PMC:7161517 / 13808-14761 JSONTXT

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{"project":"2_test","denotations":[{"id":"32305401-15833808-55252952","span":{"begin":353,"end":355},"obj":"15833808"},{"id":"32305401-15833808-55252953","span":{"begin":588,"end":590},"obj":"15833808"},{"id":"32305401-15833808-55252954","span":{"begin":949,"end":951},"obj":"15833808"}],"text":"Similar upregulation of ACE2 was observed in studies focused on the effects of ARB treatment. Spontaneously hypertensive rats treated with olmesartan demonstrated a 5-fold greater expression of ACE2 mRNA and increased Ang1-7 in their thoracic aortas, whereas those treated with atenolol and hydralazine exhibited no change in ACE2 expression or Ang1-7 (44). Comparison of vessel wall dimensions showed that olmesartan selectively reduced the thoracic aorta media-to-lumen ratio, whereas vascular hypertrophy was unchanged in spontaneously hypertensive rats given atenolol or hydralazine (44). There was no change in ACE2/Ang1-7 expression and/or activity in the carotid arteries of the treated animals. The possibility that the effects of olmesartan on vascular ACE2 gene and protein expression were the result of reduced arterial blood pressure was ruled out because of the comparative effect observed in mice treated with atenolol or hydralazine (44)."}