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To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.
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PMID:Cardiac performance in rats with renal hypertension. 13 Oct 7

1. Mean arterial pressure, heart rate, cardiac output (dye-dilution technique), stroke volume, total peripheral resistance (TPR), utero-placental blood supply (microsphere technique) and foetal weights were determined 2 days before expected birth in normotensive control (NC) rats, spontaneously hypertensive (SH) rats, rats with short-standing renal hypertension induced early in pregnancy and rats with established renal hypertension induced 4 weeks before pregnancy. Non-pregnant rats in comparable states served as controls. 2. In normal pregnancy cardiac output increased by 33% and blood pressure and TPR decreased by 17 and 38% respectively. The same principal changes were noted in SH rats and those with short-standing renal hypertension, but no changes were found in rats with established renal hypertension during pregnancy. 3. Myometrial and placental blood supply was lower in all hypertensive groups compared with NC rats, the reduction being 46 and 36% in SH rats and in rats with established renal hypertension as much as 74 and 68% respectively. 4. In SH rats foetal weights were reduced compared with NC rats, but despite the 68% reduction of placental blood flow in rats with established renal hypertension foetal weights were here unchanged.
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PMID:Circulatory changes during pregnancy in spontaneously and renal hypertensive rats. 54 Apr 52

On account of the complex effective mechanism the control of dihydralazin is performed particularly with regard to the changes of the plasma-renin-activity. The examinations were carried out in 7 patients each with renal and essential hypertension. The plasma-renin-activity, the behaviour of blood pressure, the stroke volume and the minute volume as well as the peripheral arterial resistance should be examined concerning the influence of two doses of dihydralazin and with regard to the influence of the basic disease to the above mentioned parameters. The plasma-renin-activity is decreased as well as increased by dihydralazin. Baroreceptors are made responsible for the renin regulation. Already with 4.125 mg dihydralazin (1/8 ampoule Depressan) nearly the same permanent effect reducing the blood pressure is to be achieved as with a double dosage. Stroke volume and minute volume are reduced by dihydralazin. The peripheral arterial resistance decreases in no case, but in the renal hypertension it shows a rising tendency. With the help of these examinations it shall particularly referred to the fact that the therapeutic mechanism of the slowly beginning and long lasting decrease of blood pressure is not yet be fully clarified.
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PMID:[Hemodynamic parameters and plasma-renin activity following intravenous dihydralazine administration--a contribution to the regulation of renin]. 63 99

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.
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PMID:What makes the renin-angiotensin system a pathogenic factor? 69 4

Cardiac output, total peripheral vascular resistance, renal, extrarenal, forearm muscle and skin hemodynamics and an indicator of the splanchic vascular resistance were estimated in 20 subjects with chronic renal disease without signs of chronic renal failure and without anemia. The data were compared with a group of subjects with essential hypertension. The high blood pressure of chronic renal disease of mild or moderate severity was maintained in the first place by a high cardiac output, this being due to a rise of the stroke volume, while the heart rate was only slightly increased. The total peripheral vascular resistance was within the normal range in most of the subjects. The vascular resistance in the skin was slightly raised, that in the splanchnic area and muscle unchanged in renal hypertension. The possible pathogenic mechanisms are considered.
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PMID:General and regional hemodynamics in hypertension in chronic renal disease. 119 19

Results are presented on the treatment with Inderal of 57 patients with essential hypertension and symptomatic renal hypertension in whom the changes in central and renal haemodynamics were carefully traced. In all the patients with renal hypertension (chronic pyelonephritis, chronic glomerulonephritis) the function of the kidneys was adequate. Inderal when used in a daily dose of 120--160 mg produces a hypotensive effect in patients with stage IB and IIA essential hypertension with unstable symptomatic renal hypertension who have a predominantly hyperkinetic type of the circulation. In such cases the haemodynamic changes manifest themselves in a considerable reduction of the cardiac output at the expense of a slower pulse rate and decreased stroke volume; the total peripheral resistance was moderately elevated. In patients with stage IIB of essential hypertension and in those with persistent and severe symptomatic renal hypertension the hypotensive effect of Inderal given in a daily dose of 480 mg and sometimes even higher was accompanied by a statistically significant decrease in the total peripheral resistance and a moderate reduction of the cardiac output and cardiac index at the expense of a slower pulse rate.
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PMID:[Use of inderal for the treatment of different forms of arterial hypertension]. 119 58

