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

Elastic tissue content and distribution were studied by electron microscopy of small arteries and arterioles of kidneys obtained from normotensive Wistar and spontaneously hypertensive rats, normal dogs and patients with hypertension and glomerular diseases. Specificity and sensitivity of silver tetraphenyl porphyrin sulfonate stain are discussed. This specific electron microscopy technique should prove useful in analysis of elastic tissue in pathologic states of other organs, especially where elastic tissue normally appears to be sparse or absent.
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PMID:An electron microscopic technique for the study of elastic tissue in small arteries and arterioles of the kidney. 6 48

15-hydroxy-prostaglandin-dehydrogenase (PGDH) activity was studied in rat kidney homogenates during the development of hypertension, within 20 days after left renal artery constriction by a solid silver clip. In the ischemic kidney PGDH activity increased at day 6, reached maximum at day 10, then progressively at day 15 and returned to normal levels at day 20. No difference was found between contralateral kidneys and kidneys of normotensive control rats. Variations of PGDH activity did not seem to be related to either renal perfusion pressure or renin production. Increased PGDH activity may be a consequence of an enzyme induction following increased PG-synthetase activity, or it could be viewed as a defence mechanism, according to the hypothesis of a prohypertensive effect of PG in the rat.
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PMID:Kidney 15-hydroxy-prostaglandin-dehydrogenase activity during the development of experimental hypertension in the rat. 47 77

1. The protective action of the renal medulla was studied in one-kidney renal-clip hypertension in rats with unilateral hereditary hydronephrosis and almost complete atrophy of the medulla of the affected kidney. 2. Rats were unilaterally nephrectomized. The first group had a normal kidney remaining, and the animals from the second and third groups were left with a hydronephrotic kidney and received renomedullary and renocortical autotransplants respectively. Two weeks later all rats were made hypertensive by placing a silver clip (0.2 mm) on the renal artery. 3. From the fourth day after clipping until the end of the experiment blood pressure was found to be significantly (P less than 0.01) lower in rats with medullary transplants than in the other groups. No differences in renal excretory function, plasma volume and plasma renin activity were found between the groups either before or during development of hypertension (5 and 21 days after clipping). Early in the course of hypertension (5 days) cardiac output was significantly (P less than 0.05) lower in the rats with medullary transplants than in the other groups, although an increase in plasma volume was noted in all three groups. At that time no difference in total peripheral resistance was found between the groups. 4. The results are consistent with the hypothesis that the renomedullary antihypertensive substance(s) mitigates hypertension by preventing a hypertensive haemodynamic response to sodium/volume overload.
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PMID:The mechanism of renomedullary antihypertensive action: haemodynamic studies in hydronephrotic rats with one-kidney renal-clip hypertension. 63 67

The development of collaterals to an ischemic kidney was studied in rabbits with two-kidney Goldblatt hypertension. Hypertension was produced by applying a silver clip of 0.9 mm in internal diameter on the left renal artery with the right kidney intact. Peri-ureteric collaterals were found at autopsy in 27 (32.9%) of 82 animals that were killed 7 days (early stage) and in 30 (40.5%) of 74 animals that were killed in more than 70 days (late stage) after clipping. The average blood pressure was 123.8 +/- 2.6 (SE) mmHg in animals with collaterals vs. 125.3 +/- 2.1 mmHg in animals without them in the early stage, and 142.5 +/- 4.4 mm Hg in animals with collaterals vs. 122.6 +/- 3.3 mmHg in animals without them in the late stage. These results indicate that the collaterals to an ischemic kidney develop independently of the rises in blood pressure during the first week and the presence of collaterals is associated with moderate to severe hypertension in the late stage.
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PMID:Peri-ureteric collateral vessels in rabbits with experimental renal hypertension. 92 16

