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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to their role as highly potent antihypertensive drugs, calcium antagonists may also play an important future role in the area of tissue protection and preservation. Calcium antagonists exert favorable effects on renal hemodynamics related to their reversal of renal vasoconstrictors. Calcium antagonists are also capable of blocking intracellular calcium overload induced by various types of ischemic or toxic stimuli. Features such as these may be of substantial value in ameliorating acute renal insufficiency secondary to renal ischemia, iodinated radiographic contrast agents, or the administration of various nephrotoxic drugs. The latter includes agents such as the aminoglycoside antibiotics, cyclosporine A, and the cancer chemotherapeutic agent cisplatin. Recent prospective, controlled studies from our group indicate that calcium antagonists protected against postischemic acute renal failure in the setting of cadaveric renal transplantation. Moreover, in a prospective, randomized, controlled clinical trial, we were able to demonstrate that the prophylactic use of nitrendipine reduced the decrease in GFR in patients receiving radiographic contrast agents. Calcium antagonists may also play a beneficial role in preventing progressive renal disease. Data from a number of studies conducted in experimental animals, as well as information from clinical trials, support such a view. Although the mechanisms of action of calcium antagonists in the setting of chronic renal failure are not yet fully established, their beneficial effects may be related to protective actions such as the reduction in renal hypertrophy, modulation of mesangial cell uptake of macromolecules, changes in permselectivity of the glomerulus, and a decreased free radical formation. These various aspects will be the topic in this review.
J Cardiovasc Pharmacol 1991
PMID:Renal protection with the calcium antagonists. 172 49

Reperfusion after renal ischemia is characterized by a preglomerular vasoconstriction. As endothelin-1 (ET-1) is a potent preglomerular vasoconstrictor, we designed a study to investigate the role of ET-1 in postischemic renal vasoconstriction. Renal ischemia was induced by 45 min of left renal artery clamping in anesthetized rats. After ischemia, renal blood flow was restored to only 61 +/- 4% of its preischemic value. The sensitivity to exogenous ET-1 after renal ischemia was decreased, but much less than the sensitivity to angiotensin II, which almost lost its vasoconstrictor effect, and to norepinephrine, which became a vasodilator. In addition, the binding affinity of [125I]ET-1 in the kidney increased significantly after renal ischemia, despite no change in the density of binding sites. These findings may be in favor of a role of endogenous ET-1 in postischemic renal vasoconstriction.
J Cardiovasc Pharmacol 1991
PMID:Relative preservation of the responsiveness to endothelin-1 during reperfusion following renal ischemia in the rat. 172 66

Endothelin (ET-1), a recently discovered endothelium-derived peptide, has been reported to produce potent vasoconstriction in various isolated vessels of experimental animals. Cicletanine (CIC) is a novel antihypertensive agent. This study concerns the effect of CIC on the vascular actions of ET-1 (0.2 nM/kg) and epinephrine (1 microgram/kg) in normotensive Wistar rats. The hemodynamic effects of ET-1 and epinephrine were also tested in the presence of molsidomine (MOL), a vasodilator that releases nitric oxide. Rats were treated for 15 days with CIC (10 mg/kg/day) or gum arabic p.o. Subsequently, the animals were anesthetized and renal and aortic blood flow (BF) determined by pulsed Doppler flowmetry. ET-1 or epinephrine was injected. After return to the basal level, MOL (5 mg/kg) was injected; 10 min later, the mean arterial pressure (MAP) was decreased and then ET-1 or epinephrine was administered. The vascular resistance was calculated by the MAP/BF ratio and expressed as a percentage. In CIC-treated rats, ET-1 induced a renal vasoconstriction smaller than in control rats (+27.2 +/- 5.95 and +60.4 +/- 11.95%, respectively, p less than 0.01). In the presence of MOL, ET-1 produced a smaller increase in MAP (+9.7 +/- 1.34 and +16.9 +/- 2.49 mm Hg, p less than 0.05). Epinephrine injected after MOL in CIC-treated rats induced a smaller renal vasoconstriction than in control rats (+98.8 +/- 29.83 and 185 +/- 30.33%, p less than 0.05). Thus, CIC partially reduced the hypertensive and renal vasoconstrictor effects of ET-1. A combination of CIC and MOL diminished the renal effects of epinephrine. In conclusion, CIC could be used to attenuate the hypertensive status or renal ischemia disorders where ET-1 seems to be implicated.
J Cardiovasc Pharmacol 1991
PMID:Cicletanine modulates endothelin-induced renal vasoconstriction in the rat. 172 68

