Blood Pressure In Recipients Research Articles

Gut microbiota and arterial hypertension (a literature review)

The aim of the work was to analyze and collate literature data on the role of the gut microbiota disorders in the pathogenesis of arterial hypertension and to determine the prospects for further research.Results. The article presents the results of studies that indicate the significant role of various components of the gut microbiota disorders in the development of arterial hypertension in experimental animals and humans. The accumulated data allow for consideration of the gut microiota as a part of a complex system involved in the regulation of blood pressure. Studies using fecal microbiota transplantation showed that the fecal microbiome transfer from hypertensive animals or patients with arterial hypertension to normotensive animals led to an increase in blood pressure in the latter. At the same time, transplantation of microbiota from normotensive animals to hypertensive resulted in a decrease in blood pressure in recipients. It was revealed that the leading dysbiotic factors that play the most significant role in the mechanisms of arterial hypertension development are the composition of the gut microbiota, the Firmicutes/Bacteroidetes ratio, the state of the tight junction proteins in the gut epithelium, the gut epithelial permeability to lipopolysaccharides, endotoxinemia, subclinical systemic inflammation, the levels of trimethylamine N-oxide and short-chain fatty acids production, as well as the relationship between the latter and specific Olfr and GPR receptors.Conclusions. The analyzed results of the studies indicate the involvement of gut microbiota disorders in the pathogenesis of arterial hypertension. However, the role of individual components of the gut microbiota in the mechanisms of blood pressure regulation and the development of hypertensive damage to target organs and complications remains poorly understood. Promising areas of the research are the development of informative methods for assessing the state of gut microbiota and fundamentally new approaches for reducing the risk of hypertension development and progression by the correction of occurring disorders.

Ambulatory Blood Pressure Monitoring: Profiles in Chronic Kidney Disease Patients and Utility in Management.

Optimal control of blood pressure (BP) may reduce the risk of progression of CKD. Misclassification of hypertension (HTN) and status of control may result in suboptimal management. Clinic or home BP may overestimate or underestimate status of control compared with ambulatory BP monitoring (ABPM), which is considered the gold standard. The latter relates not only to the superiority of ABPM concerning outcome prognosis but also to its ability to accurately diagnose white coat and masked HTN, which is critical in assuring adequate BP control. However, ABPM has not gained widespread use in practice because of limited third-party reimbursement and a paucity of high quality randomized controlled intervention studies evaluating its use. Herein, we review HTN phenotypes that have been identified in patients with CKD, and the potential value of ABPM in this high-risk population.

A cornerstone in the history of hypertension: the seventieth anniversary of the discovery of angiotensin

In 1939, two independent teams, in Buenos Aires and Indianapolis, identified the polypeptide angiotensin. In 1934, Goldblatt et al. demonstrated that partial occlusion of the renal arteries produces hypertension in dogs, and Houssay in 1936 predicted the presence of a humoral mechanism and, with Fasciolo, demonstrated that the ischemic kidneys released a pressor substance that increased the recipient's blood pressure. Later on, Taquini proved that the rise in blood pressure that follows the re-establishment of circulation in kidneys was also produced by a plasmatic substance from the venous blood of acute ischemic kidneys and it was called 'hypertensin'. Then, they proved that it was the result of an enzymatic reaction in which renin was the enzyme and plasma the substrate. At the same time, in 1939, Page et al. postulated that renin activated by plasma becomes vasoactive and the substance was called 'angiotonin'. Page's group began in 1937, with the purification of renin, studying its renal hemodynamic effects. Later on, Page et al. acknowledged in 1943 the enzymatic nature of the system and renamed their so-called renin-activator as renin substrate. Both groups fused the two original names into 'angiotensin' during a meeting at Michigan in 1958, making the 'adventure of the discovery of angiotensin' a reality.

