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Identification of genes encoding zinc finger motifs in the cardiovascular system.

The Zn2+-finger DNA-binding domain has been identified in several developmental control proteins, transcription factors and gene products associated with diseases, as well as in several RNA-binding proteins. We applied library screening, expressed sequence tagging (EST sequencing), Zn2+-binding assays and Northern blot hybridization, in order to characterize novel cDNA clones of the human cardiovascular system which contain Zn2+-finger motifs. An embryonic (8-10 weeks gestation) heart lambda ZAP Express cDNA library was screened with an oligonucleotide probe deduced from a consensus amino acid sequence which is highly conserved for Zn2+-finger proteins, and approximately 350 positive clones were isolated from 1 x 10(4) plaque-forming units (pfu) initially plated. The isolated clones were classified as known and novel following single pass automated DNA sequencing. Analysis of Northern blot hybridization delineated the tissue specificity of these clones, as well as their association with cardiac growth and development. Existence of Zn2+-finger motifs in the novel clones was confirmed by Zn2+-binding assay. In this report, we present the characterization of eight novel clones, including the complete cDNA sequences of one of these clones (HHZ-123).

Amino Acid Sequence↗

[Protective effect of dietary monounsaturated fatty acid on cardiovascular system].

Monounsaturated fatty acid(MUFA) is a sort of fatty acids, including a double bond in its carbon chain. Substantial evidence exists to suggest that MUFA can positively regulate the metabolism of serum lipids, decrease the susceptibility of LDL to oxidative modification, protect the artery endothelium, and decrease prothrombotic environment. The protective effect of MUFA to the cardiovascular system was introduced in the paper.

Blood Coagulation↗

[Functional disorders of the cardiovascular system and their correction in patients after gastric resection in stomach ulcer].

The examination of 88 patients with chronic gastric ulcers in the early postoperative period has revealed different changes of central hemodynamics, functional capacity of the myocardium and microcirculation in cases with bleeding gastric ulcer and associated ischemic heart disease. When correcting the disturbances of the cardiovascular system the main mechanism of functional disturbances of the circulation system should be taken into consideration (hypovolemia, hyperdynamics or hypodynamics of the myocardium, disturbance of microcirculation).

Adult↗

[Use of indicators of anaerobic metabolism in the evaluation of the functional reserve of the cardiovascular system in patients operated on in the past for congenital heart defects].

The correlation of most important parameters of the central hemodynamics with the intensity of anaerobic metabolism was studied in 65 patients operated on having congenital heart diseases and in 37 healthy patients under increased physical exercise. A mild decrease of the functional reserve of the cardiovascular system (by 7-15%) was revealed in the patients as compared with the control group.

Ductus Arteriosus, Patent↗

[Comparative study of the vegetative reactivity of the cardiovascular system in carotid-sinus and exercise tests].

The sinocarotid test test was used to study the vegetative supply and reactivity in 111 practically normal subjects aged 20 to 29 years. The vegetative supply was also examined with the aid of the standard equally graded submaximal exercise test. As regards the evaluation of the vegetative equilibrium in the cardiovascular system, the most informative was the time-course of Kerdo's index as compared with the time-course of the increments of the blood minute volume (BMV) under exercise. Dissociation of the time-course of the vegetative index exercise. Dissociation of the time-course of the vegetative index and BMV suggests the presence of disorders in the vegetative nervous system. Inadequate reaction to the standard exercise is observed in subjects with excess parasympathetic or sympathetic effects before exercise.

Adult↗

[Characteristics of the human cardiovascular system in the human diving response].

Comparative-evolutional research of diving response showed that mechanisms of its expression had much in common in humans and in animals. Firstly, it involves a reflex bradycardia, vasoconstriction of peripheral vessels, and blood flow centralization. But, unlike animals whose diving response has some typical species peculiarities, human diving response is rather diverse. Four types of cardiovascular system response to face submersion were revealed: over-reactive, reactive, paradoxical, and nonreactive. These types were chosen according to the bradycardia character. It is also supposed that the occurrence of individual maximal R--R-interval, while serving as a signal to apnea stopping, is among the reasons of apnea activity limitation.

Adolescent↗

Parathyroid hormone-related peptide and cardiovascular system.

The parathyroid hormone-related peptide (PTHrP) was initially identified in the early eighties, as the humoral mediator causing hypercalcaemia associated with malignancy. However, recently PTHrP was also shown to mediate a wide range of local paracrine/autocrine and intracrine functions in various tissues under physiological and pathological conditions. Indeed, PTHrP is a polyhormone, which can act through different receptors, including the type 1 parathyroid hormone (PTH) receptor 1 (PTH-1R). In the cardiovascular system, PTHrP appears to have potent effects on vascular smooth muscle cells and cardiomyocytes, where it participates in different pathological conditions, such as ischemia and heart failure. Therefore, it is conceivable that further studies on the regulation of PTHrP expression, characterization of its autocrine/paracrine/intracrine functions and definition of its intracellular signal transduction pathways in cardiomyocytes and cardiac vascular smooth muscle cells can elucidate the potential role of PTHrP in cardiovascular pathophysiology.

Cardiovascular Diseases↗

[Adaptation of the cardiovascular system to negative gravitation stresses during repeated antiorthostatic measures].

