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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In chloralose-anaesthetized dogs, central venous and arterial angiotensin (AII) levels were monitored by blood-bathed bioassay during venous haemorrhage of 20 ml/kg, acute renal ischaemia induced by suprarenal aortic stenosis and frusemide-induced diuresis. 2. Blockade of intrarenal dopamine receptors with ergometrine reduced markedly the increments in arterial AII associated with haemorrhage or suprarenal aortic stenosis, but did not consistently affect the corresponding increments in venous AII. 3. Ergometrine or renal denervation did not affect the increases of blood AII associated with frusemide diuresis. 4. Blockade of beta-adrenoreceptors with propranolol, by contrast, reduced blood AII increments associated with all three procedures. 5. It is suggested that renin release during moderate haemorrhage and acute suprarenal aortic stenosis is, in the dog, partly due to activation of intrarenal dopaminergic nerves. 6. The possibility is discussed that propranolol may depress renin release in the dog by an action other than that of blocking beta-adrenoreceptors.
Clin Sci Mol Med 1978 Jan
PMID:Effects of renal dopamine receptor and beta-adrenoreceptor blockade on rises in blood angiotensin after haemorrhage, renal ischaemia and frusemide diuresis in the dog. 20 30

1. Factors involved in the neural control of renin release have been reviewed. 2. Experimental evidence has been obtained that sympathetic stimulation releases renin from the kidney independently of local vasomotor changes. 3. The reflex control of renin release on postural change has been established. 4. The effect of diuretics on renin release has been studied and evidence of neural and non-neural mechanisms obtained. 5. The effect of suprarenal aortic stenosis has been studied; the findings suggest that renin release is in some way dependent on neural mechanisms. 6. The pathological significance of the neural control of renin release has been discussed.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Neural control of renin release. 80 38

1. The participation of neural mechanisms in mediating the renin release induced by reduction of renal perfusion pressure was explored in anaesthetized cats by comparing renin release from the two kidneys, one acutely denervated and the other intact. 2. Suprarenal aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and halved blood flow to both kidneys, but cause a greater release of renin from the innervated kidney than from the contralateral denervated one (increments of 72 +/- 17 and 29 +/-20 pmol/min respectively). 3. A study of the time-course of the response during aortic stenosis of 30 min duration showed early release of renin from the innervated kidney at a time (5 min) when little release occurred from the denervated one. In later samplings (15 and 30 min) the response of the innervated kidney levelled out at somewhat lower values, and that of the denervated organ progressively increased, but remained smaller than on the side with intact nerves. 4. There was no parallelism between renin release and renal vasomotor changes induced by aortic stenosis, as vasomotor changes were equal in the two kidneys and remained constant from beginning to end of stenosis. It is concluded that a significant part of the renin release induced by aortic stenosis is dependent on neural mechanisms: the neural differs from the non-neural component in being of more rapid onset and probably of shorter duration.
Clin Sci Mol Med 1976 Nov
PMID:Neural factors contributing to renin release during reduction in renal perfusion pressure and blood flow in cats. 99 43

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Role of the renal nerves in renin release during suprarenal aortic stenosis in cats. 107 17