The impact of a threatening e‐mail reprimand on the recipient's blood pressure

PurposeThis article aims to describe the effects of the communication style of the message sender (threatening or neutral), status of the sender (equal to or higher than the recipient) and the power relationship between sender and recipient (from the same department or not) on the blood pressure of the recipient of an e‐mail messageDesign/methodology/approachThe study was conducted under controlled laboratory conditions. The experiment was a mixed design, using both within and between subjects variables. The independent variable for the within subjects factor was the task that participants performed. There were three tasks: answering a questionnaire, reading a non‐threateningly worded e‐mail reprimand, and reading a threateningly worded e‐mail reprimand. Although the study used students as participants, the messages they received were from real people in a University College. Discusses the implications in the area of occupational health.FindingsDiastolic blood pressure was significantly higher (p<0.01) when recipients were reading the threateningly worded reprimand compared to reading a non‐threateningly worded reprimand. The effect of status on blood pressure was significant (p<0.05) but only for recipients in the same department as the message sender.Originality/valueThe results add to the evidence that communication style and status can have a direct impact on the recipient's physiological response.

Experimental heterotopic heart transplantation without cardiopulmonary bypass: auxiliary support for the recipient heart

Background: Auxiliary cardiac support using heterotopic heart transplant is of considerable interest, but the outcome is not known. To investigate technical feasibility and the possibility of using auxiliary support from heterotopic heart transplantation without cardiopulmonary bypass, we evaluated hemodynamics including the pressure–volume relationship in experimental animals. Methods In heterotopic heart transplantation, we tailored the donor heart by removing the pulmonary and tricuspid valves, and by wide removal of the inter-atrial septum. Next, we anastomosed the descending aorta and left atrium of the donor heart to the descending aorta and left atrium of the recipient, without using cardiopulmonary bypass. Consequently, declamping the recipient’s descending aorta allowed the donor heart to fill with blood and to start beating. We performed hemodynamic assessments including the effects of adrenergic stimulation. We measured the pressure and volume relationship of the recipient heart by closing and opening inflow of the donor left atrium to change the pre-load of the donor left ventricle. Results The donor left ventricle produced a systolic blood pressure that was augmented by the recipient blood pressure and responded to adrenergic stimulation. When inflow of the donor left atrium was opened, the pressure–volume loop of the recipient heart shifted to the left and pressure–volume area decreased. Simultaneously, the mechanical efficiency and E max (the slope of the end-systolic pressure-volume relationship) of the recipient heart increased when inflow of the donor left atrium was opened. Conclusions This transplant model, without cardiopulmonary bypass, is feasible and can be applied to transplant investigations as a working heart model on the basis of the response of adrenergic stimulation. The increased pre-load of the donor left atrium from the recipient left atrium resulted in a recipient leftward shift of the pressure–volume relationship, suggesting that this transplant model with adequate pre-load acts as auxiliary assistance in the recipient intrathoracic cavity.

How aggressively should blood pressure be treated in renal transplant recipients?

Renal transplantation is the treatment of choice for many patients with endstage renal disease. Patient survival is improved compared with dialysis for all patient ages and racial groups. Renal allograft survival is closely connected with recipient blood pressure. Blood pressure treatment goals that improve patient outcome have been defined for patients with nontransplant renal disease but not for patients with renal transplants. Extrapolating from data from nonrenal transplant patients suggests that aggressive treatment of hypertension in renal transplant patients may improve allograft and patient survival.

Association of chronic kidney graft failure with recipient blood pressure

Immunological rejection is the most important cause of kidney transplant failure. Recently, nonimmunological causes of long-term allograft failure have become more widely appreciated. In primary chronic renal disease, blood pressure is of overriding importance for long-term renal function. The role of blood pressure in determining long-term transplant outcome has not yet been established. We studied the influence of blood pressure post-transplantation on long-term kidney graft outcome in 29,751 patients. Outpatient blood pressure measurements were recorded and reported to the Collaborative Transplant Study. Graft and patient survival rates were analyzed over seven years in relation to blood pressure. Increased levels of systolic and diastolic blood pressure post-transplantation were associated with a graded increase of subsequent graft failure (P < 0.0001). Chronic graft failure was significantly associated with blood pressure even when patient death was censored (P < 0.0001). Cox regression analysis established increased blood pressure as an independent risk factor for graft failure. We conclude that post-transplant blood pressure is a highly significant predictor of long-term kidney graft outcome. Whether aggressive lowering of blood pressure improves long-term transplant outcome will have to be studied prospectively.

