ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

We compared the correlates of blood pressure in 163 young patients with insulin-dependent diabetes and in 232 of their non-diabetic siblings. A single observer recorded blood pressure in all subjects, plus all their available parents, using a standardized technique. Other variables recorded included age, weight, height, presence of diabetes and urinary albumin. The major factors accounting for over 50% of the variance of systolic blood pressure (SBP) in both groups were age, weight, paternal SBP and sex. In addition, in the diabetic group the logarithm of the random urinary albumin concentration was a significant explanatory variable. For diastolic blood pressure (DBP) approximately 16% of the variance was explained by age, weight and maternal DBP. Parental blood pressure was an important determinant of blood pressure in both the diabetic and non-diabetic sibling groups. The similarity of the correlates of blood pressure in the two groups suggests that the determinants of blood pressure in young insulin-dependent diabetic patients and in the general population are similar.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The region of intron A of the rat renin gene containing a unique tandemly repeated sequence was analysed in the Milan and Lyon hypertensive rat strains and their controls, and in several Sprague-Dawley rats, using an oligonucleotide probe complementary to the tandemly repeated sequence and a renin complementary DNA probe. In the Milan rats, the size of the Bgl II DNA fragment encompassing the tandem repeat region was the same in the hypertensive (MHS) and normotensive (MNS) strains. In the Lyon model, a difference of 1.1 kilobase (equivalent to about 28 copies of the 38 basepair tandem repeat sequence) was observed in the size of the Bgl II fragment of the hypertensive (LH) and normotensive (LN) strains. However, the finding that the size of the fragment in the Lyon low-blood-pressure (LL) strain was the same as that in the LH strain rather than the LN strain suggests that the difference between the two latter strains is not by itself a major cause of the blood pressure difference between them in the intron A tandem region. An analysis of Sprague-Dawley rats, from which the Lyon strains are derived, showed that at least three different renin gene alleles, two with Bgl II fragments of the same size as those seen in the Lyon strains, are randomly segregating in this population.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Endothelin-1 was infused into the non-dominant brachial artery in two male subjects. We then monitored intra-arterial mean blood pressure, right atrial pressure, the heart rate and forearm blood flow (by plethysmography). Endothelin-1 at a dose of 5 x 1O-14to 5 x 1O-9mol, infused over 5 min periods, elicited no major changes in mean arterial pressure, heart rate and right atrial pressure. We observed an initial increase in forearm blood flow, followed by dose-dependent decreases of 25, 34 and 42% at 5 x 10-11to 5 x 10-9mol. A higher dose of endothelin-1, 5 x 10-8mol, given to only one of the subjects, elicited sweating and vomiting. In this subject, mean arterial pressure, right atrial pressure and the heart rate did not change, while forearm blood flow increased transiently. A deep muscular pain developed in the forearm receiving the endothelin-1 infusion after 30 min (maximum 2h, duration 10 h), and this pain was intensified by touch and muscle contractions. The force of muscle contractions in the forearm was markedly reduced and a visible oedema developed. In order to investigate the mechanisms of oedema formation, endothelin-1 (10-10to 5 x 10-8mol/l) was given intra-arterially in a rat hindquarter preparation which was perfused at a constant flow rate. In the rat, endothelin-1 increased both pre- and postcapillary resistance, leading to an increase in capillary hydrostatic pressure and a marked net transcapillary fluid transfer from the perfusate to tissue. There was no sign of increased vascular permeability. These results indicate that the development of oedema in humans may be due to an increase in capillary pressure. The similarity to sarafotoxin toxicity suggests that endothelin peptides should be tested in humans with great caution until further data on their physiological or pharmacological properties are available.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

This study was aimed at evaluating the hemodynamic changes after acute inhibition of the renin—angiotensin system in hypertensive patients. Twenty-one subjects with essential hypertension were randomized into three groups of seven subjects each. In group I, the direct vascular vasodilator dihydralazine was administered at a dose of 4µg/kg per min. Groups II and III received a continuous intravenous infusion of the angiotensin converting enzyme (ACE) inhibitor perindoprilat at a dose of 1 µg/kg per min and 2.5 µg/kg per min, respectively. Brachial artery hemodynamics and aortic distensibility were evaluated non-invasively. Vascular reactivity was evaluated by the cold-pressor test. In all three groups, an identical decrease in blood pressure was observed (P < 0.001), followed by a slight (but not significant) decrease in the heart rate in both perindoprilat groups, and an important tachycardia in the dihydralazine group (P < 0.001). Brachial artery diameter was increased in the high-dose perindoprilat group from 0.437 ± 0.014 to 0.479 ± 0.013 cm (P < 0.02), but remained unchanged in the two other groups. No significant changes in brachial artery mean blood velocity and blood flow were observed. In group III, aortic distensibility increased almost twice as much as in the two other groups, but this difference was not statistically significant. The pressor response to the cold-pressor test was not modified in the three groups; the heart rate response was almost completely abolished in groups II and III, but increased in the dihydralazine group (P < 0.01). These results suggest that (1) intravenous administration of perindoprilat decreases blood pressure without increasing the heart rate, and inhibits tachycardia during the cold-pressor test, and (2) since only higher doses of ACE inhibitor may be capable of inducing vasodilatation in the large arteries, despite having an identical hypotensive effect and the same degree of plasma ACE inhibition, the two different doses of perindoprilat induced different vascular effects. We propose that higher doses of perindoprilat may be necessary in order to inhibit vascular ACE, or to stimulate vasodilating systems.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

