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Biomedical subjects

S C Textor

Publications and source records attributed to S C Textor.

At least 55 records · Page 3Linked to original sources
PubMed1994

Systemic and renal effects of nifedipine in cyclosporine-associated hypertension.

Cyclosporine induces hypertension and wide-spread vasoconstriction after transplantation in addition to reducing kidney function. We studied hemodynamic, renal, and hormonal effects of monotherapy with nifedipine XL (n = 37) in liver transplant recipients within a year after transplant (median, 4.4 months). Systemic hemodynamics were determined with thoracic electrical bioimpedance. Blood pressure before therapy was 172 +/- 4/108 +/- 2 mm Hg. Sixty-four percent of recipients achieved blood pressures less than 140/90 mm Hg mediated by a fall in systemic vascular resistance index (2427 +/- 245 dyne.s.cm-5.m-2 in responders versus 2905 +/- 281 in nonresponders, P < .01). Despite the fall in systemic vascular resistance, glomerular filtration rates were not changed during nifedipine therapy, as measured by both creatinine and iothalamate clearances. Urinary prostacyclin (6-ketoprostaglandin F1 alpha) was suppressed below normal from 2468 +/- 323 ng/d before transplant to 1103 +/- 99 ng/d (P < .01) after transplant and did not change during nifedipine therapy. Urinary thromboxane B2 and plasma renin activity also fell after transplant and remained low during nifedipine. These data demonstrate that nifedipine can reverse systemic vasoconstriction associated with hypertension after transplantation. Systemic effects were not transmitted to the kidney sufficiently to improve glomerular filtration rate or reverse hormonal changes within the kidney. Hence, vascular and functional regulation of the kidney was dissociated from the systemic circulation during nifedipine administration after transplantation.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Resolution of posttransplant hypertension after liver transplantation despite impaired glomerular filtration.

Hypertension developing after transplantation is characterized by widespread vasoconstriction including the kidney. Late resolution (mean, 29 +/- 4 months) of posttransplant hypertension has been observed in 15 (Group I) of 278 subjects monitored after liver transplantation. These studies were undertaken to define the systemic and renal changes associated with resolution, as compared with a group matched for age, sex, and time after transplant who remained hypertensive (Group II; N = 15) or a group who never developed hypertension (Group III; N = 23). Blood pressure during resolution paralleled changes in the systemic resistance index, which fell from 3,052 +/- 548 to 1,872 +/- 205 dyne/s.cm5/m2 (P < 0.01). GFR and RBF remained low, despite the resolution of hypertension, and renal vascular resistance did not change. Circulating endothelin levels remained above normal in all transplant recipients (Group I, 11.9 +/- 3.0 versus normal subjects, 7.0 +/- 1.1 pg/mL; P < 0.05), and urinary prostacyclin excretion was suppressed (880 +/- 120 versus 2,247 +/- 187 ng/day; P < 0.01). No hormonal differences were apparent between transplant groups. These results demonstrate the capacity for systemic vasodilation to occur after transplantation, independent of vascular tone in the kidney. They further suggest that renal vasoconstriction and impaired GFR alone are not sufficient to explain de novo hypertension after transplantation.

Adult↗
PubMed1994

Renovascular hypertension.

Renal artery stenosis, particularly related to advancing atherosclerotic disease, is a common concern to internists seeing patients with worsening hypertension and deteriorating renal function. Understanding the hormonal and hemodynamic consequences of critical vascular lesions allows better selection of antihypertensive therapy. With the application of potent antihypertensive agents--especially those that block the renin-angiotensin system, such as ACE inhibitors or the soon-to-be-released angiotensin receptor antagonists--blood pressure control often is not the primary reason to consider renal revascularization. Instead, protection of renal function beyond a critical level of arterial stenosis is becoming the main indication for both percutaneous angioplasty and surgical revascularization. Both procedures pose hazards, so optimal management of the patient with renovascular hypertension depends on achieving a balance between the risks and benefits to the individual patient. It remains incumbent upon the internist to weigh the cardiovascular and cerebrovascular risks against both the gains in blood pressure control and the likely progression of renal compromise during the patient's lifetime. Improved understanding of the outcomes of medical therapy versus revascularization depends on future prospective studies.

Animals↗
PubMed1993

Systemic and renal hemodynamic differences between FK506 and cyclosporine in liver transplant recipients.