Beta-adrenoceptor density and affinity, studied by H3-CGP 12177 binding, and adenylate cyclase activity were measured in 12 left ventricles of rabbits with heart failure and compared to 13 left ventricles of control (C) rabbits. Heart failure (HF) was induced by a double volume (aortic insufficiency) plus pressure (aortic stenosis 14 days later) overload. Left ventricular mass was increased in HF by 67% above C. Saturation curves with CGP 12177 showed a 36% decrease in beta-adrenoceptor density (C = 61.5 +/- 5.4 fmol/mg prot., P less than 0.05) but competition curves with isoproterenol were not different in HF and C. Basal and Gpp(NH)p stimulated adenylate cyclase activity were decreased by 36% and 22% respectively in rabbits with heart failure as compared with control animals and cAMP production was significantly smaller in failing left ventricles than in control left ventricles both after NaF stimulation (C: 161.3 +/- 24.9 pmols/mg/min; HF: 98.8 +/- 7.0 pmols/mg/min; P less than 0.05) and even more after forskolin stimulation (C: 159.1 +/- 23.9 and HF: 60.8 +/- 7.3 pmols/mg/min; P less than 0.01). Although isoproterenol stimulated ACA was smaller in HF than in C, EC50 was similar in both groups (1.6 x 10(-7) M). We conclude that in the early stage of heart failure in the rabbit, although adrenoceptor density is decreased, there are no changes of affinity of beta-adrenoceptors for isoproterenol and the major alteration of cAMP production appears to lie down-stream the receptor level with a markedly impaired stimulation of adenylate cyclase activity by forskolin.
J Mol Cell Cardiol 1991 May
PMID:Beta-adrenoceptors and adenylate cyclase activity in hypertrophied and failing rabbit left ventricle. 167 57

The cardiac changes resulting from mechanical overload of the left ventricle have been well documented and a variety of compensatory mechanisms described. These include a decrease in maximum velocity (V0) of shortening in the absence of reduction in active tension (P0), and a reversible decrease in myofibrillar adenosine triphosphatase activity resulting from isoenzymic shift from, predominantly, a form of myosin with high ATPase activity (V1) to another with low (V3). The thermodynamic advantage of the transition is the hypertrophied muscle possesses a more energy-efficient form of contraction. These reversible transitions resulted from altered gene expression of isoenzymic forms of myosin heavy chain. It must be borne in mind that the adaptational modifications just described appear to occur only in smaller animals such as the rat, that possesses several myosin isozymes. In large mammals it is mainly the V3 form of myosin that is present, which does not change with altered contractile state. Responses of the large arteries to hypertension have been poorly studied. This is surprising when one recalls that degenerative disease of such vessels, that include the aorta, carotids and ileo-femoral arteries is almost an obligatory concomitant of hypertension. Such studies as have been carried out indicate that hyperplasia is specific for abdominal aortic stenosis while hypertrophy is found in aortic smooth muscle in rats with systemic hypertension. Mechanically, an increase in V0 with no change in P0 have been reported; an increase in myofibrillar ATPase activity was also reported. Though two myosin heavy chain isozymes have been found in aortic smooth muscle densitometry did not reveal any difference in distribution between tissues from control and hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem 1990 Mar 05
PMID:Cardiovascular adaptations to mechanical overload. 213 92

Stereological techniques were used to determine quantitatively the changes in subcellular organelles in the hypertrophied swine heart. Hypertrophy was induced by aortic stenosis. In addition, the animals were stressed by exercising twice weekly on the treadmill for 30 days. The controls were normal animals which were neither exercised nor had aortic stenosis. Tissue samples from the left ventricle and interventricular septum were processed for electron microscopy. Relative volumes of myofibrils, mitochondria, transverse tubular system (T-system) sarcoplasmic reticulum (SR), and clear intracellular space (ICS) were measured. Significant differences in the volumes of all the components except the T-system were found between experimental and control animals in the epicardial and endocardial regions of the left ventricle and interventricular septum. Mitochondria and myofibrils were significantly decreased in the exercise stressed hypertrophied hearts as reported in ischemia, while SR and ICS were significantly increased. These findings suggest that ischemic injury occurs in all regions of the hypertrophied heart wall subjected to acute exercise stress, not solely the endocardial region as previous qualitative studies suggested.
Virchows Arch B Cell Pathol Incl Mol Pathol 1982
PMID:Effect of acute exercise stress in cardiac hypertrophy. II. Quantitative ultrastructural changes in the myocardial cell. 612 35

