Hypertensive Vascular Changes Research Articles

5 Ocular Changes in Hemodialysis Patients

Chronic renal failure is characterized by numerous disorders that involve many organs. In dialysis patients, some disorders could be the consequence of the dialysis treatment per se. The aim of our study was to evaluate the ocular changes in hemodialysis patients.In 64 patients undergoing hemodialysis (30 female and 34 male), aged 24–83 years (mean 58 years) and on hemodialysis 1–213 months (mean 47 months), complete ocular examination was performed: visual acuity (VA), intraocular pressure (IOP), biomicroscopic examination, and fundoscopy. All patients were on hemodialysis 3 times a week, for 4 hours; bicarbonate dialysate was used with 1.5 mmol/L Ca concentration. Most of the patients were on calcitriol therapy and calcium carbonate were used as phosphate binders. Heparin was used during hemodialysis in all patients in a dose up to 4000 i.u. Visual acuity was impaired in 84% of patients; mean IOP was 15 mmHg (right eye) and 14 mmHg (left eye) (normal vale 11–20 mmHg). Thirty‐nine patients (60%) have cataracts, 6 of them were operated. Hypertensive vascular changes were seen in 44 (68%) patients and in 6 patients age related macular degeneration was observed. Diabetic nonprolipherative or prolipherative changes were seen in 5 of 7 diabetic patients. In 3 patients, argon laser coagulopathy was performed. Ocular calcifications were found in 14 patients. No correlation of ocular calcification and parathyroid hormone PTH level or calcium–phosphate product was observed.Patients with CRF or who are receiving dialysis represent a unique group of patients. Pathologic changes could be found in many organs; therefore, we suggest more frequent complete ocular examination in dialysis patients.

Vascular cognitive impairment: introduction.

One of the greatest advances in the understanding of cognitive disorders comes from the realization that Alzheimer disease (AD) and vascular cognitive impairment share common risk factors. This opens the door to a common approach to both and promises that if vascular risk factors are controlled, then not only strokes but also cognitive impairment could be prevented. It also has become evident that AD pathology and vascular lesions often coexist in the brains of the elderly. Less certain is whether the effects are additive or multiplicative. Gorelick1 reviews and categorizes systematically the different …

Pathogenesis of structural vascular changes in hypertension

Pathogenesis of structural vascular changes in hypertension

Prolonged Nitric Oxide Inhalation Fails to Regress Hypoxic Vascular Remodeling in Rat Lung

The purpose of present study was to investigate whether long-term nitric oxide (NO) inhalation during the recovery in air might improve the regression of chronic hypoxic pulmonary hypertension (PH) and vascular changes. The rats were exposed to 10 ppm of NO in air for 10 days (n = 12) and 30 days (n = 4), or 40 ppm of NO in air for 10 days (n = 6) and 30 days (n = 12) following 10 days of hypobaric hypoxia (380 mm Hg, 10% oxygen). For each NO group, air control rats following hypoxic exposure were studied at the same time (n = 13, 11, 9, and 11, respectively). Normal air rats (n = 6) without hypoxic exposure and rats (n = 7) following 10 days of hypoxic exposure were used as normal and chronic hypoxic control groups, respectively. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. An additional 16 rats were used to investigate the recovery of pulmonary artery pressure with (n = 8) and without NO inhalation (n = 8) after 10 days of hypobaric hypoxia. Long-term hypoxia-induced PH, right ventricular hypertrophy (RVH), and hypertensive pulmonary vascular changes, each of which regressed partly after recovery in room air. There were no differences among rats with and without NO during each recovery period in RVH, medial wall thickness of muscular artery, and the percentages of muscularized arteries at the alveolar wall and duct levels. Continuous inhaled 40 ppm NO decreased pulmonary artery pressure from 40.1 +/- 1.1 to 29.9 +/- 3.8 mm Hg (mean +/- SE) [n = 8], which was not different in the rats without NO inhalation (n = 8). Urine nitrate level was higher in rats that had inhaled NO. Continuous NO inhalation showed no effect on regression of pulmonary vascular remodeling in chronic hypoxic PH after returning to room air.

Pathogenesis of structural vascular changes in hypertension.