Immunosuppression after transplantation is complicated by hypertension and nephrotoxicity, reflecting widespread vasoconstriction associated with CsA. FK506 is a novel alternative immunosuppressive agent, structurally unrelated to CsA. These studies compared systemic and renal vascular changes developing in the initial 4 weeks after liver transplantation in patients treated with FK506 (plus PRED) and CsA (plus PRED and AZA). We studied arterial pressure, cardiac index (pulsed doppler ultrasound), and systemic resistance index (SVRI) before and weekly after liver transplant in 32 patients treated with CsA (2 mg/kg initial dose plus PRED; median dose at week 4, 30 mg/day) and 14 patients treated with FK506 (0.15 mg/kg/day initial dose and PRED; mean week 4 dose, 12.5). Renal plasma flow and glomerular filtration rate (GFR) were measured by clearance of para-amino hippurate and 125-iothalamate. Renin activity, aldosterone, and urinary prostanoids were measured by RIA. Pretransplant pressures and hemodynamics reflected low SVRI and increased cardiac index typical of end-stage liver disease. After transplantation, SVRI and pressures rose in both groups, but after week 2, SVRI was lower in patients treated with FK506. This was associated with less prevalent clinical hypertension during the subsequent 4 months (4/14 FK506 (28%) vs. 25/32 (78%) CsA, P < 0.01). By contrast, renal blood flow and GFR fell in both treatment groups similarly, whereas renal vascular resistance rose. Urinary 6-keto-PG-F1-alpha was suppressed in all transplant recipients, but to a greater degree in FK506-treated patients. This value correlated directly to post-transplant GFR (r = 0.48, P < 0.001). These data indicate that FK506-based immunosuppression differs from CsA by inducing less systemic vasoconstriction and hypertension. Renal vasoconstrictive effects were at least as great as those seen with CsA, however, and indicate that nephrotoxicity will remain a common feature to both regimens.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Renovascular hypertension.

Renovascular disease, particularly when associated with atherosclerosis, is a common cofactor in accelerating hypertension and deteriorating renal function. With increased longevity and effective antihypertensive medications, the prevalence of vascular lesions affecting renal viability is increasing, possibly accounting for 15% of end-stage renal disease. Renal vascular lesions alter renin release and multiple associated mechanisms related to adrenergic and vascular regulation. Several new diagnostic modalities, including captopril renography, duplex ultrasonography, and magnetic resonance angiography, are being applied for noninvasive diagnosis. Advances in interventional radiologic procedures, including endovascular stents and surgical revascularization, offer the potential for both improved blood pressure management and salvage of renal function. Optimal management of renovascular disease depends on careful assessment of the progression of each patient and associated risk of intervention.

Angioplasty, Balloon↗
PubMed1993

De novo hypertension after liver transplantation.

Hypertension develops in most patients after transplantation when immunosuppression is based on cyclosporine and prednisone. The pathogenesis appears to be multifactorial but involves rapidly rising vasoconstrictor tone in renal and systemic vascular beds. Much of this tone reflects abnormal vascular function, characterized by impaired prostacyclin and EDRF effects, in conjunction with increased vasoconstriction due to endothelin and possibly other factors. Effective management of the transplant recipient depends on preventing excessive vasoconstriction, usually with calcium channel blocking agents.

Adult↗
PubMed1992

Renal hemodynamics, urinary eicosanoids, and endothelin after liver transplantation.

Patients with hepatic cirrhosis develop widespread abnormalities in kidney function and vasoactive hormones. These change rapidly after liver transplantation during immunosuppression with cyclosporine. The role of changing eicosanoid excretion and endothelin levels in regulating renal function after transplantation in humans remains uncertain. We studied 32 patients with regard to renal hemodynamics, glomerular filtration, urinary prostacyclin (6-keto-PG-F1-alpha), thromboxane (TBX2), and endothelin before and during the first four weeks after orthotopic liver transplantation. Arterial pressure rose from 106 +/- 2/61 +/- 2 to 146 +/- 4/81 +/- 2 mmHg, (P less than .001), while renal blood flow fell (686 +/- 38 to 453 +/- 24 ml/min/1.73 m2, P less than .05), as did GFR. Pretransplant excretion of 6-keto and TBX2 was above that of normal subjects and fell progressively after transplant, as did plasma renin activity and aldosterone. The 6-keto levels fell below normal after two weeks. The ratio of TBX2/6-keto remained elevated compared with normal subjects throughout the month after transplant (1.54 +/- 0.38 vs. 0.54 +/- 0.07, P less than .01). Endothelin levels rose during the first week (7.4 +/- 1.4 vs. 12.4 +/- 2.7 pg/ml, P less than .05), but fell back to baseline thereafter. These results indicate that high levels of urinary eicosanoids in patients with liver disease fall rapidly after liver transplantation during CsA immunosuppression. Unlike results in many experimental models, these data suggest that renal vasoconstriction in humans may be associated primarily with suppression in renal prostacyclin excretion rather than stimulation of thromboxane.

