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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensinogen is the most important component of the renin-angiotensin system present in the cerebrospinal fluid (CSF) of the rat. Its physiological significance as well as its origin have not been clearly elucidated. In this experiment we have examined plasma renin activity (PRA) and plasma and CSF angiotensinogen concentration under the following experimental conditions in male rats of the Wistar strain: 1) adrenalectomy (Adx) 4 days prior to sample collection; controls were sham Adx animals; 2) nephrectomy (Nx) 48 hours before blood and CSF collection; controls were sham Nx rats; 3) DOC-salt treatment (Cortexon depot, 50 mg/kg.s.c. twice a week) plus saline to drink was given during 4 weeks; controls were intact rats; 4) DOC-salt plus captopril: captopril (100 mg/kg/day) in the drinking fluid was added to the treatment of experimental and control animals of Group 3; 5) two-kidney, two clip hypertension: silver clips placed in both renal arteries 8 weeks before samples collection; control: sham-operated rats; 6) water deprivation: rats deprived of water for 5 days; controls: intact rats; 7) peripheral sympathectomy: 6-hydroxydopamine (6-HODA) injected s.c. from birth until 16 weeks of age, adrenodemedullectomy and adrenal denervation performed at 8 weeks; controls were vehicle-injected animals. Determination of angiotensinogen concentration in plasma and CSF was accomplished by incubation of the samples with excess hog renin. The angiotensin I released as well as PRA were evaluated using an specific radioimmunoassay technique. PRA was significantly increased by Adx, captopril treatment, and water deprivation, and was almost suppressed by Nx, DOC-salt, and DOC-salt plus captopril treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Angiotensinogen concentration in the cerebrospinal fluid in different experimental conditions in the rat. 636 Aug 80

One-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) Goldblatt hypertension was produced in rats by placing 0.30, 0.25, or 0.20 mm silver clips on the left renal artery. Mean arterial pressure (MAP) and plasma renin activity (PRA) were measured in conscious rats 24 to 28 days after clipping. The MAP in control rats (n = 38) was 116 +/- 1 mm Hg (mean +/- SEM). The 0.30, 0.25, and 0.20 mm clips produced MAPs of 133 +/- 2, 161 +/- 5, and 189 +/- 5 mm Hg, respectively, in 1K1C rats, and 123 +/- 2, 129 +/- 3, and 172 +/- 5 mm Hg in 2K1C rats (n = 17-20). When 1K1C and 2K1C groups were compared, MAP was significantly greater in 1K1C rats at all clip sizes. No treatment group's PRA was different than control (4.8 +/- 0.4 ng AI/ml/hr), except for the 0.20 mm 2K1C rats (16.2 +/- 3.1 ng AI/ml/hr). Renal artery pressure (RAP) was measured in another series of experiments and was not different from control in all but the 0.20 mm 1K1C rats. With identical clip sizes, 2K1C rats showed smaller pressure gradients than 1K1C across the clips: 0.30 mm, 8.5 +/- 1.7 vs 10.7 +/- 1.9 mm Hg; 0.25 mm, 16.5 +/- 1.2 vs 42.1 +/- 7.5 mm Hg; 0.20 mm, 51 +/- 5.3 vs 79.1 +/- 5.7 mm Hg (n = 8-12). Therefore, both the increase in MAP and the pressure gradient across the clip were greater in the 1K1C rats at every clip size.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Effects of graded renal artery constriction on blood pressure, renal artery pressure, and plasma renin activity in Goldblatt hypertension. 636 82

Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6-9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia. Principal responses were as follows: mean arterial pressure (MAP) was 193 +/- 4 mmHg awake and decreased to 114 +/- 3 mmHg and 135 +/- 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 +/- 3 mmHg and to 69 +/- 3 mmHg and 96 +/- 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 +/- 1.3 ng X ml-1 X h-1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renovascular hypertension: effect of halothane and enflurane. 642 15

