Abstract P256: Structural Alterations of Subcutaneous Small Resistance Arteries in Resistant Hypertension

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Carolina De Ciuceis ◽  
Claudia Rossini ◽  
Maria Lorenza Muiesan ◽  
Massimo Salvetti ◽  
Enzo Porteri ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Resistant Hypertension ◽  
Subcutaneous Tissue ◽  
Blood Pressure Monitoring ◽  
Response To Treatment ◽  
Large Artery ◽  
Resistance Arteries ◽  
Hypertensive Patients ◽  
Structural Alterations ◽  
Small Resistance

Background: It is was suggested that, in resistant hypertension, the presence of particularly pronounced microvascular alterations may contribute to explain the relative lack of response to treatment Patients and Methods: We investigated a population of 94 treated essential hypertensive patients. Secondary forms of hypertension were excluded, and in all patients a 24-hour blood pressure monitoring was performed in order to exclude a white coat effect. In all patients, we evaluated small resistance arteries morphology by a wire micromyographic approach. Subcutaneous tissue was obtained by local biopsy or during election surgery and subcutaneous small resistance arteries were dissected and mounted on a myograph; the media to lumen ratio (M/L) was then measured. We subdived our patents according to the presence or not of resistant hypertension (clinic blood pressure values above 140/90 mm Hg despite administration of three antihypertensive agent including a diuretic and 24-hour blood pressure values >130/80 mm Hg). Sixteen patients had true resistant hypertension, and were compared with the remaining 78 patients with non-resistant hypertension. Results: are summarized in the Table, The two groups were also different in terms of mean age (57±12 vs. 67±7 years, p=0.016 and pulse pressure/stroke volume, a rough index of large artery distensibility: 0.63±0.31 vs. 0.90±0.33, p=0.02). Conclusion: Hypertensive patients with true resistant hypertension have greater microvascular structural alterations compared with non-resistant hypertensive patients. This could partly explain the resistance to treatment and the high cardiovascular risk observed in these patients.

P2.2 RESISTANT HYPERTENSION AND STRUCTURAL ALTERATIONS OF SUBCUTANEOUS SMALL RESISTANCE ARTERIES

2015 ◽  
Vol 12 (C) ◽  
pp. 6
Author(s):  
Claudia Agabiti Rosei ◽  
Carolina De Ciuceis ◽  
Claudia Rossini ◽  
Maria Lorenza Muiesan ◽  
Massimo Salvetti ◽  
...  
Keyword(s):  
Resistant Hypertension ◽  
Resistance Arteries ◽  
Structural Alterations ◽  
Small Resistance

P2.1 AGING AND STRUCTURAL ALTERATIONS OF SUBCUTANEOUS SMALL RESISTANCE ARTERIES IN HYPERTENSIVE PATIENTS

2015 ◽  
Vol 12 (C) ◽  
pp. 6
Author(s):  
Carolina De Ciuceis ◽  
Claudia Rossini ◽  
Claudia Agabiti Rosei ◽  
Enzo Porteri ◽  
Alice Gavazzi ◽  
...  
Keyword(s):  
Resistance Arteries ◽  
Hypertensive Patients ◽  
Structural Alterations ◽  
Small Resistance

Abstract P258: Essential Hypertension Induces Early Functional and Structural Vascular Aging in Small Resistance Arteries

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Agostino Virdis ◽  
Rosa Maria Bruno ◽  
Emiliano Duranti ◽  
Stefano Taddei
Keyword(s):  
Repeated Measures ◽  
Vascular Function ◽  
Age Groups ◽  
Progression Rate ◽  
Resistance Arteries ◽  
Hypertensive Patients ◽  
Repeated Measures Anova ◽  
Structural Alterations ◽  
Small Resistance ◽  
Subcutaneous Adipose

