Sex-Specific Modulation of Blood Pressure and the Renin-Angiotensin System by ACE (Angiotensin-Converting Enzyme) 2
Hong Ji, Aline M. A. de Souza, Bilkish Bajaj, Wei Zheng, Xie Wu, Robert Charles Speth, Kathryn Sandberg
Abstract
Hong Ji, Aline M. A. de Souza, Bilkish Bajaj, Wei Zheng, Xie Wu, Robert Charles Speth, Kathryn Sandberg
Abstract
We showed ACE (angiotensin-converting enzyme) 2 is higher in the kidney of male compared with female mice. To further investigate this sex difference, we examined the role of ACE2 in Ang-[1–8] (angiotensin [1–8])–induced hypertension and regulation of the renin-angiotensin system in the kidney of WT (wild type) and Ace2 KO (knockout) mice. Mean arterial pressure rose faster in WT male than WT female mice after Ang-[1–8] infusion. This sex difference was attenuated in ACE2 KO mice. Ang-[1–8] infusion reduced glomerular AT1R (angiotensin type 1 receptor) binding in WT female mice by 30%, and deletion of Ace2 abolished this effect. In contrast, Ang-[1–8] infusion increased glomerular AT1R binding in WT male mice by 1.2-fold, and this effect of Ang-[1–8] persisted in Ace2 KO male mice (1.3-fold). ACE2 also had an effect on renal protein expression of the neutral endopeptidase NEP (neprilysin), the enzyme that catabolizes Ang-[1–10] (angiotensin [1–10]), the precursor of Ang-[1–8]. Ang-[1–8] infusion downregulated NEP protein expression by 20% in WT male, whereas there was a slight increase in NEP expression in WT female mice. Deletion of Ace2 resulted in lowered NEP expression after Ang-[1-8] infusion in both sexes. These findings suggest sex-specific ACE2 regulation of the renin-angiotensin system contributes to female protection from Ang-[1–8]–induced hypertension. These findings have ramifications for the current coronavirus disease 2019 (COVID-19) pandemic, especially in hypertension since ACE2 is the SARS-CoV-2 receptor and hypertension is a major risk factor for poor outcomes.
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We showed ACE (angiotensin-converting enzyme) 2 is higher in the kidney of male compared with female mice. To further investigate this sex difference, we examined the role of ACE2 in Ang-[1–8] (angiotensin [1–8])–induced hypertension and regulation of the renin-angiotensin system in the kidney of WT (wild type) and Ace2 KO (knockout) mice. Mean arterial pressure rose faster in WT male than WT female mice after Ang-[1–8] infusion. This sex difference was attenuated in ACE2 KO mice. Ang-[1–8] infusion reduced glomerular AT1R (angiotensin type 1 receptor) binding in WT female mice by 30%, and deletion of Ace2 abolished this effect. In contrast, Ang-[1–8] infusion increased glomerular AT1R binding in WT male mice by 1.2-fold, and this effect of Ang-[1–8] persisted in Ace2 KO male mice (1.3-fold). ACE2 also had an effect on renal protein expression of the neutral endopeptidase NEP (neprilysin), the enzyme that catabolizes Ang-[1–10] (angiotensin [1–10]), the precursor of Ang-[1–8]. Ang-[1–8] infusion downregulated NEP protein expression by 20% in WT male, whereas there was a slight increase in NEP expression in WT female mice. Deletion of Ace2 resulted in lowered NEP expression after Ang-[1-8] infusion in both sexes. These findings suggest sex-specific ACE2 regulation of the renin-angiotensin system contributes to female protection from Ang-[1–8]–induced hypertension. These findings have ramifications for the current coronavirus disease 2019 (COVID-19) pandemic, especially in hypertension since ACE2 is the SARS-CoV-2 receptor and hypertension is a major risk factor for poor outcomes.
Key concepts: Renin–angiotensin system, Blood pressure, Internal medicine, Endocrinology, Angiotensin-converting enzyme, Angiotensin II, Enzyme, Medicine