The regional distribution of the peripheral vascular resistance was studied in normotensive and hypertensive Wistar rats. Two models of experimental hypertension were investigated: (I) in 32 animals the right renal artery was constricted by a silver clip (two-kidney Goldblatt hypertension); (II) in 46 animals the left kidney was removed and the right renal artery was clipped as in the first group (one-kidney Goldblatt hypertension). The normotensive control group comprised 61 untreated animals of the same strain and age. The distribution of cardiac output to 14 tissues was determined by means of the particle distribution technique. The resistance was increased in all regions investigated, a decreased or unchanged resistance was not observed. For most of the investigated tissues the regional resistance was increased exactly in proportion to the total peripheral resistance (TPR). Exceptions to this were found in 2 regions where the change of local resistance deviated from that of TPR: the splanchnic area and the skeletal muscle. In both cases the 2 models differed from each other. In the two-kidney model the increase of resistance in the splanchnic circulation was more intense than in other organs. In contrast, in the one-kidney model the local change of resistance was less than that of TPR. The change of skeletal muscle resistance was not significantly different from the change of TPR in the two-kidney model, while in the one-kidney model the increase of local resistance was significantly higher than that of TPR. It is concluded that the etiology of the abnormal resistance is different in the 2 models investigated and that known extrinsinc pressor factors may play a role in the two-kidney, but not in the one-kidney Goldblatt hypertension.
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PMID:Regional distribution of vascular resistance in two models of experimental renovascular hypertension. 94 22

Serial, clinical, clinicopathologic and histologic studies performed simultaneously following onset of PS-AGN in children for a period of up to 144 months revealed no evidence of progression to chronic glomerulonephritis. Although acute morphologic changes were more severe in renal tissue obtained from patients with AGN following streptococcal upper respiratory infection than following pyoderma, the acute manifestations in both groups subsided 6 to 12 weeks after onset. Cumulative morphologic healing occurred in 20% of patients at 24 months, in 43% at 48 months after onset of PS-AGN; 1 patient who was unhealed at 49 months was lost to follow-up. In 2 patients (6%), acute histologic exacerbations without clinical signs occurred within 24 months after onset. Subsequent healing was documented histologically. Addis counts remained abnormal in a high percentage of patients throughout the 12 years of observation and did not correlate with the histologic findings of renal biopsy tissue. The occasional demonstration of renal vascular disease and/or hypertension may merely reflect the early development of spontaneous essential hypertension although the possibility of a relationship to the previous attack of PS-AGN is intriguing. This question cannot be answered at this time. Renal biopsy studies are more dependable than Addis counts in assessing the course of PS-AGN. The significance of persistence of immunofluorescent and/or electron microscopic changes (subepithelial dense deposits) many years after onset in 58% of 12 patients studied, at a time when a majority of patients (84%) revealed healing by light microscopy, remains to be assessed.
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PMID:Prognosis of acute poststreptococcal glomerulonephritis in childhood: prospective study and review of the literature. 100 3

1. The sodium and water excretion rates of rabbit kidneys were studied when isolated and perfused at known pressure with blood from another normal anaesthetized rabbit. Studies at several different perfusion pressures confirmed that a small rise in perfusion pressure caused a large rise in sodium excretion and that the potential sodium-excreting ability of the isolated kidney was high. The curve obtained could be closely fitted by a quadratic equation which allowed an estimate to be made of the blood pressure below which no urine is formed, i.e. the 'theoretical perfusion pressure threshold'. For normal kidneys this was 55-4 mmHg. 2. A group of rabbits had a silver clip applied to the left renal artery and, 3-6 weeks later, the eight most hypertensive animals were selected to provide their kidneys for perfusion. Both kidneys were perfused simultaneously. The clip on the left renal artery was removed immediately before perfusion and the cannula placed distal to the stenosis in the post-stenotic dilatation. The function curves of these kidneys were compared with the curves obtained from normal kidneys. 3. The untouched kidney contralateral to the clip was found to require a significantly higher perfusion pressure (71-7 mmHg) for it to achieve a given sodium excretion rate and, surprisingly, the clipped kidney showed a similar functional change (76-4 mmHg). In other words the positions of both function curves were shifted though their slopes were not much changed. 4. Both kidneys in single-clip-hypertension appear to adapt or reset their sodium excretory behaviour. The resetting in the untouched kidney allows hypertension to be sustained without undue sodium loss. Aldosterone probably contributes little to the resetting. We infer, indirectly, that the normal kidney may, to a significant extent, restrain sodium excretion by virtue of its sympathetic innervation. We also opine that the kidney cannot be assigned fixed intrinsic functional properties on which a renal sodium-handling theory of long-term blood pressure regulation can be firmly based.
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PMID:The relation between the excretion of sodium and water and the perfusion pressure in the isolated, blood-perfused, rabbit kidney, with special reference to changes occurring in clip-hypertension. 125 32

