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)

Renovascular hypertension is the most prevalent form of curable hypertension. Despite some unanswered questions, there is a growing consensus about the need to identify patients with renovascular hypertension so that a specific therapy can be recommended. The renin-angiotensin system is the chief pathophysiologic mechanism responsible for hypertension in patients with renal ischemia but other, yet poorly defined, mechanisms may be operative. Most patients with renovascular hypertension do not present with typical or discriminative clinical features. Thus, many physicians do not perform work-up to uncover renovascular disease even if diagnosis is dictated by patients' clinical course. It is difficult to make the proper diagnosis unless there is a high index of suspicion and certain procedures are performed. How can we, then, select a few patients for the work-up from the vast sea of people with hypertension? The identification of such patients and the pursuit of a renovascular etiology is a matter of clinical judgment. Delineation of renovascular hypertension should be undertaken only after careful deliberation. When clinical clues suggestive of renovascular hypertension are present, appropriate diagnostic tests should be undertaken in patients who are candidates for PTRA or surgery. Captopril-stimulated PRA test is done first. If the test is positive (and in some clinically relevant circumstances even if it is not done or is negative), DSA should be obtained. IV-DSA is being steadily replaced by the superior IA-DSA. The need for renal vein renin determination varies from center to center, but when carefully performed, it yields meaningful information. Ultimately, a conventional arteriogram is done to define the extent of renal artery stenosis and to assess intrarenal vascular anatomy. For selected patients, the benefit-risk ratio clearly outweighs the cost considerations. The spectrum of renovascular hypertension is variable, further compounding the diagnostic indications and contraindications. At one end of this spectrum are those patients in whom surgical therapy is likely to be beneficial, and at the other end are the patients who have relative contraindications to surgery. In between lies the vast gray zone that constitutes a great judgmental challenge in clinical medicine. What is to be done with the patients who have mild to moderate renovascular hypertension whose BP is controlled on medical therapy? There are some patients who may benefit from renovascular repair despite the nonlateralization of renal vein renins. What is the mechanism underlying their hypertension?(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renovascular hypertension. 306 42

Nineteen mongrel dogs had 30 minutes of thoracic aortic occlusion to determine the effects that blockade of the renin-angiotensin system may have on preserving spinal cord blood flow and function during a period of temporary spinal cord ischemia. Cross-clamping of the thoracic aorta causes renal ischemia and activates the renin-angiotensin system with resulting increased production of angiotensin II. Angiotensin II is a potent peripheral constrictor and elevated levels may constrict collateral spinal cord circulation. At the time of aortic cross-clamping, 10 dogs received 100 mg/kg of MK422 (intravenous enalapril maleate), a converting enzyme inhibitor, and nine animals served as controls. The blockade of the renin-angiotensin system had no preserving effects on spinal cord flow as measured by microspheres and on spinal cord function as graded with the Tarlov scale. However, the paraplegic animals all had significantly increased lower thoracic and lumbar spinal cord flows 30 minutes after clamp release when compared with those animals that remained neurologically intact. In conclusion, marked hyperemia occurring after a period of hypoperfusion may lead to spinal cord edema and compartment syndrome with resulting paraplegia.
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PMID:The effect of hyperemia on spinal cord function after temporary thoracic aortic occlusion. 317 89

The pathway of renin biosynthesis and secretion in normal and ischemic human kidneys has been investigated by pulse-labeling experiments. The results indicate that in normal human kidney, preprorenin is rapidly processed to 47-kDa prorenin. Microradiosequencing showed that this molecule was generated by cleavage between Gly-23 and Leu-24, yielding a 43-amino acid proregion. Analysis of prorenin secreted by the kidney tissue yielded an identical sequence, indicating that prorenin is secreted without any further proteolysis. An examination of the kinetics of processing and secretion suggested that a majority of the newly synthesized prorenin is quickly secreted, while only a small fraction is processed intracellularly to the mature renin. The differences in secretion kinetics between prorenin and mature renin and the selective inhibition of prorenin secretion by monensin suggest that they are secreted independently via two pathways: a constitutive pathway probably from the Golgi or protogranules that rapidly release prorenin and a regulated pathway that secretes mature renin from the mature granules. A comparison of the kinetics of processing between normal and ischemic tissues suggests that renal ischemia leads to an overall increase in the rate of processing of prorenin to mature renin. In addition, prolonged biosynthetic labeling of renin in the ischemic kidney yielded two smaller molecular weight immunoreactive forms suggestive of renin fragments that may be degradative products. These fragments were not detected in normal kidney tissue labeled for similar lengths of time.
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PMID:Human renin biosynthesis and secretion in normal and ischemic kidneys. 331 96

