans and in 1,873 non-Hispanic whites from the San Antonio Heart Study, a population-based study of cardiovascular disease and diabetes. By all four definitions, the crude prevalence of hypertension in both sexes was lower in Mexican-Americans than in non-Hispanic whites, although only two of the eight pairwise comparisons were statistically significant However, after adjusting for the potentially confounding effects of age, body mass index, and non-insulin-dependent diabetes mellitus, Mexican-Americans did have a statistically significant lower prevalence of both systolic and diastolic hypertension than did non-Hispanic whites in both sexes (odds ratios ranging from 0.66 to 0.71 depending on the definition of hypertension). The cause of this lower prevalence is unknown, but study of this ethnic group with elevated levels of risk factors for hypertension (obesity, hyperinsulinemia, and diabetes) may provide additional insights into the etiology of hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Twenty-two patients with normal plasma renln and essential hypertension were classified as “salt-sensitive” (SS) (n=9) or “non-salt-sensitive” (NSS) (n=13) from an increase in mean blood pressure with changes in sodium intake from 25 to 250 meq/day. With the high sodium diet, the SS patients gained more weight (/?<0.05), retained more sodium (p<0.05), and had a greater increase in cardiac output (p<0.05). Despite the markedly increased cardiac output, systemic vascular resistance did not change with sodium loads in the SS patients, whereas the NSS patients had a significant decrease in systemic vascular resistance. Thus, the greater increase in blood pressure with sodium loads in SS patients can be attributed not only to an increase in cardiac output, possibly resulting from greater sodium retention, but also to inappropriately elevated systemic vascular resistance. Concomitant with a greater increase in cardiac output, the SS patients had a greater increase in forearm blood flow with sodium loading than the NSS patients (p<0.02). In contrast, blood flow to the kidney and the liver was not significantly changed in either group; renal (p<0.05) and hepatic (p<0.01) vascular resistance increased significantly in SS patients but remained unchanged in NSS patients. Thus, evidence presented suggests that the greater increase in blood pressure with sodium loads seems to be characterized by a very inhomogenous distribution of local flow and resistance in SS patients; renal and hepatic blood flow remains essentially unchanged and skeletal muscle blood flow receives almost all of the increase in cardiac output Moreover, systemic vascular resistance changes did not reflect the resistance of individual beds because vasoconstriction appeared in the kidney and the splanchnic area but was masked by prominent vasodilation in the skeletal muscle. Because this hemodynamic pattern is similar to the pattern evoked during defense reaction, it is suggested that sympathetic overactivity on a selective basis might be involved in the impaired renal function for sodium excretion and the increase in blood pressure with sodium loads in SS patients.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Cytosolic free calcium concentration ([Ca2+t) and muscle tension were simultaneously measured in aortic tissue isolated from spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY) rats, and SHR chronically treated with a novel angiotensin converting enzyme inhibitor, CS-622. In the presence of 2.5 mM Ca2+in the bathing solution, aortic [Ca2+], measured with fura-2 was higher in SHR than in WKY rats, and it was almost the same in CS-622-treated SHR and untreated WKY rats. Increase of external Ca2+concentration from zero to 2.5 mM elicited a contraction in SHR aortas but not in aortas from both CS-622-treated SHR and untreated WKY rats. When the aortas were contracted by 60 mM K+, however, [Ca2+], as well as developed tension was similar in the three groups. CGP-28392 (10−6M), a Ca2+channel activator, induced a rhythmic activity superimposed on a gradual increase of [Ca2+], and tension in SHR aortas but not in the aortas of CS-622-treated SHR or untreated WKY rats. Nicardipine (10∼7 M) decreased the resting [Ca2+], and the resting tone in SHR aortas, but not in WKY rat aortas. These results suggest that SHR aortas have a higher myogenic tone due to increased [Ca2+], than WKY rat aortas and that the increased [Ca2+], is attributed to alterations of dihydropyridine-sensitive Ca2+ channels in SHR aortas. Further, the decrease of the vascular tone induced by long-term administration of the angiotensin converting enzyme inhibitor may be due to a reduction of increased [Ca2+], in SHR.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Three groups of spontaneously hypertensive rats (SHR) were given enalapril (25 mg/kg/day) from 4 to 9 weeks, 4 to 14 weeks, and 14 to 20 weeks of age. The drug was stopped and observations continued for another 16–21 weeks. At selected times, we measured blood pressure, in vitro hindquarter vascular resistance properties, left ventricular weight/body weight ratio, and skeletal muscle vessel norepinephrine kinetics in treated and untreated SHR and in Wistar-Kyoto (WKY) rats. At the end of each treatment period, all cardiovascular variables were close to values of WKY rats and well below those of untreated SHR, and the norepinephrine or fractional rate constant was about 25% below those levels. After enalapril was stopped, blood pressure and left ventricular weight/body weight ratio increased in parallel to levels ranging from 30% to 50% of the normal difference between untreated SHR and WKY rats. However, in SHR treated from 4 to 9 weeks and from 4 to 14 weeks of age, hindquarter resistance properties remained close to WKY rat levels for the entire observation period of 16–21 weeks after treatment, suggesting suppression of the enhanced resistance responses of SHR (amplifier properties). In SHR treated from 14 to 20 weeks of age, suppression of amplifier properties was more transient, and they redeveloped partially 5–6 weeks after cessation of therapy. When enalapril was given up to 14 weeks of age, the long-term suppression of amplifier properties was probably mainly through prevention of smooth muscle hypertrophy in resistance vessels and possibly through other mechanisms (eg., “rarefaction”). After that age, its therapeutic action was similar to that of other antihypertenslve drugs where, after drug withdrawal, there is a slow pressure rise in parallel with redevelopment of vascular and cardiac hypertrophy.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Diuretic therapy may enhance renin release by various mechanisms, principally contraction of extracellular fluid volume and its effects, including a fall in arterial pressure. Awake hydropenic or volume-expanded rats received diuretics (amiloride and hydrochlorothiazide) that are known inhibitors of NaCl transport beyond the macula densa; also the well-known Na+-K+-2 Cl″ transport system inhibitor furosemide was administered. We also evaluated the effect of a dose of ethacrynic acid (a drug that shares the same mechanism of action as furosemide but is not diuretic in the rat). The direct action of the diuretics on renin-producing cells was examined in isolated glomeruli; a rise in renin release was observed with the calmodulin inhibitor trifluoperazine (10−5M). Renin release in intact hydropenic rats was not altered by diuretic therapy, but furosemide increased plasma renin activity in hydropenic as well as in volume-expanded rats. This demonstrates the importance of furosemide inhibition of transport in the macula densa for its renin secretory action. None of the diuretics (amiloride, hydrochlorothiazide, ethacrynic acid, or furosemide) elicited changes in renin release from glomeruli (10−6to 10−3M); amiloride and hydrochlorothiazide (10−4to 10−3M) did not change renin release from slices, but 10−3M ethacrynic acid and furosemide increased renin secretion in this preparation. This suggests that an effect on the macula densa is essential in loop diuretic-mediated renin release. Because ethacrynic acid is not diuretic (at the doses used in this study) but increases renin release from slices, the study raises the possibility that a direct effect of some diuretics on tubular structures (i.e., macula densa) may cause the production of substances that are ultimately responsible for mediating renin release from renin-containing cells.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of an orally active inhibitor (UK 79300) of the neutral metalloendopeptidase EC 3.4.24.11 were investigated in six healthy male volunteers maintained on a constant diet (150 mmol sodium/day and 80 mmol potassium/day). Subjects were studied in a random order, single-blind study on two occasions, each 48 hours in length, when they were given UK 79300 (25 or 50 mg p.o.) or placebo at 12-hour intervals (each agent for 24 hours). The endopeptidase inhibitor enhanced plasma concentrations of atrial natriuretic factor in association with suppression of both plasma renin activity and aldosterone concentrations. Twenty-four-hour urinary excretion of sodium was doubled by UK 79300, and the urinary excretion rates of phosphorus, atrial natriuretic factor immunoreactivity, and cyclic guanosine monophosphate were also significantly enhanced, whereas urinary aldosterone excretion was halved. The profile of biological effects closely paralleled those previously reported with low dose infusions of atrial natriuretic factor in humans and animals. Therapeutic trials of such inhibitors are now indicated for hypertension or heart failure together with further studies to clarify the underlying mechanisms of action.