The effects of regression of cardiac hypertrophy on myocardial contractility and ventricular myosin isoenzymes were investigated in rats with renovascular hypertension. Six-week-old male Wistar rats were made hypertensive by constriction of one renal artery with a silver clip. Regression of cardiac hypertrophy was induced following the lowering of blood pressure by nephrectomy on the affected side 5-6 weeks after constriction of the renal artery and was maintained for 5-6 weeks. In contrast, myocardial hypertrophy was induced by 10-11 weeks of the hypertensive state. Isometric developed tension of isolated left ventricular papillary muscles was measured, while they were being perfused with Tyrode solution. Left ventricular myosin isoenzymes were separated by pyrophosphate gel electrophoresis. The ventricular to body weight ratio of the nephrectomized group was significantly lower than that of the hypertensive group, although it was greater than that of age-matched normal control rats. There were no significant differences in the isometric developed tension among three groups, the nephrectomized, hypertensive, and normal control rats. However, dT/dtmax tended to decrease in the hypertensive rats and recovered to normal in the nephrectomized rats. The left ventricular myosin isoenzyme pattern was shifted toward VM-3 in hypertensive rats and was shifted back toward VM-1 again in nephrectomized rats.
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PMID:Effects of regression of cardiac hypertrophy on myocardial contractility and ventricular myosin isoenzymes. 148 59

To determine the effects of moderate versus severe dietary sodium restriction on the development of 2-kidney, 1-clip (2K,1C) hypertension, young male Wistar rats were placed on diets containing 9, 26, or 101 (control) mumol sodium/g food. Three days later, a solid silver clip (i.d. 0.20 mm) was placed on the left renal artery and diets were continued up to 6 weeks. Adult rats received a 0.25-mm clip. In young clipped rats receiving the 101 mumol/g diet, blood pressure (BP), plasma renin activity (PRA), and BP response to captopril were increased as early as 1 week after clipping and increased further over time. Moderate sodium restriction (26 mumol sodium/g) led to only a slight delay in the development of hypertension; the levels of BP and PRA, the BP response to captopril, and the extent of cardiac hypertrophy achieved by 6 weeks were not different between the 2K, 1C rats receiving 26 or 101 mumol sodium/g. Sodium restriction to 9 mumol/g decreased rate of growth and completely prevented the rise in BP and in left ventricular weight. At 3 and 6 weeks the severely sodium-restricted rats had significantly higher PRA levels than the 2K, 1C control group. However, the BP response to captopril was attenuated relative to the other hypertensive groups. In adult rats, this level of sodium restriction had a small, but significant effect on body weight, but still prevented the increase in BP and in left ventricular weight. In conclusion, dietary sodium restriction can prevent the development of 2K,1C hypertension in both young and adult rats, but only if the restriction is severe. This effect may relate to a marked reduction in the pressor effectiveness of the renin-angiotensin system by low sodium intake per se or by associated metabolic or other changes.
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PMID:Dietary sodium restriction and the development of two-kidney, one-clip hypertension in young versus adult rats. 149 15

Pyrrolizidine alkaloids such as monocrotaline are bioactivated in the liver, resulting in veno-occlusive disease of the liver, pulmonary arterial hypertension, and right ventricular hypertrophy. We have searched for the formation of a reactive, alkylating pyrrole intermediate in the metabolism of monocrotaline by isolated rat liver microsomes, using the sulfhydryl-containing resin, thiopropyl sepharose 6B, as a trapping agent. Control experiments show that a toxic, chemically reactive, alkylating pyrrole such as dehydromonocrotaline binds covalently to the resin via a thioether bond, but that a less toxic, poorly alkylating pyrrole, such as dehydroretronecine, does not. Isolated hepatic microsomes metabolize monocrotaline to produce a pyrrole that binds to the resin, and that can be detected by means of the Ehrlich color reagent (p-dimethylaminobenzaldehyde). The pyrrole is releasable by silver nitrate treatment, thereby establishing it to be bound via a thioether linkage. In buffered ethanolic silver nitrate the major product is 7-ethoxy-1-hydroxymethyl-6,7-dihydro-5H-pyrrolizine (O7-ethyldehydroretronecine). This establishes that the thioether linkage is at the 7-position. The same product is obtained on release of the resin-bound pyrrole formed from the reaction of dehydromonocrotaline with the resin, thereby establishing the intermediacy of dehydromonocrotaline in the metabolism of monocrotaline.
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PMID:Detection of a reactive pyrrole in the hepatic metabolism of the pyrrolizidine alkaloid, monocrotaline. 164 51


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