The cerebral, pulmonary, liver and peripheral circulation was studied simultaneously in 12 test subjects (aged 24--30) rheographically, photoplethysmographically and rheoplethysmographically; arterial pressure was measured by the Korotkoff method. The measurements were carried out during three antiorthostatic tests at --15degrees for 20 min or --30degrees for 20 min. It was shown that the cardiovascular system can adapt to repeated antiorthostatic exposures. The adaptation includes more significant decrease of the heart rate, increase in the systolic and pulse arterial pressure, fall of the diastolic arterial pressure, more marked reduction of antiorthostatically induced increase of blood filling and congestion of cerebral and pulmonary vessels, lesser decrease of their tone and blood redistribution into the vessels of the liver, upper and lower limbs. From the point of view of the adaptive effect repeated exposures to --15degrees are more effective.

Adaptation, Physiological↗

Effects of losartan on the cardiovascular system, renal haemodynamics and function and lung liquid flow in fetal sheep.

1. The angiotensin type 1 (AT1) receptor antagonist, losartan (10 mg/kg) was infused intravenously into nine chronically catheterized fetal sheep (125-132 days gestation). Losartan reduced the fetal systolic (P <0.01) and diastolic (P <0.01) pressor response to 5 microg angiotensin II (AngII) i.v. from 27.4 +/- 1.5 to 7.4+/-0.9 and from 17.5 +/- 1.3 to 5.4 +/- 0.6 mmHg, respectively, after 1 h and to 6.1 +/- 0.5 and 4.4 +/- 0.5 mmHg, respectively, after 2 h. Maternal pressor responses to 5 microg AngII i.v. were unchanged. Fetal mean arterial pressure decreased (P <0.05) after losartan administration, but fetal heart rate did not change. 2. Fetal haematocrit increased (P <0.05), fetal PO2 decreased (P <0.01), PCO2 did not change and pH decreased (P <0.01), as did plasma bicarbonate levels (P <0.01) following administration of losartan. Thus, losartan induced a fetal metabolic acidosis. 3. Fetal placental blood flow did not change following administration of losartan. In the fetal kidney, losartan caused a decrease in vascular resistance (P <0.01) and an increase in blood flow (P <0.05). Glomerular filtration rate decreased (P <0.05); thus, filtration fraction decreased (P <0.01). There was no change in the fractional reabsorption of sodium and glomerulotubular balance was maintained. Free water clearance decreased (P <0.01) and became negative. Urine flow decreased (P <0.01), the excretion rates of sodium, potassium and chloride did not change, but the urinary sodium: potassium ratio decreased (P <0.05). There was a decrease in lung liquid flow (P <0.05) following losartan. 4. It is concluded that the fetal renin-angiotensin system (RAS) is important in the maintenance of fetal arterial pressure, the regulation of fetal renal blood flow and is essential in the maintenance of fetal glomerular function. Further, these actions of AngII are mediated via functional AT1 receptors. These effects of losartan on the fetal cardiovascular system, renal blood flow and function are similar to those observed following captopril administration. Thus, the effects of angiotensin converting enzyme (ACE) inhibition in the foetus are due to the blockade of the fetal RAS and are independent of any direct effects on bradykinin or prostaglandin levels.

Animals↗

Hormone replacement therapy and the cardiovascular system. Nonlipid effects.

Coronary heart disease (CHD) is the leading cause of death in women, and the risk of this disease rises markedly after loss of ovarian function. Hormone replacement therapy (HRT) can reduce the incidence of CHD in postmenopausal women by 50%. HRT causes changes in lipids and lipoproteins, but it is now clear that many other effects of gonadal steroid hormones have important influences on the cardiovascular system. These nonlipid effects include a variety of changes in other metabolic risk factors for CHD, as well as direct arterial effects. Insulin resistance and hyperinsulinaemia may be pivotal disturbances in the pathogenesis of CHD. Estradiol reverses the effects of menopause on glucose and insulin metabolism, resulting in an increase in pancreatic insulin secretion and a decrease in insulin resistance, although other types of estrogen may not do this. Androgenic progestogens may oppose this potentially beneficial effect on insulin resistance. Central obesity is linked with many CHD risk factors, and HRT reverses the increased fat distribution that results from loss of ovarian function at the menopause. HRT may also improve the balance between coagulation and fibrinolysis, resulting in a reduction in arterial thrombosis. Finally, estradiol acts directly on the arterial wall, modifying both endothelium-dependent and calcium-dependent processes. These actions result in improved blood flow and reduced blood pressure and, importantly, have the potential to reduce myocardial ischaemia.

Adipose Tissue↗

Biosynthesis of catecholamines, uptake of 3H-noradrenaline, and reactivity of cardiovascular system of the rat after chronic and acute treatment with a new antidepressant agent, IPF C-45.

The effect of acute and chronic treatment of rats with IPF C-45 on the following biochemical and pharmacological parameters was tested: catecholamine concentration in brain, heart and adrenals, 3H-noradrenaline uptake by cardiac muscle, the action on catecholamine synthesis following treatment with alpha-methyl-p-tyrosine, reactivity of cardiovascular system to catecholamines and isoproterenol-induced tachycardia. Given chronically, IPF C-45 does not affect noradrenaline uptake by the cardiac muscle. Both chronic and acute administration of the drug decelerates catecholamine biosynthesis by inhibition of tyrosine hydroxylase activity. It seems that the action of IPF C-45, a benzonaphthyridone derivative, affects catecholamine metabolism in a manner distinctly different from that of tricyclic antidepressant drugs.

Adrenal Glands↗