The pathogenic role of angiotensin II (ANG II), dietary sodium chloride, sympathetic activation, obesity and aldosterone in the development of structural vascular changes (SVCs) in hypertension is considered from three perspectives (criteria): their utility in predicting hypertension and its complications (predictability); the effect of their inhibition or removal on the reversal of SVCs (reversibility); and their ability to induce SVCs in experimental animals (reproducibility). Only ANG II meets all three criteria. Importantly, ANG II increases preglomerular vascular resistance by inducing structural changes in renal cortical resistance arteries and arterioles. High salt intake, by dilating and thereby stiffening some arteries, may play a role in the development of systolic hypertension with aging, but does not produce structural changes in renal cortical resistance vessels. While high circulating levels of norepinephrine are associated with SVCs, the experimental evidence for the role of sympathetic nerve stimulation in the development of SVCs is inconclusive. Obesity is associated with hypertension, but is not known to be associated with SVCs. Salt-loading is required for aldosterone to produce SVCs, but vascular pathology in this experimental model differs from that in benign essential hypertension. The findings of this review indicate that SVCs in extra-renal sites by themselves do not lead to hypertension; structural changes in renal cortical arteries and arterioles that increase preglomerular vascular resistance are needed. Progressive trophic stimulation of preglomerular resistance vessels by itself may lead to hypertension. ANG II is prime candidate for such stimulus.

Relación entre la gravedad de la hipertensión arterial esencial y la prevalencia de hiperuricemia

Hyperuricemia has been associated with an increased risk of cardiovascular disease in hypertensive patients. However, the relation between serum urate and severity of hypertension has not been conclusively defined as yet. We aimed at finding out whether there exists an independent relationship between changes in the prevalence of hyperuricemia and severity of hypertension. We studied 3 cohorts of patients aged 35 to 60 years with essential hypertension diagnosed at a university hospital in Madrid, Spain. The first cohort (before 1981) included 325 patients, the second (from 1981 to 1989) comprised 271 patients and the third cohort (from 1990 to 1999) included 545 patients. Disease severity ranged from 1 to 6 according to blood pressure levels at diagnosis (WHO/ISH grades 1, 2 or 3 were assigned 1, 2 or 3 points, respectively) and target organ damage (left ventricular hypertrophy, hypertensive retinal vascular changes, and proteinuria above 300 mg/day; one point each). Mean serum urate concentrations in the 3 cohorts were 6.6, 5.8 and 5.5 mg/dL, respectively (p < 0.05 for all comparisons). 39% of patients in the first cohort had a serum urate concentration > 7.0 mg/dL whereas only 18.1% patients in the third group showed hyperuricemia (difference: 20.9%; 95% CI, 10.1 to 32.3; p < 0.05). Severity of hypertension was higher in the first cohort (mean SD, 2.50 1.31 points) than in the third group (1.96 1.06 points; p < 0.05), with the second cohort showing an intermediate severity (2.23 1.01 points). Serum urate levels were directly related to the severity of hypertension in the 3 groups (r = 0.08, p < 0.05). In a multivariate analysis, after adjustment for confounding variables, serum urate had no significant association with severity of hypertension. However, target organ damage, systolic blood pressure and serum creatinine were all independent predictors of severity. Favourable changes in the severity of hypertension for a time period significantly correlate with decreases in hyperuricemia prevalence in the same period. On the other hand, hyperuricemia appears to be an indirect marker of hypertensive renal damage.

Novel signaling pathways contributing to vascular changes in hypertension.

In hypertension, increased peripheral resistance maintains elevated levels of arterial blood pressure. The increase in peripheral resistance results, in part, from abnormal constrictor and dilator responses and vascular remodeling. In this review, we consider four cellular signaling pathways as possible explanations for these abnormal vascular responses: (1) augmented signaling via the epidermal growth factor receptor to cause remodeling of the cerebrovasculature; (2) reduced sphingolipid signaling leading to blunted vasodilation and increased smooth muscle proliferation; (3) increased signaling via Rho/Rho kinase leading to enhanced vasoconstriction, and (4) a relative state of microtubular depolymerization favoring vasoconstriction in hypertension. These novel cell signaling pathways provide new pharmacological targets to reduce total peripheral vascular resistance in hypertension.

Role of pulse pressure in determining structural vascular changes in hypertension

Role of pulse pressure in determining structural vascular changes in hypertension

Estradiol improves pulmonary hemodynamics and vascular remodeling in perinatal pulmonary hypertension.