Wistar female rats were made hypertensive by applying a silver clip to the left renal artery and removing the right kidney. In aortas, the proliferation fraction of smooth muscle cells, DNA synthesis and wet weight have been correlated with the blood pressure increase subsequent to the operation. A wave of proliferation of smooth muscle cells in the aortic media is triggered immediately after the highest increased rate of blood pressure. When blood pressure stabilizes at high values, the metabolism of nucleic acid within the aortic media resumes its normal level but the arterial changes previously established persist. The sequence of pathological events responsible for these changes could be: increment of blood pressure; increase in wall stress; proliferation of smooth muscle cells; thickening of arterial wall; correction of the wall stress; end of proliferation. The consequence of this early proliferation of aortic smooth muscle cells is not clear but it is probably one of the mechanisms through which high blood pressure is sustained. It can also participate in atherogenesis, being in this way one of the bases of the well-known relationship between hypertension and atherosclerosis.
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PMID:Kinetics of proliferation of rat aortic smooth muscle cells in Goldblatt one-kidney, one-clip hypertension. 688 19

1. In two experiments severe hypertension (systolic blood pressure 180 mmHg) was induced in rats by constricting one renal artery with a silver clip (two-kidney, one clip hypertension; 2KIC). Blood pressure, plasma renin activity (PRA) and body weight were measured for 35 days after clipping. Plasma sodium concentration and carcass sodium content were measured at the conclusion of the experiment. To determine the relationship between sodium intake, PRA and the development of severe hypertension, half of the rats were given a normal diet and water to drink; the other half were given a low sodium diet and 0.9% saline to drink. 2. In both experiments, two patterns of responses were observed. Group (1) had reduced growth rate, and marked elevation of PRA. Some, but not all of these animals had histological evidence of malignant nephrosclerosis in the untouched kidney. In the other group (11), weight gain was normal and PRA was normal or only slightly elevated. 3. Group 1 animals drinking saline, had raised carcass sodium levels, whereas those drinking water had no increase in carcass sodium. 4. The results confirm that hypertension in the 2KIC model is not always associated with a raised PRA. 5. The coexistence of a raised PRA and increased total body sodium suggests that the PRA does not rise as a result of sodium depletion in this model.
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PMID:Sodium balance and plasma renin activity during the development of two-kidney Goldblatt hypertension in rats. 699 58

Cumulative water- and electrolyte balance, plasma creatinine (PC), plasma renin activity (PRA), urinary prostaglandins (PGs) E2, and F2alpha and kallikrein (K) were studied in 40 male Wistar CHbb THOM rats (250 +/- 4 g SE). A solid silver clip (0.25 mm lumen) was applied to both renal arteries in 18 animals; 13 rats were sham-operated and nine remained intact. The analyses were performed during a control period and up to 10 days after surgery. Blood pressure (BP) recorded on the 10th and 12th day of the study increased significantly in clipped rats with respect to sham rats (p less than 0.001);PC and PRA measured on the 11th day were not significantly different. A positive cumulative water "balance" )p less than 0.01) and sodium balance (p less than 0.02) was found in clipped rats when compared with sham rats in the first 5 days of the experimental period. Significantly higher values of PGE2 urinary excretion were observed in sham rats vs clipped rats on the 2nd and 5th day after surgery (p less than 0.02). On the 2nd day after surgery, K urinary excretion was significantly lower in clipped rats than in sham rats (p less than 0.02). No significant changes were observed in PGF2alpha excretion. The absence of significant difference in PRA 10 days after bilateral renal artery stenosis points to a lack of any fundamental role of circulating angiotensin II at this stage of the development of hypertension. The significant water- and salt retention in the first 5 days after clipping suggests that it might be involved in the pathogenesis of this model. Early changes in PGs E2 and F2alpha and K appear to be related more to intrarenal adjustments soon after surgery than to the increase in BP.
Hypertension
PMID:Initial mechanisms in hypertension after bilateral renal ischemia in the rat. 702 18

Ablation of tissue surrounding the anteroventral third cerebral ventricle (AV3V) has been demonstrated to prevent and reverse renal hypertension in the rat. The contribution of this brain area to the maintenance of hypertension in other species has not been examined. In the present investigation, an attempt was made to produce two-kidney, one clip renal hypertension in rabbits with histologically and functionally defined AV3V destruction. Electrolytic lesion of the AV3V in rabbits produced effects closely resembling those previously seen in rats: increased plasma volume and plasma sodium, temporary adipsia, no change in resting arterial pressure or heart rate, and significant attenuation of pressor responsiveness to angiotensin II (AII) delivered intracranially. However, the increase in arterial pressure observed over a 4-week period following the application of a 0.5 mm silver clip to the left renal artery (opposite kidney intact) was identical in 12 AV3V-lesioned and 12 sham-operated rabbits. Hypertension development was not accompanied by significant sodium retention, water retention, or plasma/extracellular fluid volume expansion in either group of rabbits. Pressor responses to intravenous infusions of AII and norepinephrine were identical in sham and AV3V-X rabbits. Thus, destruction of the AV3V, and the attendant reduction in the central pressor action of AII, does not alter the pattern of development of two-kidney, one clip renal hypertension in the rabbit. The contrasting results in rats and rabbits could be explained by the differing contribution of the area postrema to the pressor action of AII in the two species.
Hypertension
PMID:Influence of forebrain periventricular lesions on the development of renal hypertension in rabbits. 706 Nov 22