It is known that renal ischemia enhances the production of adenosine, which is further metabolized by xanthine oxidase, and that the inhibition of this metabolizing enzyme by allopurinol ameliorates the consequences of renal ischemia. This study was undertaken to define the effect of allopurinol on the renal responses to adenosine. It was found that 5 minutes of intrarenal infusion of adenosine in control dogs produced a typical biphasic response characterized by an initial vasoconstriction, decreasing renal blood flow by 46.3% +/- 6.0%, followed by vasodilation, increasing renal blood flow by 8.5% +/- 3.6% above the control levels. Adenosine infusion was also accompanied by a significant reduction of plasma renin activity, from 8.4 +/- 0.6 ng/ml/hour to 3.8 +/- 0.4 ng/ml/hour. The administration of an intravenous infusion of 50 mg allopurinol did not alter the vasoconstrictor phase of adenosine--the average decrease was 41.1% +/- 3.3%; however, it prevented much of the vasodilation because renal blood flow over the 5 minutes remained 17.9% +/- 5.0% less than the levels recorded before adenosine infusion. Allopurinol also prevented the decrease of plasma renin activity, for which the average values recorded before and after adenosine were 9.6 +/- 0.6 ng/ml/hour and 8.2 +/- 0.6 ng/ml/hour, respectively. The results of this study indicate that allopurinol exerts specific effects on the vasodilatory component of adenosine and prevents the adenosine-suppressive effect on the renin-angiotensin system.
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PMID:Effect of allopurinol on the renovascular responses to adenosine. 351 11

In coarctation, bipedal exercise induces a pressure triad: exaggerated systolic arm hypertension, unchanging leg pressure, and markedly increased systolic gradient. Constancy of leg pressure derives from the lower body sharing the poststenotic compartment with the kidneys. Exercise-induced poststenotic hypotension stimulates the juxtaglomerular apparatus (JGA) to raise renal pressure to pre-exercise levels. Ambulation during the greater part of each day stimulates the JGA repetitively. Thereby, this chronic Single-Kidney-Goldblatt model is modified by increased plasma renin, fluid volumes, and cardiac output. It also accounts for hyper-responsive renin output after renin blockage and for mild poststenotic hypertension. Hypertension after repair which corrected the resting gradient, is almost always associated with the exercise triad, indicating that renal ischemia exists during ambulation. Thus, residual hypertension usually means residual coarctation. Mesenteric ischemia complicating postoperative paradoxic hypertension is probably due to spasm in the superior mesenteric artery and not to fixed occlusion of necrotizing arteritis.
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PMID:Coarctation hypertension is renovascular, modified by ambulation. Coarctation hypertension renovascular variant. 352 15

Renal parenchyma, and the juxtaglomerular apparatus in particular, was studied in 23 patients with verified diagnosis of pheochromocytoma. Intraoperative renal biopsy was performed in 21 cases, and kidneys obtained at nephrectomy or autopsy were examined in 2 cases. Twenty-one patients were examined following the removal of pheochromocytoma (2 patients died). Arterial BP returned to normal in 86.4%, and residual hypertension due to continuous hyperfunction of the juxtaglomerular apparatus in the presence of hypertensive angiosclerosis was recorded in 13.6%. Tubular epithelial atrophy of varying markedness, associated with renal ischemia, was detected in all cases. The pathogenetic contribution of the renin-angiotensin system to pre- and postoperative hypertension in pheochromocytoma patients is discussed.
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PMID:[Residual hypertension after removal of a pheochromocytoma (morphologic study of the kidneys)]. 368 71

