Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After the development of blood pressure measurements in humans, the association of high blood pressure with renal disease was established. Injection of extracts of various organs in an attempt to replace their secretions was common in the 19th century, and it was therefore natural for Tigerstedt and Bergman to investigate the effects of renal extracts. In this way, they discovered renin. This paper covers the methods by which its mode of action was uncovered, as well as its relation to renal ischemia and hypertension.
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PMID:Evolution of renin. 184 50

Recovery from renal ischemia requires regeneration of damaged tubular epithelium. Previous studies have examined the expression of proto-oncogenes and growth factors after ischemia, but the response of genes coding for structural and functional genes has not been scrutinized. Rats were subjected to 40 minutes of renal artery occlusion and 60 minutes to 96 hours of reperfusion. Total RNA was isolated and mRNA for the structural protein actin, the enzymes superoxide dismutase and renin, the proto-oncogene c-fos, the nuclear protein histone H2b, and the putative marker for cell injury TRPM-2 was quantitated by Northern hybridization. Expression of the proto-oncogene c-fos was seen early but for only short duration. Histone gene expression was not markedly increased until 24 hours after ischemia, but remained increased for several days. Renin mRNA was undetectable one hour after ischemia, but was present in normal amounts at 24 and 48 hours. In contrast, superoxide dismutase mRNA was present in decreased amounts 24, 48, and 96 hours after ischemia. TRPM-2 gene expression was greatly increased 24 to 72 hours after ischemia and began decreasing at 96 hours. This selective sequence of gene expression or repression after renal ischemia might maximize the proliferative repair process. This information will be useful for designing therapies to further enhance recovery from acute renal injury.
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PMID:Differential gene expression in the recovery from ischemic renal injury. 191 Jan 24

The study included 15 patients with nephrogenic hypertension of various genesis. 13 of them had unilateral disease, 2 bilateral one. The diagnosis was established from the data provided by a single captopril test, radionuclide and angiographic examinations. The blood for renin and prostaglandin quantitation was obtained from the renal veins and infrarenal portion of the vena cava inferior. The results show that in unilateral renal lesions prostaglandin E secretion on the affected side was significantly lower than on the contralateral side (p less than 0.05). Plasma renin activity in 3 patients with a contracted kidney was significantly lower on the affected side (p less than 0.05), though the rest 10 patients were reported to exhibit opposite results. No significant relationships occurred in the levels of prostaglandins I2, F2 alpha, thromboxane A2. It is suggested that renal ischemia may inhibit synthesis of depressor prostaglandin E2 in renal medullary interstice. A separate analysis is presented of plasma renin and prostaglandin activity in 2 cases of nephrogenic hypertension as a result of bilateral renal affection.
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PMID:[The diagnostic importance of determining prostaglandins in patients with nephrogenic arterial hypertension]. 194 11

In 12 patients with unilateral significant renal ischemia plasma levels of atrial natriuretic peptide (ANP) were estimated in renal vein blood of the ischemic (IK) and contralateral kidney (NK) and in arterial blood under supine and upright conditions. Plasma ANP levels in renal vein blood were compared with plasma renin activity (PRA) of the same blood samples. Plasma ANP levels in renal vein blood of the contralateral kidney (87 +/- 9 pg/ml) were significantly lower than in arterial blood (131 +/- 11 pg/ml) and renal vein blood of the ischemic kidney (139 +/- 16 pg/ml). In contrast plasma ANP concentrations in renal vein blood of the ischemic kidney were slightly or markedly higher than in arterial blood. A positive correlation was found between the ratio of plasma ANP in renal vein blood of the IK to that of the NK under supine condition and the respective ratio of PRA. Data presented in this paper suggest the presence of abnormal handling of ANP by an ischemic kidney and that plasma ANP levels in renal vein blood may be a marker of renal ischemia.
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PMID:Plasma level of atrial natriuretic peptide in renal venous blood--marker of kidney ischemia? 214 10

