Work

L-arginase induces vascular dysfunction in old spontaneously hypertensive rats.

Year: 2019

Type: article

Abstract: BACKGROUND: Aging is a major non-modifiable risk factor for hypertension. Changes in aging are similar to those seen in hypertension in the vasculature. Also, aging increases the vascular dysfunction that occurs in hypertension. L-arginase action reduces substrate (L-arginine) availability for the formation of nitric oxide (NO). This reduces the level of NO and leads to reduced vasodilation and ultimately, vascular dysfunction. This study examines the hypothesis that age-dependent vascular dysfunction in SHRs is mediated by arginase. METHODS: M). RESULTS: MAP increased during aging in the SHRs p<0.05 but not in the Wistar rats. Arginase impaired the endothelium-dependent relaxation responses of thoracic aortic and MRA arterial rings to Ach in the old Wistars and SHRs (Emax aorta: 29.42±2.19% vs 7.94±1.86%). Arginase also impaired endothelium-independent relaxation response to SNP in the old SHRs only (Emax aorta: 88.62±4.10% vs 31.45±10.61%). We also observed no differences in the serum arginase activity in the four groups of rats. On the contrary, arginase activity in the aortae of young Wistar rats was reduced compared to other groups. CONCLUSIONS: Arginase impairs both endothelium-dependent and -independent vasorelaxation responses, through the NO signaling pathway.

Source: Journal of African Association of Physiological Sciences

Authors: O Arishe, J McKenzie, F Priviero, A B Ebeigbe, R Clinton Webb

Institutions: Augusta University, University of Benin

Language: English

Topic: Nitric Oxide and Endothelin Effects

Subfield: Physiology (medical)

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: diamond

Funder: National Heart, Lung, and Blood Institute

Award: Damage-Associated Molecular Patterns in Hypertension