Genetically hypertensive rats have been found in previous studies to be more susceptible than normotensive rats to the formation of lesions of the inner ear as a result of excess noise. The present study was designed to investigate whether or not that susceptibility is a direct result of the high blood pressure. Hypertension was induced in 28 Sprague-Dawley rats by placing a 0.25 mm wide silver clip on one renal artery. Systolic blood pressure was measured indirectly by a tail-cuff technique 3 weeks after the operation and again after noise exposure. The animals were kept for one month in noise conditions (100 dB Leq (lin)) simulating those in an industrial milieu. The frequency range was adjusted to correlate to the hearing range of the rat. Auditory sensitivity was assessed electrophysiologically by recording auditory brain stem response to pulses of 1/3-octave filtered full-cycle sine waves. The results showed no correlation between hearing loss and systolic blood pressure. There was no difference between the audiograms obtained from rats with a systolic pressure below 160 mmHg and those obtained from rats with systolic pressures of between 170 and 255 mmHg. These results do not support the hypothesis that high blood pressure is a mechanism underlying noise-induced hearing loss.
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PMID:Noise-induced hearing loss in rats with renal hypertension. 714 37

Right ventricular hypertrophy, and by inference pulmonary arterial hypertension, were induced in female Wistar Albino rats by subjecting them to a barometric pressure of 380 mmHg for four weeks. A control group was kept at normal barometric pressure for a similar period of time. The cell boundaries of the endothelial lining of the aorta, pulmonary trunk and inferior vena cava were stained in situ by a modified silver method of Poole et al. (1958). Photomicrographs of the intimal surfaces of these blood vessels at a standard magnification were used to determine the length, breadth and area of the cells. In the control rats the endothelial cells were found to have a characteristic shape and size in each of the three vessels studied. Those of the aorta were small and elongated in the direction of blood flow with tapering ends. The endothelial cells of the inferior vena cava were rectangular. Those of the pulmonary trunk were polygonal and had tessellated borders. In the test rats with right ventricular hypertrophy induced by chronic hypoxia the endothelial cell pavement pattern of the pulmonary trunk changed to resemble that of the aorta. It is considered that this was an expression of the acquired pulmonary hypertension, the fusiform shape appearing appropriate for an elevated pressure.
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PMID:Endothelial cell pavement pattern in the pulmonary trunk in rats in chronic hypoxia. 721 38

Arterial dilatation distal to a stenosis has been known as poststenotic dilatation (PSD). This paper describes arterial constriction enough to produce PSD, time course of PSD, structural changes of the dilated segments and influence of hypertension on the development of PSD. These problems were studied in 2 experimental protocols. In protocol I, 87 carotid arteries of 45 rabbits were constricted by silver clip of 0.65 to 2.0 mm in diameter. The arterial diameter was measured at the sites both proximal and distal to the constriction after 3 days to 8 weeks. In protocol II, 22 carotid arteries of 12 rabbits with experimental one-or two-kidney Goldblatt hypertension were constricted and the development of PSD was compared with age matched controls. Remarkable PSD developed in arteries with moderate stenosis of 45 to 60% constriction. The degree of dilatation expressed as ratio of distal to proximal diameter reached about 1.5 at the end of the second week and remained unchanged thereafter. Destruction of the elastic fibers with intimal hyperplasia was observed in the dilated segments even at the early stages of the PSD. Both mild and severe stenosis failed to produce prominent PSD. In protocol II, the PSD averaged 1.18 +/- 0.05 (mean +/- SE) in hypertensive, and 1.32 +/- 0.03 in normotensive animals (p less than 0.05). The result suggests that chronic hypertension decreases the distensibility of the arteries.
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PMID:Experimental production of poststenotic dilatation in the carotid arteries of rabbits. 721 22


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