Renal effects of 1,4-dihydropyridine (DHP)-type calcium antagonists (nitrendipine and nisoldipine) were analyzed in diverse conditions, such as long-term antihypertensive treatment, acute saline-loading, and acute renal failure in rats. In spontaneously hypertensive rats (SHR), 60-week treatment with nitrendipine resulted in normotensive blood pressure values without increasing body weight, an indicator of salt-water retention, or increasing plasma renin activity and plasma aldosterone concentration compared with the untreated rats. After acute saline-loading of normotensive or hypertensive rats, administration of calcium antagonists nitrendipine and nisoldipine increased urinary volume and sodium excretion. This was in contrast to the effects observed with the vasodilator minoxidil, with which salt-water retention was shown. In acute renal failure induced by 60-min renal ischemia in uninephrectomized rats, administration of nisoldipine decreased mortality rate and improved kidney function. The increase in renal tissue calcium content and the decrease in ATP content associated with the renal failure was abolished by nisoldipine treatment. In conclusion, renal protective effects are present with DHP-type calcium antagonists; however, mechanisms in situations such as hypertension or acute renal failure might be different and deserve further analysis.
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PMID:Renal effects of 1,4-dihydropyridines in animal models of hypertension and renal failure. 244 Nov 91

The effect of ketanserin (Kt) has been analyzed during the development of two-kidney-two-clip (2k-2c) renovascular hypertension in the rat. Male Wistar rats were divided into four experimental groups: (1) clip Kt (ClKt) (n = 12)--A silver clip (0.25 mm width) was placed in each renal artery 3 days after beginning the administration of Kt (10 mg/kg/day) in the drinking water; (2) sham Kt (ShKt) (n = 13)--Similar to group 1, but the clips were placed in, and immediately removed from, the renal arteries; (3) untreated clip (UCl) (n = 10)--Similar to group 1, but the rats drank water; (4) untreated sham (USh) (n = 10)--Similar to group 2, but the rats drank water. Blood pressure (BP) was measured before surgery and was followed weekly for 7 weeks. At the end of this period, blood and cerebrospinal fluid (CSF) samples were obtained in all the animals. Plasma renin activity (PRA) and plasma and CSF angiotensinogen concentration (AoC) were evaluated. The results have shown that Kt partially inhibited the increase in BP induced by bilateral renal ischemia (BP: UCl rats 180.5 +/- 12.4 versus ClKt rats 149.8 +/- 5.1 mm Hg; p less than 0.01; USh rats 116.7 +/- 3.7; ShKt rats 114.4 +/- 5.0 mm Hg). PRA was similar in hypertensive and control rats whether or not they had received Kt. AoC in plasma was decreased in clipped treated and untreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic administration of ketanserin and the development of two-kidney-two-clip Goldblatt renovascular hypertension in the rat. 244 74

In a 22 years old woman with recent hypertension, a timed intravenous pyelogram revealed an asymptomatic obstructive ureteropelvic junction. Preoperative renal vein catheterization demonstrated excessive renin release from the diseased kidney and low release from the other one, suggesting that corrective ureteral surgery should return blood pressure to normal levels. Moderately impaired glomerular filtration rate improved after surgery as a consequence of suppressed hydronephrosis and bilateral renal ischemia. Thus we conclude that in young people, asymptomatic unilateral hydronephrosis can lead to hypertension and renal failure like renal artery stenosis. In the other cases of urinary flow obstruction, secondary hypertension remains to be explained by both inappropriate production of renin and water chronic retention.
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PMID:[Arterial hypertension with renin hypersecretion secondary to pyelo-ureteral syndrome. Cure after corrective surgery]. 269 10

The authors studied clinical and biological data occurring in 165 patients observed during 23 years and afflicted with polyarteritis nodosa. Hypertension was present in 52 patients (31.5%) and seven of them suffered from malignant hypertension (4%). Mean age of patients (6 male, 1 female), with malignant hypertension was 38 +/- years old. Mean follow up was 49 +/- 28 months including 26 +/- 21 months after discontinuation of treatment of polyarteritis nodosa. Malignant hypertension occurred during the first year of evolution of polyarteritis nodosa. Renal insufficiency was present in 5 of 7 patients. Proteinuria was greater than 1 gr/d in 4 cases. Renal arteriography was performed in 6 patients and showed in every case renal ischemia and microaneurysms in five. In 4 patients measurements of plasma renin activity and of aldosterone were obtained. A stimulation of those hormones was demonstrated. Some symptoms of polyarteritis nodosa were present with a high incidence in case of malignant hypertension: digestive signs (6/7), orchitis (3/6). HBs antigen was present in 6 cases and hepatitis in 5. Captopril was effective in every case, alone or associated with other treatments. Follow up of hypertension went from 8 months to 4 years. At present time 6 patients are alive and one is lost of follow up. A treatment is necessary in 6 of 7 patients. Creatininemia is greater than 300 micromol/l in 4 patients. A successful kidney transplantation was performed in one case. Our study shows a close relation between malignant hypertension observed in polyarteritis nodosa, vascular nephropathy, digestive and urologic signs. Hepatitis B virus could be responsible of those manifestations.
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PMID:[Malignant arterial hypertension in periarteritis nodosa. Incidence, clinicobiologic parameters and prognosis based on a series of 165 cases]. 287 20