Partial ligation of the ductus arteriosus (DA) in the fetal lamb causes sustained elevation of pulmonary vascular resistance (PVR) and hypertensive structural changes in small pulmonary arteries, providing an animal model for persistent pulmonary hypertension of the newborn. Based on its vasodilator and antimitogenic properties in other experimental studies, we hypothesized that estradiol (E(2)) would attenuate the pulmonary vascular structural and hemodynamic changes caused by pulmonary hypertension in utero. To test our hypothesis, we treated chronically instrumented fetal lambs (128 days, term = 147 days) with daily infusions of E(2) (10 microg; E(2) group, n = 6) or saline (control group, n = 5) after partial ligation of the DA. We measured intrauterine pulmonary and systemic artery pressures in both groups throughout the study period. After 8 days, we delivered the study animals by cesarean section to measure their hemodynamic responses to birth-related stimuli. Although pulmonary and systemic arterial pressures were not different in utero, fetal PVR immediately before ventilation was reduced in the E(2)-treated group (2.43 +/- 0.79 vs. 1.48 +/- 0.26 mmHg. ml(-1). min, control vs. E(2), P < 0.05). During the subsequent delivery study, PVR was lower in the E(2)-treated group in response to ventilation with hypoxic gas but was not different between groups with ventilation with 100% O(2). During mechanical ventilation after delivery, arterial partial O(2) pressure was higher in E(2) animals than controls (41 +/- 11 vs. 80 +/- 35 Torr, control vs. E(2), P < 0. 05). Morphometric studies of hypertensive vascular changes revealed that E(2) treatment decreased wall thickness of small pulmonary arteries (59 +/- 1 vs. 48 +/- 1%, control vs. E(2), P < 0.01). We conclude that chronic E(2) treatment in utero attenuates the pulmonary hemodynamic and histological changes caused by DA ligation in fetal lambs.

Effects of cilazapril on the retinal vessels in spontaneously hypertensive rats: Corrosion cast and scanning electron microscopic study

The effects of the long-term oral angiotensin-converting enzyme inhibitor, cilazapril, on retinal circulation in stroke-prone spontaneously hypertensive (SHR-SP) rats were assessed by scanning electron microscopy (SEM), corrosion casts and transmission electron microscopy (TEM). Two groups of 20 male SHR-SP rats were compared. One group was treated with 10 mg/kg/day of cilazapril from 4 to 40 weeks of age, and the other group received no treatment. A third group of male Wistar-Kyoto (WKY) rats served as age-matched controls. At regular intervals the rats were weighed, and their systolic blood pressure was measured. Cilazapril normalized systolic arterial pressure to 121 ± 2.7 mm Hg (SD) in the treated SHR-SP rats. There was no significant difference in body weight between the two groups of SHR-SP. In the 40-week-old SHR-SP rats without treatment corrosion cast and SEM revealed hypertensive retinal vascular changes. In the 40-week-old SHR-SP rats treated with cilazapril, these changes were markedly decreased to the level seen in WKY rats. The differences in caliber of retinal capillaries between the treated SHR-SP and untreated SHR-SP rats were statistically significant (p < .0001). TEM in the cilazapril-treated SHR-SP rats revealed intact basement membranes (0.29 ± 0.057 μ m) of the endothelial cells and pericytes, but in the untreated SHR-SP rats the basement membrane was thickened (0.51 ± 0.123 μm) (p < .0001) and the pericytes damaged. Our results show that the long-term administration of cilazapril decreased systolic arterial pressure to a nearly normal level and prevented hypertensive retinal vascular changes, probably by improving endothelial function. The effects of cilazapril on the retinal vasculature are described for the first time. SEM of corrosion casts is a valuable technique for showing the effects of some drugs on the vasculature easily, precisely and three-dimensionally.

Inhaled nitric oxide and aerosolized prostaglandin therapies

Inhaled nitric oxide (NO) therapy is becoming an indispensable measure in neonatal intensive care to rescue critically ill neonates with hypoxemic respiratory failure. Inhaled NO improves oxygenation and reduces pulmonary hypertension, but it also may have the following beneficial effects: (1) decreasing pulmonary capillary pressure; (2) inhibiting pulmonary microvascular leaks; (3) inhibiting pulmonary leukocyte aggregation and adhesion; (4) inhibiting pulmonary platelet aggregation and adhesion; and (5) inhibiting hypertensive pulmonary vascular changes. Inhaled NO therapy has been receiving much attention as a preventive measure for acute respiratory distress syndrome and pulmonary hypertensive diseases. The indices for improvement of oxygenation and the measures for augmentation of oxygenation during inhaled NO are beginning to be described, but no device for inhaled NO therapy exists which can be used easily and safely by anyone. Aerosolized prostaglandin therapy has not yet been established either. Neither therapy should be performed without obtaining informed consent and institutional approval.

