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Irigoyen, M. C.

Publications and source records attributed to Irigoyen, M. C..

2 recordsLinked to original sources

Sex-related differences in vascular remodeling of sodium overloaded normotensive mice

Background and Aims: Primary hypertension affect about 20% of adults in developed societies and, associated with high salt intake, leads to vascular remodeling, an adaptive physiological response of blood vessels that driven by repair, inflammation, or cell growth, is but may contribute to vascular diseases over time. This study examined vascular remodeling in the aorta and cardiac arteries, focused on gender-specific responses to sodium overload. Methods and Results: Adult male and female C57Bl/6 mice were divided into six groups: control with filtered water (Cont M; Cont F), 1% NaCl for two weeks (Salt-2 M; Salt-2 F), and 1% NaCl for twelve weeks (Salt-12 M; Salt-12 F). Blood pressure (BP) and heart rate (HR) were measured using tail plethysmography, and metabolic cages recorded 24-hour water intake and urine output. Morphometric analysis of the aorta and cardiac arteries included assessments of elastic laminae and collagen fibers, using Weigert van Gieson and Picrosirius staining. No changes in BP and HR were observed. Sodium intake increased water consumption in both genders after two weeks, but only males showed increased urine output. Vascular responses differed: males exhibited delayed increases in aortic elastic lamellae, while females showed earlier changes. Elastic lamellae in cardiac arteries remained unchanged. Collagen deposition increased in aortic walls for both genders but decreased by 50% in male cardiac arteries. Males showed thick collagen fibers, while females had thin and thick fibers. Conclusion: High sodium intake caused arterial stiffness through distinct mechanisms in males and females, even in normotensive animals.

physiology↗

Early inflammatory response mediated by Angiotensin II in cardiac arteries of normotensive mice.

To verify if a low dose of angiotensin II (Ang II) can induce an inflammatory response in cardiac arteries, even though blood pressure remains at normal values. Were used C57Bl/6J male mice treated with a low dose of Ang II (30ng/kg IP) and AT1R blockers. Blood pressure was recorded after 10, 30, 60min, 2 and 6hours after Saline or Ang II injection. Time curve (30 and 60min, 2, 6, 12, 24, and 48hours after treatment) for expression of inflammatory markers was evaluated in cardiac arteries (TGF-{beta}, IL-1{beta}, IL-6, TNF- and ICAM-1) by immunohistochemistry and western blot. Serum TNF- and IL-6 were analyzed by ELISA. Although Ang II did not alter blood pressure, local TGF- and IL-6 presented an early increase in cardiac arteries. IL-1{beta} and ICAM-1 participated in a late response to Ang II (12 hours). Ang II group showed a systemic increase of IL-6 30 to 60 minutes after treatment. AT1 and AT2 receptor blockers (losartan, 20mg/kg, and PD123.319, 15mg/kg) were given alone or concomitant to Ang II. This combination showed that Ang II increases TGF-{beta} and IL-6 by acting on the AT1 receptor in a fast response. IL-1{beta} regulation by Ang II seems to be mediated by both AT1 and AT2 receptors. The results suggest that, independently of hemodynamic influences, Ang II, acting on AT1R, leads to the expression of inflammatory markers in cardiac vessels. AT2 receptor seems to be involved in the counterbalance of AT1R during modulation of IL-1{beta} production in cardiac arteries.

physiology↗