The neurohormonal contribution to high blood pressure was investigated in 9 conscious two-kidney, two-clip Goldblatt (2K2C) hypertensive dogs during evolution of the benign and malignant phases after application of bilateral renal clips (BRC). Serial measurements were taken of the plasma renin activity (PRA), plasma angiotensin I-immunoreactivity (Ang I-ir), plasma angiotensin II-ir (Ang II-ir), renin substrate (RS) catecholamines [epinephrine (Epi) and norepinephrine (NE)] and vasopressin (AVP). Immediately after BRC, the elevation of the blood pressure (86 +/- 3 to 110 +/- 3 mmHg, p less than 0.01) was associated with an increase in heart rate (93 +/- 3 to 114 +/- 9 beats/min, p less than 0.01). These hemodynamic changes were accompanied by increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP. The renin angiotensin system was activated throughout the 3 week period following BRC, as indicated by increases in PRA, Ang I-ir and Ang II-ir. Catecholamines were elevated immediately after BRC, followed by a return toward the control values. AVP underwent a slight but not significant elevation after BRC, which was sustained during the 3 weeks. Production of malignant hypertension was affected by occlusion of one of the adjustable renal clips 3 weeks after BRC. A marked elevation of the blood pressure was associated with significant increases in PRA, Ang I-ir, Ang II-ir, Epi, NE and AVP, compared with the pre-occlusion values. In addition, pharmacologic experiments were performed in 6 of 9 dogs. Administration of angiotensin I converting enzyme inhibitor (SQ 14225) reduced the blood pressure both in the benign and malignant phases of 2K2C renovascular hypertension, and a ganglionic blocking agent (hexamethonium) also decreased the blood pressure. However, a specific, vascular acting AVP antagonist failed to reduce the blood pressure significantly. From this study, it seems likely that severe renal ischemia caused by renal clipping caused the activation of the renin-angiotensin and the sympathetic nervous system and elevation of serum vasopressin. However, there are no apparent differences between the benign and malignant phases of renovascular hypertension, except for the marked elevation of neurohormone levels in malignant hypertension.
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PMID:Characterization of neurohormonal changes following the production of the benign and malignant phases of two-kidney, two-clip Goldblatt hypertension. 288 73

Our previous studies support the hypothesis that activation of the renin-angiotensin system by renal ischemia elevates adenosine levels and that adenosine acts in a negative feedback loop to limit renin release and to mitigate some of the hypertension-producing effects of angiotensin II. To further test this hypothesis, we compared the time course of caffeine-induced increases in plasma renin activity with the time course of changes in plasma levels of adenosine in two models of renin-dependent renovascular hypertension. Also, we compared the effects of caffeine on plasma renin activity and arterial blood pressure in renin-dependent versus renin-independent renovascular hypertension. In comparison to sham-operated rats, plasma levels of adenosine in the left and right renal veins and aorta were elevated severalfold in two-kidney, one clip rats (2K1C) 1 week after left renal artery clipping. However, adenosine levels declined during the second and third weeks after clipping. In 2K1C rats treated chronically with caffeine, plasma renin activity was markedly elevated during the first week after operation as compared to non-caffeine-treated 2K1C rats. However, during the second and third weeks after clipping, caffeine had lesser effects on plasma renin activity. A temporal relationship between plasma adenosine levels and caffeine-induced hyperreninemia was also observed in rats with aortic ligation. Caffeine accelerated hypertension in 2K1C rats and rats with aortic ligation (renin-dependent renovascular hypertension), but it had no effect on plasma renin activity or blood pressure in one-kidney, one clip rats (renin-independent renovascular hypertension). These results lend further support to the hypothesis that adenosine functions to mitigate the renin-angiotensin system in renin-dependent renovascular hypertension.
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PMID:Adenosine in renin-dependent renovascular hypertension. 304 93


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