ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Intracellular cations regulate a variety of functions in myocytes, and abnormalities in ionic homeostatic control have been implicated in several cardiac disease processes. These include cardiac hypertrophy, some of the cardiomyopathies and reperfusion injury following myocardial ischaemia.Topics under review:Current understanding of the sarcolemmal transport mechanisms which generate transmembrane electrochemical gradients for Ca2 +, H+and K+is reviewed. Both active, ATP-dependent membrane ion transport and secondary active transport are described. The importance of the sarcolemmal Na+—K+pump in maintaining transmembrane gradients for Na+and K+is emphasized, and we describe how the electrochemical energy stored in the Na+gradient generated by the pump is utilized by ion-exchange processes in which a tightly coupled exchange of extracellular Na+for intracellular Ca2+or H+occurs. We also describe cotransport processes in which coupled obligatory transport of Na+, K+and Cl−occurs in the same direction. Physiological and pharmacological properties of sarcolemmal ion transport mechanisms are reviewed and reference is given to possible clinical implications.

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective and design:It has been hypothesized that risk factors for coronary heart disease in men are linked and that the underlying factor linking them may be an alteration in the sex hormone milieu. As a test of this hypothesis, sex hormones and fibrinogen, factor VII and plasminogen activator inhibitor (PAI-1), hemostatic factors recently shown to be risk factors for myocardial infarction, were measured in men with hypertension and in healthy control subjects.Results:The fasting serum testosterone and free testosterone levels were decreased and the plasma factor VII and PAI-1 levels increased in the men with hypertension.Conclusion:These findings are consistent with the stated hypothesis.

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:To study the effects of chronic insulin administration without sugar supplementation on blood pressure and response to acute saline loading in normal rats.Design:Design: Comparison of blood pressure, insulin and glucose levels in 24 insulin-treated and 12 control rats on regular rat chow (not supplemented with sugar).Methods:Sustained-release insulin implants (or sham implantation for the control rats) were administered subcutaneously. The sustained-release insulin implant size was gradually increased. Tail-cuff systolic blood pressure, insulin and glucose were measured twice a week for 8 weeks, after which intra-arterial blood pressure was recorded under resting conditions and 2 h after saline loading in seven insulin-treated and seven control rats.Results:Insulin-treated rats had a 1.2- to twofold increase in insulin without hypoglycaemia, a small but significant increase in glucose levels being found at weeks 6 and 8. When the rats were killed (week 8) triglyceride and fructosamine levels were increased in the insulin-treated rats in comparison with controls. Neither tail-cuff systolic blood pressure nor resting intra-arterial blood pressure differed between the two groups. However, acute saline loading resulted in significantly higher blood pressure in the insulin-treated rats, without altering renal Na+excretion.Conclusions:Insulin-treated rats had a 1.2- to twofold increase in insulin without hypoglycaemia, a small but significant increase in glucose levels being found at weeks 6 and 8. When the rats were killed (week 8) triglyceride and fructosamine levels were increased in the insulin-treated rats in comparison with controls. Neither tail-cuff systolic blood pressure nor resting intra-arterial blood pressure differed between the two groups. However, acute saline loading resulted in significantly higher blood pressure in the insulin-treated rats, without altering renal Na+excretion.

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective:Chronic parathyroidectomy (PTX) attenuates blood pressure and increases vascular force generation. The mechanism is not understood. We tested the hypothesis that PTX-induced changes in blood pressure and vessel contractility result from rapid changes in serum parameters induced by PTX, and the hypothesis that the endothelium-derived factors contribute to PTX-induced enhancement of force generation in the spontaneously hypertensive rat (SHR).Design:Chronic PTX or sham surgery was performed on 5-week-old male SHR, and subacute PTX was performed on 13- to 14-week-old SHR. The following experimental parameters were measured 5—6 weeks after chronic and 2 days after subacute PTX: systolic blood pressure, serum Ca2 +, 1,25-dihydroxyvitamin D3(vitD) and mesenteric resistance artery contractility.Results:Results: Chronic PTX significantly reduced blood pressure, body weight and serum Ca2 +compared with sham surgery; subacute PTX reduced only serum Ca2 +and vitD. Compared with sham surgery, the mesenteric resistance artery following chronic PTX showed increased active stress responses to norepinephrine and serotonin that were not associated with changes in free intracellular Ca2 +, but were abolished by endothelial denudation. Subacute PTX did not affect the active stress response to norepinephrine or endothelin. Low-dose acetylcholine induced relaxation that was attenuated in the chronic, but not the subacute, PTX subgroup compared with the sham-operated subgroup. High-dose acetylcholine induced contraction that was significantly greater in the chronic, but not subacute, PTX rats than in sham-operated rats. Indomethacin abolished the acetylcholine-induced contraction in all groups, but did not improve the impaired relaxation response of the chronic PTX subgroup.Conclusions:The PTX-induced decrease in blood pressure and increase in force generation do not result from acute changes initiated by reduction of serum parathyroid hormone, vitD or Ca2 +. Moreover, the PTX-induced increase in force generation results from a decrease in the production of a non-cyclo-oxygenase endothelium-dependent relaxing factor.

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Objective and design:The aim of the study was to assess the role of angiotensin II (Ang II) in the maintenance of cardiovascular hypertrophy and the abnormal vascular amplifier properties in spontaneously hypertensive rats (SHR) with established hypertension. Losartan, a type 1 Ang II receptor antagonist, was administered to SHR and Wistar—Kyoto (WKY) rats, and its effects on blood pressure, cardiac hypertrophy, vascular morphology and hindquarter vascular amplifier properties assessed at the end of treatment and 3 months later.Methods:Losartan was administered for 6 weeks to 14-week-old SHR (60mg/kg per day orally). A bio-equivalent dose (20 mg/kg per day orally) was administered to age-matched WKY rats. Systolic blood pressure (SBP) was measured in conscious rats by tail-cuff plethysmography. Morphological changes were assessed both in the heart, from the ratio of the weight of the left ventricular wall plus septum to body weight, and in blood vessels from the medial cross-sectional areas of the abdominal aorta and mesenteric arteries. Vascular amplifier properties were measured by perfusion of the rat hindquarters under conditions of full dilation (papaverine hydrochloride) and incremental constriction with methoxamine hydrochloride.Results:Losartan lowered SBP in SHR to normotensive WKY rat levels during treatment. Left ventricular hypertrophy and aortic cross-sectional area were reduced at the end of treatment to WKY rat levels; mesenteric artery cross-sectional area was reduced to a lesser extent. The abnormal hindquarter vascular amplifier properties of the SHR were normalized by losartan. Three months after treatment ended, SBP had returned to untreated SHR levels. Left ventricular hypertrophy and the abnormal hindquarter vascular amplifier properties had also partially redeveloped.Conclusions:Our findings support the hypothesis that Ang II contributes to the maintenance of cardiovascular hypertrophy and the abnormal vascular amplifier properties in SHR with established hypertension. However, its role appears to be variable and to depend on the type of vascular bed. Other, pressure-independent, factors may also contribute to vascular hypertrophy.

ISSN:0263-6352    

出版商:OVID    

年代:1993

数据来源: OVID