Activation of the intestinal tissue renin-angiotensin system by transient sodium loading in salt-sensitive rats

Abstract

Background: The renal tissue renin-angiotensin system is known to be activated by salt loading in salt-sensitive rats; however, the response in other organs remains unclear. Method: Spontaneously hypertensive rats were subjected to normal tap water or transient high-salt-concentration water from 6 to 14 weeks of age and were thereafter given normal tap water. From 18 to 20 weeks of age, rats given water with a high salt concentration were treated with an angiotensin II type 1 receptor blocker, valsartan. Results: Sustained blood pressure elevation by transient salt loading coincided with a persistent decrease in the fecal sodium content and sustained excess of the circulating volume in spontaneously hypertensive rats. Administration of valsartan sustainably reduced the blood pressure and normalized the fecal sodium levels. Notably, transient salt loading persistently induced the intestinal tissue renin-angiotensin system and enhanced sodium transporter expression exclusively in the small intestine of salt-sensitive rats, suggesting the potential connection of intestinal sodium absorption to salt sensitivity. Conclusion: These results reveal the previously unappreciated contribution of the intestinal tissue renin-angiotensin system to sodium homeostasis and blood pressure regulation in the pathophysiology of salt-sensitive hypertension.

Antihypertensives and Antibiotics: Impact on Intestinal Dysfunction and Hypertension

“…69 Moreover the effects of this short-term treatment were sustained 8 weeks after cessation of treatment. 69 Thus reducing sodium absorption may be another pathway via which RAAS blockade lowers BP.…”

“…In SHRs, salt loading caused a reduction in fecal sodium excretion (indicative of increased absorption) and increased BP and activation of the local gut RAAS. 69 These effects of salt loading in SHRs were reversed by 2 weeks of AT1R blockade, alongside downregulation of the NHE3 in the small intestine and colon. 69 Moreover the effects of this short-term treatment were sustained 8 weeks after cessation of treatment.…”

“…69 These effects of salt loading in SHRs were reversed by 2 weeks of AT1R blockade, alongside downregulation of the NHE3 in the small intestine and colon. 69 Moreover the effects of this short-term treatment were sustained 8 weeks after cessation of treatment. 69 Thus reducing sodium absorption may be another pathway via which RAAS blockade lowers BP.…”

Determining ACE-2 Level and Some Relevant Biochemical Parameters and studying the effect of Gender in Iraqi Diabetic Patients with Glomeruli and Renal Tubules Fibrosis as Early Prediction Marker

“…For instance, in CKD, plasma aldosterone is frequently increased without an increase in plasma renin, which may be brought on by metabolic acidosis due to hypokalemia 43 . Additionally, local angiotensin II (ANG II) synthesis in the kidneys may cause CKD to activate the intrarenal renin-angiotensin system (RAS).Additionally, it has been noted that a high salt diet can activate the mineralocorticoid receptor without the help of aldosterone 44 . ANG II, aldosterone, and MR activate Na+ transport proteins in the kidney, including Na + , Cl − 45 .…”

“Greedy Organs Hypothesis” for sugar and salt in the pathophysiology of non-communicable diseases in relation to sodium-glucose co-transporters in the intestines and the kidney

“…We recently demonstrated that salt also increases the expression of SGLT1 in the intestines [ 31 ]. High salt intake for 8 weeks to rats increased the expression of SGLT1 along with Na + -H + -exchanger (NHE)3 through the up-regulation of intestinal renin angiotensin system (RAS).…”