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

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.

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

Artery Research ◽

10.1016/j.artres.2015.10.209 ◽

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

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Effects of a Long-Term Treatment With Aliskiren or Ramipril on Structural Alterations of Subcutaneous Small-Resistance Arteries of Diabetic Hypertensive Patients

Hypertension ◽

10.1161/hypertensionaha.114.03380 ◽

2014 ◽

Vol 64 (4) ◽

pp. 717-724 ◽

Cited By ~ 16

Author(s):

Carolina De Ciuceis ◽

Carmine Savoia ◽

Emanuele Arrabito ◽

Enzo Porteri ◽

Monica Mazza ◽

...

Keyword(s):

Term Treatment ◽

Resistance Arteries ◽

Hypertensive Patients ◽

Structural Alterations ◽

Long Term Treatment ◽

Small Resistance

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

Hypertension ◽

10.1161/hyp.66.suppl_1.p256 ◽

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.

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

Journal of Hypertension ◽

10.1097/hjh.0b013e32833c2177 ◽

2010 ◽

Vol 28 (9) ◽

pp. 1951-1958 ◽

Cited By ~ 13

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

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Lack of Prognostic Role of Endothelial Dysfunction in Subcutaneous Small Resistance Arteries of Hypertensive Patients

High Blood Pressure & Cardiovascular Prevention ◽

10.2165/00151642-200512030-00155 ◽

2005 ◽

Vol 12 (3) ◽

pp. 188

Author(s):

C. De Ciuceis ◽

E. Porteri ◽

D. Rizzoni ◽

G. E.M Boari ◽

F. Zani ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Resistance Arteries ◽

Prognostic Role ◽

Hypertensive Patients ◽

Small Resistance

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Abstract P287: Endothelial Dysfunction in Small Resistance Arteries of Patients with Severe Obesity: Role of Arginase

Hypertension ◽

10.1161/hyp.68.suppl_1.p287 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Agostino Virdis ◽

Emiliano Duranti ◽

Monica Nannipieri ◽

Marco Anselmino ◽

Andrea Grazi ◽

...

Keyword(s):

Endothelial Dysfunction ◽

Severe Obesity ◽

Subcutaneous Tissue ◽

Age Groups ◽

Inhibitory Effect ◽

Resistance Arteries ◽

Small Arteries ◽

Laparoscopic Surgical Procedure ◽

Small Resistance

Nitric oxide (NO) is produced by endothelial NO synthase (eNOS) using the aminoacid L-Arginine. Arginase (Arg) also uses L-Arginine as substrate, converting it in L-Ornitine and urea. An increased Arg activity causes a progressive L-Arginine depletion, which in turn determines a lower NO bioavailability. Studies in murine models of obesity identify Arg as a determinant of endothelial dysfunction. In this study, we evaluated whether Arg might play a role in determining the lower bioavailability of NO in small resistance arteries isolated from subcutaneous tissue of patients with severe obesity (Ob), split in age groups (younger than 30 aa, range 21-29, n=5; older than 30 aa, range 35-56, n=5) vs normoweight controls (Ctrl younger 30 years, range 20-29, n=5; older than 30 yrs, range 36-58, n=5). Each patient underwent a subcutaneous biopsy during a laparoscopic surgical procedure. Small arteries, isolated from periadvential fat, were evaluated on a pressurized micromyograph. Endothelium-dependent vasodilation (VD) was assessed by acetylcholine (Ach, 0,001-100μM). NO availability was assessed by repeating Ach with L-NAME (100μM). Ach was also infused in the presence of norNOHA (10μM, Arg inhibitor). In Ctrl, VD induced by Ach was inhibited by L-NAME and not modified by norNOHA. Ob younger exhibited a reduced VD induced by Ach vs Ctrl of the same age, a reduced inhibition by L-NAME, and a potentiating effect by norNOHA, which also normalized the inhibitory effect of L-NAME on Ach. In Ob older, VD induced by Ach was reduced vs Ob younger, resistant to L-NAME and not modified by norNOHA. In conclusions, in small arteries from younger Ob, the Arg inhibition improves endothelial function by increasing the NO availability, while in older Ob Arg does not seem to play any role in endothelial dysfunction.

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