Hypertensive structural changes in systemic precapillary resistance vessels

To discuss recent findings that seem to question the importance of structural vascular changes for the raised resistance observed in hypertension. First, in daily life situations, the proximal resistance sections, which are the main site for vasoconstrictor fibre effects, are also the main site for structural elevation of resistance in hypertension. The most distal ones are crucially important for local flow distribution, and their unaltered design suggests that they are usually protected from pressure elevations by a raised resistance upstream. Furthermore, recent findings indicate that central neurohormonal mechanisms are much more important than myogenic ones for inducing hypertension at least in spontaneously hypertensive rats. Second, the function of structurally altered resistance vessels is often misunderstood, mainly because the haemodynamic importance of wall distensibility is disregarded. Vascular geometric design and distensibility tend to be altered to an 'ideal' extent, so that with ordinary changes in smooth muscle activity a normal flow range is maintained, despite elevations in both perfusion and transmural pressures and in resistance. Third, the rapid normalization of blood pressure on declipping of two-kidney, one clip or of one-kidney, one clip renally hypertensive rats by no means refutes the haemodynamic importance of a prevailing structural upward resetting. Declipping leads to a powerful and prolonged release of vasodilator-sympathoinhibitory medullipins, which create a subnormal smooth muscle tone. Because the structurally hyper-reactive resistance vessels now operate along a steeper resistance curve the pressure fall becomes, if anything, accentuated, which opens the way for structural regression. Fourth, the highly sophisticated and often differentiated neurohormonal control system usually explains why vasoactive agents, for example, do not regularly produce exaggerated pressure changes in vivo, even in the presence of hypertensive structural changes. In addition, counteracting effects by endothelial mechanosensitive mechanisms seem to be of great importance in these situations. The arguments and views outlined recently do not, on closer scrutiny and for the reasons given, really challenge the importance of structural vascular changes in hypertension in vivo and may, indeed, in some respects serve to support this concept.

Influence of hypertensive vascular changes in intratesticular arteries on spermatogenesis in SHRSP.

1. The process of the spermatogenetic damage induced by hypertensive vascular changes was studied with stroke-prone spontaneously hypertensive rats (SHRSP). 2. In SHRSP, hypertensive changes in intratesticular arterioles developed from 19 weeks of age. 3. At 23 weeks of age, a severe reduction in the number of mature and immature spermatids was observed. 4. The transferrin concentration in testicular cytosol was decreased at 23 weeks of age, suggesting that Sertoli cell function in SHRSP had regressed. 5. In conclusion, it was suggested that the decline in Sertoli cell function as a result of hypertensive vascular changes is part of the mechanism whereby spermatogenic damage occurs in SHRSP.

Protective effects of manidipine on spermatogenesis in stroke-prone spontaneously hypertensive rats.

1. We evaluated the protective effects of manidipine on spermatogenic damage induced by the hypertensive vascular changes in stroke-prone spontaneously hypertensive rats (SHRSP). 2. Blood pressure reached more than 250 mmHg in SHRSP at 15 weeks of age, and thereafter the hypertensive changes in testicular arterioles developed. Manidipine reduced both the blood pressure and the hypertensive vascular changes. 3. Although immature and mature spermatids greatly diminished in SHRSP at 23 weeks of age, manidipine could preserve almost normal spermatogenesis even at 23 weeks of age. Transferrin concentration in testicular cytosol, which was considered to be indicative of the Sertoli cell function, in SHRSP with manidipine administration was significantly higher than that in SHRSP with no treatment at 23 weeks of age. 4. In conclusion, manidipine could prevent the development of the hypertensive changes in intratesticular arterioles and maintain normal Sertoli cell function. As a result, manidipine protected spermatogenic damage in SHRSP.

OCULAR FUNDUS CHANGES IN MALIGNANT OR PRECOCIOUS STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS AFTER ADMINISTRATION OF ANTIHYPERTENSIVE DRUGS

1. Malignant or precocious stroke-prone spontaneously hypertensive rats (M-SHRSP) showed hypertensive ocular fundus changes with severe hypertension, but various anti-hypertensive drugs given over a proper period improved funduscopic findings. 2. We treated a M-SHRSP with SQ29,852 (an angiotensin converting enzyme inhibitor, ACEI) or manidipine (a calcium antagonist) and observed hypertensive vascular changes in the fundus. 3. The M-SHRSP treated with anti-hypertensive drugs lived longer and the hypertensive fundic changes improved in both groups. But there were some differences of histochemical staining reaction on the endothelial cell-surface and mucopolysaccharides accumulations between the treated group of ACEI and the group treated with the calcium antagonist. 4. In the treated group with calcium antagonist, the anionic ion functions of the endothelial cell-surface were impaired and organic retinal or choroidal damages appeared to have deteriorated.