Unilateral parenchymatous kidney disease associated with high blood pressure represents a potentially curable form of hypertension. Surgery may normalize blood pressure in a substantial number of these patients. Curable renal parenchymatous hypertension includes unilateral tubulointerstitial kidney diseases such as chronic pyelonephritis, reflux nephropathy, segmental hypoplasia and radiation nephritis, hydronephrosis, simple renal cysts, traumatic kidney lesions and renal tumors associated with high blood pressure. Renal ischemia and in turn activation of the renin angiotensin system is involved in the pathogenesis of hypertension in most of these patients. In patients with unilateral kidney disease and hypertension, both an operative and a medical therapeutic approach have a high success rate. Good candidates for nephrectomy are young patients with severe hypertension, strict unilateral disease, normal plasma creatinine levels and minimal function of the involved kidney. In unilateral hydronephrosis reconstructive surgery or nephrectomy may cure or improve hypertension in the vast majority of the patients. Surgically correctable hypertension has also been reported in some patients with large renal cysts and renal tumors (hemangiopericytoma, Wilm's tumor, hypernephroma, renal pelvic tumor).
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PMID:Curable renal parenchymatous hypertension: current diagnosis and management. 390 29

Water-electrolyte balance, plasma renin activity and urinary catecholamine excretion were studied for a period of 10 weeks after clipping the renal artery in the rat. Two groups of rats were examined; in Group I, a silver clip was applied on the left renal artery leaving the contralateral kidney untouched; in Group II, both renal arteries were clipped. Neither water-salt retention nor the increase inthe activity of the renin-angiotensin system or in the neural tone seem to be essential in the development of high arterial pressure after renal ischemia. All these factors would seem to be secondary mechanisms the contribution of which would depend on the experimental model or the hypertensive period under consideration.
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PMID:Water-salt balance, plasma renin activity and catecholamine excretion in renovascular hypertension in the rat. 616 29

To examine the role of the renal vascular receptor in the control of renin secretion in the rat, a denervated, nonfiltering kidney model (DNFK) was developed. The left kidney was subjected to a 2-hr period of total renal ischemia followed by ureteral ligation and section Denervation was accomplished by stripping all visible nerves and painting the renal vessels with 5% phenol. Forty-eight hours later lissamine green dye was injected iv and failed to appear in either the cortical or medullary tubules, indicating that glomerular filtration had ceased. Histological study of these kidneys revealed diffuse tubular necrosis with extensive intratubular cast formation. Norepinephrine content of the DNFK was reduced 91% compared to the contralateral normal kidney (P less than 0.001). In another group of anesthetized rats with a single DNFK, 15 min of suprarenal aortic constriction (SAC) increased plasma renin activity (PRA) from 3.4 +/- 0.6 to 11.5 +/- 1.6 ng AI/ml/hr; in a time control series, PRA was unchanged. To exclude the influence of adrenal catecholamines in this response, bilateral adrenalectomy was performed in a separate group of animals with a DNFK. In this series, SAC also markedly increased PRA. The present data indicate that in the rat the macula densa, the renal nerves, and adrenal catecholamines were not essential for the hyperreninemia induced by a reduction in renal perfusion pressure.
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PMID:A denervated nonfiltering kidney preparation in the rat: a model for study of renin release. 634 93

Blood pressure and supine plasma renin were measured in fourteen children aged seven to eighteen years whose hydronephrosis had been relieved surgically two to eleven years previously. Values did not differ significantly from age matched controls. It has been suggested that renal ischemia may persist after relief of hydronephrosis but our results show that hyperreninemia rarely occurs within two to eleven years of effective surgery. Further studies of blood pressure and renin after this period of time remain to be done.
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PMID:Plasma renin activity in children after surgical relief of hydronephrosis. 635 74


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