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The objective of our study was to determine the genetic influence on blood pressure in spontaneously hypertensive rats (SHR), and normotensive Wistar-Kyoto (WKY) rats using genetic crosses. Blood pressure was measured by tail sphygmomanometry from 8 to 20 weeks of age. Blood pressure was significantly higher from 12 to 20 weeks in the male offspring derived from WKY mothers x SHR fathers as compared with male offspring derived from SHR mothersxWKY fathers (180±4 versus 160±5 mm Hg, /?<0.01). There was no significant difference between the blood pressure of the F, females, further supporting Y chromosome linkage and not parental imprinting. The blood pressure data from F2 males derived from reciprocal crosses of parental strains were consistent with the presence of a Y-Iinked locus, but not with an X-linked locus controlling blood pressure. The data strongly suggest that hypertension in the SHR has two primary components of equal magnitude, one consisting of a small number of autosomal loci with a second Y-linked component

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The present experiments were designed to test the hypothesis that adrenal epinephrine contributes to the development of hypertension in the Dahl salt-sensitive (DS) rat All studies were carried out in conscious male DS and Dahl salt-resistant (DR) rats weighing 200–240 g. An indwelling femoral arterial catheter was placed for blood sampling and measurement of blood pressure. After 5 days of either a high salt (7% NaCl) or a normal salt (1% NaCl) dietary regimen, DS and DR rats were subjected to an acute stress paradigm (graded electrical footshock). There were no differences in basal plasma catecholamine concentrations or in the acute pressor responses to graded footshock between the four substrain/diet groups. However, in both DS and DR rats, plasma epinephrine responses to acute footshock were greater on a 7% than on a 1% NaCl diet Additional groups of DS rats were treated with an inhibitor of adrenal phenylethanolamine JV-methyltransferase, SK&F 29,661 (1–2 g/kg body wt/day) or with vehicle. Three days after placement of an arterial catheter, rats were placed on a 7% NaCl diet, and blood pressure was measured daily for an additional 3 weeks. Although SK&F 29,661 treatment was effective in reducing adrenal epinephrine content and apparent release by approximately 80%, treatment did not alter the time course of salt-induced changes in blood pressure. We conclude that: 1) acute pressor responses to mild stress do not differ between DS and DR rats and are not enhanced by high dietary NaCl intake, 2) 5 days of high salt diet induces an apparent increase in adrenomedullary responsiveness to mild stress that is independent of DS or DR substrain, and 3) epinephrine of adrenal origin is not essential for the development of salt-sensitive hypertension in the DS rat

ISSN:0194-911X    

出版商:OVID    

年代:1990

数据来源: OVID