Growth and Function of En Bloc Infant Kidney Transplants: A Preliminary Study

We evaluated the growth and function of 21 pairs of en bloc infant kidneys transplanted into adult recipients. Serum creatinine, 99mtechnetium-diethylenetriaminepentaacetic acid glomerular filtration rates, kidney volumes and resistive indexes were determined at 1 to 3, 3 to 6 and beyond 6 months, and compared using repeated measures analysis of variance tests. En bloc kidneys grew at a statistically significant rate (p < 0.001), for example nearly 2-fold in 3 to 6 months (209 +/- 69 cc from 132 +/- 70 cc), and approaching 3-fold at 6 months and longer (325 +/- 106 cc). Similarly, the glomerular filtration rates increased almost 4-fold (83 +/- 52 ml. from 23 +/- 11 ml. per minute) and 5-fold (121 +/- 45 ml., p < 0.001), respectively, during the same periods. Resistive indexes remained at normal range (0.60 to 0.63). Recipient blood pressure was normal. Our study shows that infant en bloc kidney transplants grow rapidly and provide excellent function to the adult recipient.

Source of kidney determines blood pressure in young renal transplanted rats.

Recipients of a renal graft from adult stroke-prone spontaneously hypertensive rat (SHRSP) but not normotensive Wistar-Kyoto rat (WKY) donors have been shown to develop posttransplantation hypertension. To investigate whether hypertension would also travel with the kidneys from young prehypertensive SHRSP and whether the age-related increase in blood pressure in F1 hybrids (F1H) bred from SHRSP and WKY parents was attenuated by early bilateral nephrectomy and transplantation of a WKY kidney, we transplanted kidneys from 14 male SHRSP and 16 WKY donors aged 35-42 days to young male F1H. Recipients had both native kidneys removed. Fifteen unilaterally nephrectomized nontransplanted F1H served as controls. At the time when kidneys were harvested for transplantation, systolic blood pressures in young SHRSP and WKY donors were not significantly different (114 +/- 5 vs. 113 +/- 3 mmHg). After transplantation, recipients of an SHRSP kidney rapidly developed posttransplantation hypertension with systolic blood pressures above 180 mmHg at 3 mo after transplantation. In contrast, systolic blood pressure in recipients of a WKY kidney rose only slightly with increasing age and remained significantly lower than in non-transplanted controls. Transplanted rats exhibited normal weight gain, and renal function (glomerular filtration rate, renal blood flow) in grafted kidneys was well preserved; plasma renin activity was reduced compared with nontransplanted controls. These data demonstrate that 1) hypertension can be transmitted to normotensive recipients by transplantation of a kidney from young prehypertensive SHRSP donors and 2) the age-related increase in arterial pressure in F1H is attenuated by early bilateral nephrectomy and transplantation of a WKY kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension transmitted by kidneys from stroke-prone spontaneously hypertensive rats.

We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar-Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension.

HYPERTENSION AFTER RENAL TRANSPLANTATION

Hypertension is a common complication after renal transplantation and is associated with increased mortality. Cyclosporine is known to be nephrotoxic and raises blood pressure in recipients of cardiac and bone marrow transplants, but there is conflicting data on the role of cyclosporine after renal transplantation. We have examined this question in patients entered into the second Oxford prospective randomized comparison of short-term cyclosporine treatment alone with conversion to azathioprine and prednisolone at 90 days (CsA group), and conventional therapy with azathioprine and prednisolone throughout (AP group). Blood pressure and antihypertensive medication were similar in the CsA and AP treatment groups during the first 90 days. Following conversion from cyclosporine, mean blood pressure fell from 155/94 to 142/81 within 7 days, and this fall correlated with the change in plasma creatinine over the same period (r = 0.44,P<0.05). Blood pressure was subsequently lower in the converted patients than in those treated with AP throughout. Six months after transplantation patients converted from cyclosporine not only had lower blood pressure but also required fewer antihypertensive drugs than AP patients. This study demonstrates that cyclosporine may elevate the blood pressure in recipients of renal transplants. This effect may either be direct or mediated through the effect of cyclosporine on renal function. Administration of corticosteroids during the first three months after transplantation is implicated as a possible cause of persisting high blood pressure.