Adult↗
PubMed1991

Elevation of plasma endothelin associated with systemic hypertension in humans following orthotopic liver transplantation.

Endothelin (ET) is a 21-amino-acid peptide of endothelial origin, is a potent systemic and renal vasoconstrictor associated with sodium retention and modulation of the renin-angiotensin-aldosterone system. The present study was designed to determine if plasma ET is elevated in humans with cirrhosis (n = 12), a state characterized by sodium retention and increased plasma renin activity (PRA) and plasma aldosterone (PA), and to determine the effect of orthotopic liver transplantation (OLT) upon plasma ET, PRA, and PA at 1, 3, and 7 days after transplantation. Plasma ET before OLT was 1.62 +/- 0.23 pg/ml, which was not different as compared with normal controls. Plasma ET significantly increased to 4.18 +/- 0.66, 3.87 +/- 0.58, and 4.07 +/- 0.61 pg/ml, respectively following OLT. PRA remained elevated throughout the postoperative course, in contrast to PA that decreased following OLT. Mean arterial pressure increased significantly from 82 +/- 4 pre-OLT to 98 +/- 4 and 103 +/- 2 mmHG on days 3 and 7 respectively.

Aldosterone↗
PubMed1991

Renal vascular response to sodium loading in sons of hypertensive parents.

Studies of normotensive offspring of hypertensive parents offer the potential to identify inherited abnormalities that contribute to essential hypertension. We compared renal and systemic hemodynamic responses to saline infusion between normotensive sons of two hypertensive parents (SOHT) and sons of two normotensive parents (SONT) selected from the general population of Rochester, Minn. Hemodynamic measurements were performed after a week of low sodium intake (10 meq/day) and were repeated after a week of high sodium intake (200 meq/day). Despite being in the normotensive range, blood pressures in SOHT were higher than those in SONT during low sodium (124 +/- 3/85 +/- 3 versus 118 +/- 2/71 +/- 2 mm Hg, p less than 0.01) and high sodium (122 +/- 3/80 +/- 3 versus 112 +/- 2/70 +/- 2 mm Hg, p less than 0.05) conditions. Higher pressures in SOHT were associated with elevated systemic and renal vascular resistance. After a high sodium diet, renal vascular resistance in SOHT rose further during acute saline infusion, whereas systemic vascular resistance did not change. After a low sodium diet, this renal vasoconstrictor response to saline infusion in SOHT was not present, and renal vascular resistance fell to levels not different from SONT. Plasma renin activity, aldosterone, and atrial natriuretic peptide did not differ between SONT and SOHT. Circulating levels of norepinephrine were higher in SOHT. These data demonstrate a renal vasoconstrictor response to saline infusion in normotensive SOHT, which depends on prior sodium intake. This alteration in renal hemodynamics may represent an inherited abnormality related to the development of hypertension.

Adult↗
PubMed1990

ACE inhibitors in renovascular hypertension.

ACE inhibition has provided many insights into the etiology and treatment of renovascular hypertension. Not only have studies using these agents profoundly expanded our understanding of the mechanisms governing preservation of renal perfusion pressures and function beyond arterial lesions, they have provided tools for more precise diagnosis and therapy in clinical practice. ACE inhibitors must be considered the agents of choice for the treatment of renovascular hypertension and provide an effective and safe medical alternative for many patients developing atherosclerotic renovascular lesions with an otherwise unacceptable risk for revascularization procedures. With the advent of widespread clinical use of these agents, however, come many new questions regarding the long-term fate of the kidney beyond vascular lesions and the need for preservation of renal function.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Altered pressor responses to NE and ANG II during cyclosporin A administration to conscious rats.

