Dietary Potassium Downregulates Angiotensin-I Converting Enzyme, Renin, and Angiotensin Converting Enzyme 2

Abstract

Background: The importance of dietary potassium in health and disease has been underestimated compared with that placed on dietary sodium. Larger effort has been made on reduction of sodium intake and less on the adequate dietary potassium intake, although natural food contains much more potassium than sodium. The benefits of a potassium-rich diet are known, however, the mechanism by which it exerts its preventive action, remains to be elucidated. With the hypothesis that dietary potassium reduces renal vasoconstrictor components of the renin-angiotensin system in the long-term, we studied the effect of high potassium diet on angiotensin-I converting enzyme, renin, and angiotensin converting enzyme 2. Methods: Sprague Dawley male rats on a normal sodium diet received normal potassium (0.9%, NK) or high potassium diet (3%, HK) for 4 weeks. Urine was collected in metabolic cages for electrolytes and urinary volume measurement. Renal tissue was used to analyze angiotensin-I converting enzyme, renin, and angiotensin converting enzyme 2 expression. Protein abundance analysis was done by Western blot; gene expression by mRNA levels by RT-qPCR. Renal distribution of angiotensin-I converting enzyme and renin was done by immunohistochemistry and morphometric analysis in coded samples.

Effects of enriched-potassium diet on cardiorespiratory outcomes in experimental non-ischemic chronic heart failure

“…It is worth noting that the present study was not intended to provide a detailed description of the molecular signaling pathways by which enriched K + diets reduced sympathoexcitation in CHF but rather to highlight its potential to improve cardiovascular and ventilatory outcomes. However, previous studies showing that dietary K + downregulates renin and angiotensin-I converting enzyme and reduce AngII generation [ 22 , 23 ] allow us to speculate that one potential mechanism associated with the beneficial effects of K + supplementation in CHF may be linked to RAS regulation. Future studies should focus on uncovering the molecular footprints related to K + supplementation and cardiovascular regulation in the setting of CHF.…”

“…Rats were randomly assigned to Sham, CHF and CHF+K + groups. Sham and CHF received standard chow diet (Prolab® RMH3000 5P00/0.9% K + ) while CHF+K + received the same formula but supplemented with 3% K + (Prolab® RMH3000 5P00/2% K + and 1% KCl in the drinking water) for 6 weeks as previously described [ 22 , 23 ]. Combination of K + supplementation in both chow and tap water has been shown to increase tolerability to high-salt diets [ 35 ].…”

Quality changes when replacing NaCl with KCl in shrimp head paste

“…Penton et al (2015) reported that high potassium intake altered plasma K + levels and led to reduced stiffness of endothelial cells and vasodilation by increasing nitric oxide (NO), while K + reduced excessive water by increasing sodium excretion, reducing sympathetic nervous system activity and hyperpolarization of endothelial and vascular smooth muscle cells leading to vasodilation, an altered response of arterial baroreceptors and reduced renal renin. Vio et al (2020) detected decreased renal renin, angiotensin I converting enzyme (ACE) and angiotensin converting enzyme II in rats that received high potassium diet (3%) compared to rats that received normal potassium (0.9%). Increasing potassium in blood was detected by inwardly rectifying potassium channels 4.1 and 5.1 (Kir 4.1 and Kir 5.1) in the basolateral membrane, leading to inhibition of the chlorine channel.…”

“…Increasing potassium in blood was detected by inwardly rectifying potassium channels 4.1 and 5.1 (Kir 4.1 and Kir 5.1) in the basolateral membrane, leading to inhibition of the chlorine channel. Accumulation of intracellular chlorine then led to inhibition of apical sodium chloride cotransporter (NCC) and decreasing sodium reabsorption (Vio et al, 2020).…”

Influence of aging on T cell response and renin-angiotensin system imbalance during SARS-CoV-2 infection

“…Similarly, this animal model has shown in the lungs the lowest level of ACE2 when compared with that in the heart, brain, and kidneys [ 41 ]. Other conditions such as dietary elements such as high potassium intake decreased ACE2 gene expression [ 42 ]. Moreover, the host genetic components that define ACE2 variants also influence its expression levels, which may also impact on COVID-19 outcome [ 43 ].…”