HYPERTENSION AFTER RENAL TRANSPLANTATION

Hypertension is a common complication after renal transplantation and is associated with increased mortality. Cyclosporine is known to be nephrotoxic and raises blood pressure in recipients of cardiac and bone marrow transplants, but there is conflicting data on the role of cyclosporine after renal transplantation. We have examined this question in patients entered into the second Oxford prospective randomized comparison of short-term cyclosporine treatment alone with conversion to azathioprine and prednisolone at 90 days (CsA group), and conventional therapy with azathioprine and prednisolone throughout (AP group). Blood pressure and antihypertensive medication were similar in the CsA and AP treatment groups during the first 90 days. Following conversion from cyclosporine, mean blood pressure fell from 155/94 to 142/81 within 7 days, and this fall correlated with the change in plasma creatinine over the same period (r = 0.44, P less than 0.05). Blood pressure was subsequently lower in the converted patients than in those treated with AP throughout. Six months after transplantation patients converted from cyclosporine not only had lower blood pressure but also required fewer antihypertensive drugs than AP patients. This study demonstrates that cyclosporine may elevate the blood pressure in recipients of renal transplants. This effect may either be direct or mediated through the effect of cyclosporine on renal function. Administration of corticosteroids during the first three months after transplantation is implicated as a possible cause of persisting high blood pressure.

Prednisolone and posttransplantation hypertension in rat renal allograft recipients.

Rat recipients of renal allografts and unilaterally nephrectomized control rats were studied to evaluate the response in blood pressure to prednisolone in diverse doses, and to determine the dosage required to achieve adequate immunosuppression without undue complication of hypertension. While a continuous infusion of 2 mg/kg/day or more of prednisolone proved effective in prolonging allograft survival time, this dosage increased the blood pressure of recipients as well as unilaterally nephrectomized control rats. In contrast to control rats, the recipients remained hypertensive after the cessation of prednisolone administration. This suggests that the high blood pressure observed during prednisolone administration was due to its hypertensive action. On the other hand, the high blood pressure remaining after cessation of the prednisolone administration is likely to be caused by an incomplete prevention of rejection. If recipients had received a transfusion of donor-strain blood prior to transplantation in combination with the infusion of 2 mg/kg/day or more of prednisolone, they became normotensive when the prednisolone infusion was ceased. By reducing the prednisolone dosage to 1 mg/kg/day in combination with donor-strain blood pretreatment, hypertension could also be eliminated during the first two weeks. In conclusion, effective immuno suppression can be achieved with prednisolone in rats, without inducing hypertension, provided prednisolone is administered at a low dosage in combination with adjuvant immunosuppression--i.e., donor-strain blood pretreatment.

Discussion of Reports on Renal Factors in Hypertension

The continuous secretion of renin by the chronically ischemic kidney was held to be unlikely in view of the experiments quoted by Dr. Kolff in which a rapid in situ transfer of an ischemic kidney to a normal dog did not raise the recipient's blood pressure. Measurable renin release was viewed rather as an acute intermittent response to a temporary reduction of renal circulation. Evidence from the classic experiment of Fasciolo, in which the transplanted chronic ischemic kidney caused hypertension in the recipient, was interpreted as showing the result of acute reduction in blood flow in the transplanted organ, rather than the chronic overproduction of renin. The depressor effect of antirenin injections in chronic renal hypertension might result from inhibition of the effect of renin on the hypothetical blood pressure regulating function of the normal kidney (Drs. Blaquier, Braun-Menéndez, Kolff). The magnitude of pressor response to injected renin and angiotonin was discussed by Drs. Langford, Wakerlin and Helmer. The pulmonary hypertension produced by renin and angiotonin and the lack of an elevation in pulmonary blood pressure in experimental renal hypertensin was discussed by Drs. Langford, Wakerlin, Sancetta, Braun-Menéndez and Stamler. Experiments disproving the importance of pulsatile flow as a stimulus to renin release were quoted by Dr. Kolff. An increase in the amount of the enzyme converting hypertensin I to its active form was considered as a possible mechanism for the production of hypertension by Drs. Leonard, Skeggs and Helmer. The relative importance of pressure per se and of renal insufficiency in the production of the necrotizing vascular lesion of malignant hypertension was discussed by Drs. Robert and Goldblatt.