We evaluated cross-sectionally whether vascular remodeling is physiologically present in normal aging, and whether hypertension causes an acceleration of the aging process for vascular function and structure. 40 essential hypertensive patients (EH, age 44.9±13.2 years; BP, 157±8/99±3 mmHg) and 36 normotensive control individuals (Ctrl, age 44.7±12.7 years; BP: 128±7/80±4 mmHg) underwent laparoscopic surgery with subcutaneous adipose tissue biopsy. Small resistance arteries were studied by pressure micromiography. Endothelium-dependent and -independent vasodilation were evaluated by dose-response curve to Acetylcholine (ACh) and sodium nitroprusside (SNP). Maximum %inhibition by L-NAME on response to Ach was calculated. Structural alterations were assessed by media-lumen ratio (M/L). EH showed a reduced vasodilation to Ach (P<0.001), but not to SNP, compared to Ctrl. In both groups, %inhibition by L-NAME on response to ACh was inversely related to age (EH, r:-0.75; P<0.0001; Ctrl, r:-0.49; P<0.0001). NO availability was significantly reduced in EH as compared to Ctrl for each age group (<30 years: 22±6% vs 30±9%, P<0.05; 31-45 years: 17±3% vs 30±3%, P<0.0001; 46-60 years: 9±4% vs 21±6%, P60 years: 4±3% vs 13±3%, P<0.05). Age-hypertension interaction (Repeated measures ANOVA) was not significant (p= 0.25). EH showed an increased M/L (P<0.001) compared to Ctrl. In both groups, M/L was positively related to age. (EH, r:0.82; P<0.0001; Ctrl, r:0.50; P<0.0001). M/L was similar in EH and Ctrl for individuals <30 years, but greater in EH than Ctrl for the other age groups (31-45 years: 6.5±0.4% vs 5.6±0.4%, P<0.0001; 46-60 years: 7.4±0.5% vs 5.8±0.2%, P60 years: 7.9±0.3% vs 6.3±0.5%, P<0.0001). There was a significant age-hypertension interaction (Repeated measures ANOVA p= 0.0009). In small resistance arteries, aging is characterized by progressive reduction in NO availability and increased M/L. In hypertensive patients, NO availability is early reduced in comparison to Ctrl, but the progression rate with age appears to be similar. Conversely, structural alterations are influenced by hypertension only after 30 years of age, but the progression rate with age is steeper in the presence of hypertension.

Structural alterations in subcutaneous small resistance arteries predict changes in the renal function of hypertensive patients

2010 ◽  
Vol 28 (9) ◽  
pp. 1951-1958 ◽  
Author(s):  
Gianluca EM Boari ◽  
Damiano Rizzoni ◽  
Carolina De Ciuceis ◽  
Enzo Porteri ◽  
Daniele Avanzi ◽  
...  
Keyword(s):  
Renal Function ◽  
Resistance Arteries ◽  
Hypertensive Patients ◽  
Structural Alterations ◽  
Small Resistance

scholarly journals Increased phosphorylation of the renal Na+-Cl−cotransporter in male kidney transplant recipient patients with hypertension: a prospective cohort

2015 ◽  
Vol 309 (10) ◽  
pp. F836-F842 ◽  
Author(s):  
Lorena Rojas-Vega ◽  
Aldo R. Jiménez-Vega ◽  
Silvana Bazúa-Valenti ◽  
Isidora Arroyo-Garza ◽  
José Victor Jiménez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Transplant ◽  
Prospective Cohort ◽  
Blood Pressure Monitoring ◽  
Kidney Transplant Recipient ◽  
Blood Levels ◽  
Kidney Transplant Recipients ◽  
Hypertensive Patients ◽  
Urinary Exosomes ◽  
Trough Blood

Evidence in rodents suggests that tacrolimus-induced posttransplant hypertension is due to upregulation of the thiazide-sensitive Na+-Cl−cotransporter NCC. Here, we analyzed whether a similar mechanism is involved in posttransplant hypertension in humans. From January 2013 to June 2014, all adult kidney transplant recipients receiving a kidney allograft were enrolled in a prospective cohort study. All patients received tacrolimus as part of the immunosuppressive therapy. Six months after surgery, we assessed general clinical and laboratory variables, tacrolimus trough blood levels, and ambulatory 24-h blood pressure monitoring. Urinary exosomes were extracted to perform Western blot analysis using total and phospho-NCC antibodies. A total of 52 patients, including 17 women and 35 men, were followed. At 6 mo after transplantation, of the 35 men, 17 developed hypertension and 18 remained normotensive, while high blood pressure was observed in only 3 of 17 women. The hypertensive patients were significantly older than the normotensive group; however, there were no significant differences in body weight, history of acute rejection, renal function, and tacrolimus trough levels. In urinary exosomes, hypertensive patients showed higher NCC expression (1.7 ± 0.19) than normotensive (1 ± 0.13) ( P = 0.0096). Also, NCC phosphorylation levels were significantly higher in the hypertensive patients (1.57 ± 0.16 vs. 1 ± 0.07; P = 0.0049). Our data show that there is a positive correlation between NCC expression/phosphorylation in urinary exosomes and the development of hypertension in posttransplant male patients treated with tacrolimus. Our results are consistent with the hypothesis that NCC activation plays a major role in tacrolimus-induced hypertension.

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