The effects of the thyroid state and of aortic stenosis on muscarinic cholinergic binding sites in heart membranes were compared (with proper controls) by simultaneously determining total and high-affinity binding sites and estimating low-affinity binding sites by difference. Hyper- and hypothyroidism induced decreased and increased concentration of high-affinity agonist binding sites, respectively, supporting the hypothesis that these sites were directly regulated by thyroid hormones. This was not the case for low-affinity binding sites, as they decreased in number in both hyper- and hypothyroidism. In hyperthyroid rats, this decreased number of low-affinity binding sites could be due to the rapidly developing cardiac hypertrophy. Indeed, cardiac hypertrophy provoked by aortic stenosis led also to a decreased concentration of low-affinity binding sites without affecting the concentration of high-affinity binding sites.
Mol Pharmacol 1982 May
PMID:Rat cardiac muscarinic receptors. II. Influence of thyroid status and cardiac hypertrophy. 621 44

The rates of synthesis (in per cent per day) of the total protein (ks) and myosin heavy chains (ke HC) and actin (ke A), isolated by preparative electrophoresis from myofibrils prepared in a relaxing medium, have been measured in rat heart ventricles after a continuous infusion of 50 microCi of (14C) Tyrosine (0.5 ml/h during 6 h). Normal values, in the sham-operated group, were for ks 19%, ke HC 23% and ke A 11%. Two to 4 days after an abdominal aortic stenosis there was an increase in the specific radioactivity of free plasma and intra-cellular tyrosine and of protein-bound tyrosine. The rate of synthesis also increased up to 37% for ks, 41% for ke HC and 21% for ke A but the ratio ke HC/ke A remained unchanged. We conclude that the normal heterogeneity of the rate of synthesis of the two main contractile proteins, at least when measured on myofibrils free from easily releasable myofilaments, was unmodified by cardiac overload, although both of these rates of synthesis were stimulated.
J Mol Cell Cardiol 1984 Oct
PMID:Myosin heavy chain and actin fractional rates of synthesis in normal and overload rat heart ventricles. 654 95

Myocardial Na+,K(+)-ATPase was studied in patients with aortic valve disease, and myocardial Na+,K(+)- and Ca(2+)-ATPase were assessed in spontaneously hypertensive rats (SHR) and hereditary cardiomyopathic hamsters using methods ensuring high enzyme recovery. Na+,K(+)-ATPase was quantified by [3H]ouabain binding to intact myocardial biopsies from patients with aortic valve disease. Aortic stenosis, regurgitation and a combination hereof were compared with normal human heart and were associated with reductions of left ventricular [3H]ouabain binding site concentration (pmol/g wet weight) of 56, 46 and 60%, respectively (p < 0.01). Na+,K(+)- and Ca(2+)-ATPases were quantified by K(+)- and Ca(2+)-dependent p-nitrophenyl phosphatase (pNPPase) activity determinations in crude myocardial homogenates from SHR and hereditary cardiomyopathic hamsters. When SHR were compared to age-matched Wistar Kyoto (WKY) rats an increase in heart-body weight ratio of 75% (p < 0.001) was associated with reductions of K(+)- and Ca(2+)-dependent pNPPase activities (mumol/min/g wet weight) of 42 (p < 0.01) and 27% (p < 0.05), respectively. When hereditary cardiomyopathic hamsters were compared to age-matched Syrian hamsters an increase in heart-body weight ratio of 69% (p < 0.001) was found to be associated with reductions in K(+)- and Ca(2+)-dependent pNPPase activities of 50 (p < 0.001) and 26% (p = 0.05), respectively. The reductions in Na+,K(+)- and Ca(2+)-ATPases were selective in relation to overall protein content and were not merely the outcome of increased myocardial mass relative to Na+,K(+)- and Ca(2+)-pumps. In conclusion, myocardial hypertrophy is in patients associated with reduced Na+,K(+)-ATPase concentration and in rodents with reduced Na+,K(+)- and Ca(2+)-ATPase concentrations. This may be of importance for development of heart failure and arrhythmia in hypertrophic heart disease.
Mol Cell Biochem 1997 Apr
PMID:Reduced concentration of myocardial Na+,K(+)-ATPase in human aortic valve disease as well as of Na+,K(+)- and Ca(2+)-ATPase in rodents with hypertrophy. 908 35


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