Based on animal experiments in rats (spontaneous and renal hypertension, experimental aortic stenosis, thyroxine and training-induced hypertrophy, and aorto-caval fistula with and without additional unilateral renal artery coarctation) as well as clinical data and literature, the functional consequences of cardiac hypertrophy and structural ventricular dilatation are analyzed and discussed. A methodological approach, developed on the basis of Frank's diagram and model calculations, permits quantitatively estimating the significance of ventricular geometry (wall thickness and inner dimensions) compared to myocardial alterations (decrease in contractility and distensibility) and hemodynamic load (preload and systolic pressure). As a rule, hypertrophy causes an increase in ventricular working capacity, which allows the heart to cope with an increased hemodynamic load without a decrease in stroke volume and without enhanced systolic stress requirement. Adverse consequences mainly concern ventricular compliance, cardiac energetics, and electrophysiological parameters. Particularly from the example of the aorto-caval fistula, it can be seen that enhanced systolic wall stress does not necessarily lead to heart failure within a few months. However, the length of time for which the additional wall stress, with correspondingly increased energy demand, can be tolerated remains to be determined. In later stages, a multitude of alterations on the cellular, tissue, and organ level occurs, affecting myocardial and ventricular mechanics and energetics, depending on the type, velocity of development, and duration of overload. A distinction should be made between the adverse alterations, which can be related to myocardial growth, and those that are not necessarily related to a certain cell size (receptors, transformation of the contractile proteins) as well as those changes that do not primarily influence the myocardial cell (arteriosclerosis, microangiopathy). Structural dilatation alone could lead to insufficiency only in the case of substantial increase in inner ventricular radius. Reduced contractility, myocardial distensibility, and increased pressure load aggravate the negative effects of dilatation in a predictable manner, as demonstrated on the basis of a representative case of dilative cardiomyopathy. Using the example of spontaneously hypertensive rats, it is shown that ventricular mass and shape are differently influenced by various blood-pressure lowering agents, e.g., atenolol, nifedipine, and dietary interventions. It is concluded from the analysis of chronic cardiac reactions that adaptive processes are, in principle, ambiguous in character, revealing negative components even in the case of regular adaptation. However, it seems unjustified to aim at a regression of hypertrophy without reducing the underlying hemodynamic overload.
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PMID:Functional consequences of cardiac hypertrophy and dilatation. 182 78

Vascular complications are rarely found in neurofibromatosis. The case of a female patient with this condition is reported, who showed systemic vascular involvement, with juvenile stroke, mesenteric infarction, and stenosis of the renal artery with consequent renal hypertension. The typical clinical and morphological features of vascular complications in neurofibromatosis are discussed.
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PMID:[Vascular involvement in neurofibromatosis 1]. 194 12

Various colonies of the spontaneously hypertensive rat (SHR) of the same age demonstrate different forms of the left ventricle (LV) in end-diastole. SHR from breeders in Australia and Switzerland exhibit concentrically hypertrophied LV, evident from an increased wall thickness to internal radius ratio (w/ri), while SHR from a Danish colony show an unchanged w/ri ratio, indicating eccentrically hypertrophied LV. These differences may be related to changes in arterial blood pressure and/or altered cardiac filling patterns. A more favourable situation seems to prevail for the eccentrically hypertrophied SHR heart compared with the concentrically hypertrophied heart, the former demonstrating enhanced cardiac function. Thus, an LV with increased diastolic diameter, as in the eccentrically hypertrophied SHR heart, can produce an elevated stroke volume for a given degree of myocardial shortening. In renal hypertension, however, LV function was depressed, probably due to a factor, possibly released upon clipping of the renal artery, that has inherent negative inotropic properties. Here, the reduction of LV performance could be explained neither by the changed LV geometrical design nor by the altered myocardial myosin isoenzyme pattern. At low aortic pressures and hence limited coronary perfusion, LV performance is attenuated in SHR and renal hypertensive rats, most likely due to the vascular structural changes within the coronary vascular bed.
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PMID:Cardiac and vascular structural adaptation in experimental hypertension. 215 38

In an attempt to clarify the developmental mechanism of cerebral aneurysms, we studied the elastic skeleton of experimentally induced cerebral aneurysms in rats under scanning electron microscopy after hot formic acid extraction followed by freeze-drying. We produced cerebral aneurysms in 19 rats by unilaterally ligating the common carotid artery, inducing renal hypertension, and feeding beta-aminopropionitrile fumarate. The first noted change was the loss of folds protruding from the internal elastic lamina. Morphologic changes of the internal elastic lamina, considered to be primarily responsible for aneurysmal formation, occurred after the loss or disintegration of the elastic skeleton of first the intima, then the media. In large aneurysms with thick domes, we found proliferation of elastic lamellae that may reduce the risk of rupture. It seems probable that the complex elastic skeleton of the arterial wall may account for the mechanical properties of the artery and that growth of an aneurysm occurs due to disintegration of the elastic skeleton and not simply to rupture of the internal elastic lamina. We believe that such changes in the elastic skeleton are a property of the functional state of the cells that produce elastin.
Stroke 1990 Dec
PMID:Elastic skeleton of intracranial cerebral aneurysms in rats. 226 79


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