Vascular responsiveness was evaluated in perfused mesenteric arteries from rats infused with dexamethasone (2 µg/day). Full dose—response curves to noradrenaline, vasopressin and potassium chloride were established. In order to investigate whether prostaglandins or noradrenaline uptake were involved in dexamethasone-induced pressor changes, vascular responses were compared before and during treatment with either indomethacin (a cyclo-oxygenase inhibitor) or desipramine (an inhibitor of neuronal catecholamine uptake). Dexamethasone-treated tissues showed an increased vascular sensitivity to noradrenaline compared with controls; the maximal response was greater and the concentrations of agonist required for a 50% response (EC50) was less in dexamethasone-treated tissues. The responses to vasopressin and potassium chloride were not affected. Systolic blood pressure in dexamethasone-treated rats was not significantly different from that in controls. Indomethacin infusion decreased the vascular responsiveness to noradrenaline in control and dexamethasone-treated rats to a similar degree. Noradrenaline responses after indomethacin treatment were not significantly different in control and dexamethasone-treated tissues. 6-Keto-prostaglandin-F1αoutput during stimulation with noradrenaline was not affected by dexamethasone. Desipramine lowered pressor responses to noradrenaline at all concentrations and decreased the maximal response in tissues from dexamethasone-treated but not control rats. However, during infusion with desipramine, the EC50for noradrenaline after dexamethasone was still less than in controls. Dexamethasone at low doses appears to selectively increase vascular sensitivity to noradrenaline in rats at a prehypertensive stage by changing prostaglandin synthesis and, possibly, neuronal uptake of noradrenaline.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of calcium and deoxycorticosterone (DOC) were studied in four groups of spontaneously hypertensive rats (SHR): control, calcium, DOC and DOC + calcium. Calcium was administered in drinking fluid as 1.5% calcium chloride, and DOC was injected weekly (25 mg/kg subcutaneously). During the 9-week study the increase in, systolic blood pressure was enhanced in the DOC and attenuated in the calcium group, but did not differ from control values in the DOC+calcium group. DOC augmented in vitro contractions of aortic and mesenteric arterial rings induced by noradrenaline and impaired relaxations in reponse to nitroprusside and acetylcholine. Calcium alone enhanced the relaxation in reponse to nitroprusside in the mesenteric artery. In the DOC + calcium group vascular contractions did not differ from control values, but the relaxations caused by nitroprusside and acetylcholine were augmented in the mesenteric artery. The activity of erythrocyte Ca2+-ATPase increased in both calcium groups. The Na+:K+ratio of tail artery tissue was reduced in the calcium group. In conclusion, calcium supplementation attenuates the development of hypertension, and prevents DOC-induced blood pressure increases in SHR by altering vascular reactivity. Changes in smooth muscle electrolyte ratios and Ca2+-ATPase activity may account for these alterations.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID

摘要:

The effects of endothelin-1 on cytosolic Ca2+and inositol 1,4,5-triphosphate (IP3) levels were investigated in cultured, untreated human endothelial cells and in endothelial cells pretreated with anti-endothelin-1 serum for 24 h to exclude the effect of endogenous endothelin-1. Endothelin-1 was found to increase the intracellular Ca2+level, either in the presence or absence of extracellular Ca2+, in endothelial cells pretreated with antiserum by the fura-2 fluorescence technique. IP3levels immediately started to rise following endothelin-1 stimulation. Resting intracellular Ca2+levels were significantly lower when the cells were pretreated with antiserum than without antiserum pretreatment. Following stimulation by endothelin-1, intracellular Ca2+and IP3levels in endothelial cells pretreated with antiserum increased significantly compared to those in untreated endothelial cells. Endothelin-1 also increased45Ca influx from the extracellular space. These results suggest that endothelin-1 increases intracellular Ca2+in endothelial cells through extracellular Ca2+-dependent mechanisms and by the release of Ca2+from intracellular stores, this presumably being induced by IP3formation.

ISSN:0263-6352    

出版商:OVID    

年代:1990

数据来源: OVID