Assessment of the cardiovascular effects of stress.

The stress response increases sympathetic nervous activity, which can adversely affect the cardiovascular system. Cardiovascular disease is due in part to stress-induced mechanisms mediated primarily through increased adrenergic stimulation. These stress-induced mechanisms include elevations in serum lipid levels, alterations in blood coagulation, atherogenesis, vascular changes in hypertension, and myocardial ischemia. Stress management interventions for hypertension are controversial; however, interventions for coronary heart disease-prone behavior patterns have proven successful. Stress management interventions have also reduced cardiovascular events, mortality, and coronary atherosclerosis. Assessment of stress includes individual interviews, which can be complemented by information derived from questionnaires and mental stress testing. Educational and relaxation strategies can prepare patients to understand and cope with stress. These approaches will hopefully decrease the occurrence of stress and, ultimately, the risk for cardiovascular disease.

Portal hypertension in children.

Portal hypertension is an uncommon but serious complication in children. The etiology may be intrahepatic or from an extrahepatic vascular occlusion. The pathophysiology is unknown, but the development of increased vascular resistance and portal flow are believed to be the primary changes. Increased portal flow is created by a decrease in systemic vascular resistance regionalized to the splanchnic vascular bed. Abnormally reduced response to vasoactive substances may be responsible. Advances in ultrasonography and endoscopy may improve our ability to evaluate portal hypertensive vascular changes. However, pharmacologic management is still limited to controlling the hemodynamic disturbances after they have occurred. Nonsurgical shunt management is increasingly being used in children, limiting the need for surgical shunt placement. Liver transplantation is now a viable option for managing end-stage disease. Future management depends on understanding the role of vasoactive substances controlling portal flow velocity, subsequent development of targeted pharmacologic therapy, and application of nonsurgical shunt technology in children. Transjugular intrahepatic portosystemic shunt placement is the next technologic advance moving from the adult into the pediatric realm.

Investigation of the arterial and venous upper arm vascular bed

Studies concerning vascular changes in hypertension and exercise have shown an increasing need to investigate the properties of a complete vascular bed in vivo. In this study, the repeatability of a non-invasive method for quantifying properties of the vascular bed of an upper arm segment, was investigated in two groups of volunteers (age 22–55 years). One group of subjects (n = 9) were measured twice at a 15 min interval. The other group (n = 8) were measured 4 times with each subject measured daily at the same time. The estimated quantities included the arterial and venous blood volume, the static arterial compliance, the myogenic response of the arm veins and the extravascular fluid volume of the tissue under an occluding cuff at the upper arm. They not only describe properties of the arterial vascular bed as a whole but also of different sized arteries functioning at different intra-arterial pressure. They were derived from the fluid shifts under the occluding cuff that arise when cuff pressure changes, as determined by electrical impedance and blood pressure measurements. The repeatability of the method was well within the physiologically acceptable range and of the same order of magnitude as that of established methods. Established methods however, provide less information about the properties of a vascular bed and result in controversial estimates of the dynamic arterial compliance. Furthermore, the method eliminates the need to match subjects in comparative studies for arterial blood pressure. These features and the sensitivity of the method for (patho)physiological changes, offer the possibility to investigate in vivo many still unknown aspects of the peripheral circulation.

Ocular disease associated with hypertension in 16 cats

ABSTRACTBetween 1990 and 1993, 16 cats were referred with acute onset blindness or intraocular haemorrhage. Blood pressure assessment, using the Doppler ultrasonic recording technique in 11 of the cats, proved these cases to be hypertensive. Fifteen cats underwent further investigation, revealing 13 with some degree of renal impairment and one as hyperthyroid. Five underwent cardiac ultrasound and all showed evidence of cardiac hypertrophy. The eyes from four of the cats were examined histologically and showed serous or haemorrhagic retinal detachments with varying degrees of retinal degeneration and a range of ocular hypertensive vascular changes. Two cats had full post mortem examinations which revealed evidence of renal and thyroid pathology.

Hypertensive Vascular Changes in the Optic Nerve of M-SHRSP

Hypertensive Vascular Changes in the Optic Nerve of M-SHRSP