The need to support the distal circulation during aortic crossclamping and the subsequent effects on hemodynamics and organ perfusion prompted our review of 51 patients who underwent repair of aneurysm of the descending thoracic aorta from 1983 through 1987. Forty-three patients had aneurysms originating distal to the left subclavian artery, and eight had aneurysms involving the distal aortic arch and the proximal descending aorta; 10 patients had emergency operation for aneurysm rupture. Three different techniques were used: Seventeen patients had left atrial-distal aorta arterial bypass with a centrifugal pump, 18 patients had a Gott shunt, and 16 patients had no circulatory support during aneurysm repair. Location and type of aneurysm, age, sex, diabetes, preoperative hypertension, and serum lipid levels were similar in the three groups. Duration of crossclamping was 54 +/- 12 minutes for left atrial-aortic assist, 45 +/- 5 for the shunt group, and 34 +/- 4 for patients without circulatory support. With crossclamping, all groups had similar and significant increases in heart rate (p less than 0.03). Proximal systolic blood pressure did not change during left atrial-aortic assist, but a transient increase occurred in patients with shunts (p less than 0.01), and a sustained increase occurred in patients without circulatory support (p less than 0.05). With crossclamp release, arterial pH and capillary pulmonary wedge pressure decreased significantly (p less than 0.05) in patients without shunt or bypass. Postoperative renal function did not vary significantly when circulatory support was used, but serum creatinine rose transiently in patients with unsupported aortic crossclamping. We conclude that support of the distal circulation during thoracic aortic crossclamping stabilizes hemodynamics and prevents systemic acidosis and renal ischemia. Further, our data suggest that the centrifugal pump may provide better protection than a passive shunt.
J Thorac Cardiovasc Surg 1990 Jun
PMID:Circulatory support during crossclamping of the descending thoracic aorta. Evidence of improved organ perfusion. 235 21

In this randomized, double-blind, placebo-controlled trial the renal function was studied in 60 patients recovering from coronary artery bypass surgery treated with a daily dose of 800 mg sulphinpyrazone (SP) or 880 mg acetylsalicylic acid (ASA) or placebo. Serum creatinine level increased (p less than 0.05) during the first 2 days of SP treatment, but returned to its baseline level within 4 days under maintained therapy; during ASA and placebo therapy no significant changes occurred. Serum urea levels decreased (p less than 0.01) during ASA and placebo treatments as time from surgery subsided; the decrease of serum urea level was delayed in the SP group compared with the ASA and placebo groups. Urinary excretion of prostaglandin E2 (PGE2) was significantly decreased (p less than 0.01) during ASA treatment; in the SP group, urinary PGE2 excretion tended also to decrease during the first days of treatment, the decrease being significant only on the 4th day (p less than 0.01). The urinary excretion of kallikrein decreased significantly only in the SP group (p less than 0.01), while the changes in the ASA and placebo group were not significant. We suggest that the rapidly reversible acute renal impairment during SP therapy was probably due to a transient renal ischemia caused by a drug-related decrease in urinary kallikrein excretion rather than by renal prostaglandin inhibition.
J Cardiovasc Pharmacol
PMID:Impairment of renal function due to sulphinpyrazone after coronary artery bypass surgery: a prospective double-blind study. 242 79

An increase in intracellular calcium has been identified as an etiologic factor in acute renal failure (ARF) and blockade of slow calcium channels has been successful in its amelioration. Diuretics may also prevent or mitigate the effects of renal ischemia. We examined the actions of a new calcium channel blocker, nitrendipine (NTR), given intravenously to rats prior to bilateral clamping of the renal pedicle for 45-60 min. Four groups of rats were studied. Group I: Rats given the vehicle only and subjected to sham surgery had a creatinine clearance (Ccr) of .93 +/- .05 ml/min (n = 20). Group II: Rats given NTR (1 or 3 mg/kg) and subjected to sham surgery had a Ccr of .65 +/- .03 ml/min (n = 17). Group III: The infusion of the vehicle alone 10-15 min before clamping resulted in a Ccr of .12 +/- .02 ml/min (n = 23, p less than .001 vs. group I). Group IV: Rats given NTR and then clamped had a Ccr of .30 +/- .04 ml/min (n = 31, p less than .001 vs. group III, p less than .001 vs. group II). Higher doses of NTR did not improve the results. We concluded that NTR partially protects against ARF, but NTR lowered Ccr compared to control rats (p less than .001, group I vs. group II).
J Cardiovasc Pharmacol 1987
PMID:Effect of nitrendipine in a rat model of ischemic acute renal failure. 244 Nov 86

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.
J Cardiovasc Pharmacol 1987
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)
J Cardiovasc Pharmacol 1987
PMID:Chronic administration of ketanserin and the development of two-kidney-two-clip Goldblatt renovascular hypertension in the rat. 244 74

Abdominal aortic aneurysm associated with a pelvic kidney was recognized and treated successfully in a 66-year-old male by keeping renal ischemia time to less than 40 minutes and implanting the renal arterial supply as a cuff with common iliac arterial anastomoses to each Dacron limb of the graft.
J Cardiovasc Surg (Torino)
PMID:Abdominal aortic aneurysm and pelvic kidney. 672 90

The case is presented of a 38-year-old male who presented with a large 10 cm x 8 cm pulsatile swelling in his abdomen. Thirteen years before, internal iliac arteries had been used to treat long segment occlusions and diseased state of both renal arteries. At the same time both kidneys had been transplanted to the iliac fossae. Digital subtraction angiography revealed a huge abdominal aortic aneurysm. Both kidneys were fully functional. As the renal transplants had been done extraperitoneally an easy transperitoneal approach was now possible. The maximum diameter of the aneurysm was 12 cm. An inclusion graft repair was carried out using a 16-mm woven Dacron graft. In the light of the favourable circumstances it was decided not to take any special protective measures against renal ischemia apart from keeping the aortic cross-clamp time short. The patient could be discharged with patent and normally functioning kidneys 10 days after surgery.
Thorac Cardiovasc Surg 1994 Apr
PMID:Abdominal aortic aneurysm repair in a patient with bilateral autotransplanted kidneys. 801 29


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