Vasoconstriction and hypertension have been prominent during cyclosporin A (CSA) administration. To evaluate whether CSA modulates vascular responsiveness to pressor stimuli in the intact organism, CSA was administered via osmotic pump (10 and 20 mg.kg-1.day-1 ip vs. olive oil vehicle) for 2 wk. After 8 days, arterial pressure and dose-response relationships to norepinephrine, angiotensin II, and bradykinin were measured in conscious animals. Despite similar initial pressures, dose-response relationships were markedly attenuated to both norepinephrine and angiotensin II. Maximal responses were not affected, indicating a rightward shift without loss of peak effect. Vasodilation with bradykinin was not diminished. These changes were not evident after an acute CSA infusion at the same dose (10 mg.kg-1.day-1 over 2 h). Treatment with verapamil (0.505 mg/kg over 2 days) lowered basal arterial pressures but did not change the effects of CSA on pressor sensitivity. Despite attenuated pressor responses, renal vascular resistance was elevated and glomerular filtration diminished during CSA administration. These observations indicate that cyclosporin modifies vascular responsiveness to pressor stimuli in the rat and may explain the relative resistance of this species to cyclosporin-induced hypertension.

Angiotensin II↗
PubMed1989

Alterations in blood pressure by derangement of the mechanisms that regulate sodium excretion.

Understanding the sequence of events responsible for pressure-related natriuresis and their pathophysiologic alterations may be useful in distinguishing various types of essential hypertension of renal origin. The perturbation of a distal step in the sequence is likely to be reflected in a simple physiologic defect. For instance, pathophysiologic alterations in the medullary production of prostaglandin E2 might directly influence natriuresis and diuresis because of its modulatory effect on tubular reabsorption of sodium and water. Perturbation of more proximal steps in the sequence could influence all the distal events as well. For instance, prostaglandin I2 and endothelium-derived relaxing factor may be produced by the preglomerular vasculature in response to alterations in renal perfusion pressure and may modulate the release of renin from the juxtaglomerular cells. Thus, variations in the production of prostaglandin I2 or endothelium-derived relaxing factor may be reflected by various renal vascular, tubular, and systemic homeostatic events related to the renin-angiotensin system.

Animals↗
PubMed1989

Management of mild hypertension.

The benefits of blood pressure reduction have been clearly established for diastolic pressures of more than 100 mm Hg. For patients with a diastolic pressure between 90 and 99 mm Hg on repeated measurements, treatment should be initiated if other risk factors are present--for example, a family history of coronary risk, increased cholesterol level, male sex, smoking, or diabetes mellitus. When the pressure seems to be labile or exaggerated in the office, home or ambulatory readings may provide confirmatory information. For persons with diastolic pressures in the range of 90 to 94 mm Hg, it may be suitable to initiate therapy with nonpharmacologic maneuvers such as sodium restriction, weight reduction, and physical conditioning. In such cases, careful follow-up of blood pressure is particularly important because it may increase later. The initial therapy for mild hypertension should be selected to minimize adverse effects and should be tailored to the individual patient. Management of all levels of hypertension must be considered in light of the associated risk factors and a concomitant effort to minimize cardiovascular risk.

Age Factors↗
PubMed1988

Post-stenotic arterial pressures, renal haemodynamics and sodium excretion during graded pressure reduction in conscious rats with one- and two-kidney coarctation hypertension.

Study of rat models of renovascular hypertension has been limited by the difficulty in measuring the post-stenotic pressures in conscious animals. We studied a model using inter-renal aortic coarctation (0.33 mm clip) in which post-stenotic (iliac) and systemic (carotid) pressures could be measured chronically. One-kidney-coarctation (1K-coarctation) rats (analagous to one-kidney, one clip hypertension) were compared to two-kidney-coarctation (2K-coarctation) and 1K-sham-coarctation groups. After coarctation, post-stenotic pressures fell to 40 +/- 4 mmHg then rose to normal over 5 days, concomitantly with a rise in systemic pressure to 141 +/- 6 mmHg. 1K-coarctation animals developed consistently higher post-stenotic pressures than 2K-coarctation rats after 6 weeks. Reduction of systemic pressures to normal with sodium nitroprusside induced major decrements in renal function in 1K-coarctation rats [effective renal plasma flow (ERPF): 4.32 +/- 0.40 to 1.41 +/- 0.28 ml/min; P less than 0.01; glomerular filtration rate (GFR), 1.56 +/- 0.18 to 0.42 +/- 0.33 ml/min, P less than 0.01], but not in 2K-coarctation or 1K-sham-coarctation groups. This produced an abrupt decrease in filtered sodium load, which combined with a decline in fractional sodium excretion during pressure reduction to make 1K-coarctation rats especially sensitive to fluctuations in renal artery pressure. We propose that a marked dependence upon post-stenotic perfusion pressures to maintain sodium homeostasis may be involved in sustaining hypertension in 1K-renovascular models. Inter-renal coarctation provides a valuable model for studying post-stenotic haemodynamic changes in chronically instrumented rats.

Animals↗