Exercise Training Prevents High Fructose-Induced Hypertension and Renal Damages in Male Dahl Salt-Sensitive Rats. 2023

Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito

High-fructose diet (HFr) causes metabolic syndrome, and HFr-induced hypertension and renal damage are exaggerated in Dahl salt-sensitive (DS) rats. Exercise training (Ex) has antihypertensive and renal protective effects in rats fed HFr; however, there has been little discussion about the DS rats, which exhibit metabolic disturbances. This study thus examined the effects of Ex on DS rats fed HFr. Male DS rats were divided into three groups. The control group was fed a control diet, and both the HFr group and the HFr-Ex group were fed an HFr (60% fructose). The HFr-Ex group also underwent treadmill running (20 m·min -1 , 60 min·d -1 , 5 d·wk -1 ). After 12 wk, renal function, histology, and renin-angiotensin system were examined. HFr increased blood pressure, urinary albumin, and creatinine clearance, and Ex inhibited these increases. HFr induced glomerular sclerosis, podocyte injury, afferent arteriole thickening, and renal interstitial fibrosis, and Ex ameliorated them. HFr reduced plasma renin activity, and Ex further reduced the activity. HFr also increased the expression of angiotensinogen, renin, angiotensin-converting enzyme (ACE), and angiotensin II type 1 receptor, and Ex restored the ACE expression to the control levels. HFr decreased the expression of ACE2, angiotensin II type 2 receptor, and Mas receptor, and Ex restored the ACE2 and Mas receptor expressions to the control levels and further decreased the angiotensin II type 2 receptor expression. HFr increased the ACE activity and decreased the ACE2 activity, and Ex restored these activities to the control levels. Ex prevents HFr-induced hypertension and renal damages in DS rats. The changes in renal renin-angiotensin system may be involved in the mechanism of the antihypertensive and renal protective effects of Ex.

UI MeSH Term Description Entries
D006973 Hypertension Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more. Blood Pressure, High,Blood Pressures, High,High Blood Pressure,High Blood Pressures
D007668 Kidney Body organ that filters blood for the secretion of URINE and that regulates ion concentrations. Kidneys
D008297 Male Males
D012083 Renin A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19. Angiotensin-Forming Enzyme,Angiotensinogenase,Big Renin,Cryorenin,Inactive Renin,Pre-Prorenin,Preprorenin,Prorenin,Angiotensin Forming Enzyme,Pre Prorenin,Renin, Big,Renin, Inactive
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D005632 Fructose A monosaccharide in sweet fruits and honey that is soluble in water, alcohol, or ether. It is used as a preservative and an intravenous infusion in parenteral feeding. Levulose,Apir Levulosa,Fleboplast Levulosa,Levulosa,Levulosa Baxter,Levulosa Braun,Levulosa Grifols,Levulosa Ibys,Levulosa Ife,Levulosa Mein,Levulosado Bieffe Medit,Levulosado Braun,Levulosado Vitulia,Plast Apyr Levulosa Mein,Levulosa, Apir,Levulosa, Fleboplast
D000085962 Angiotensin-Converting Enzyme 2 A transmembrane glycoprotein with an extracellular catalytic domain which functions as a carboxypeptidase. It cleaves a single C-terminal residue from a distinct range of substrates. The catalytic efficiency is 400-fold higher with ANGIOTENSIN II as a substrate than with ANGIOTENSIN I. Angiotensin-converting enzyme 2 is also is a functional receptor for the spike glycoprotein (SPIKE PROTEIN, CORONAVIRUS) of the CORONAVIRUSES SARS-COV, SARS-COV2, and HCOV-NL63. ACE-Related Carboxypeptidase,ACE2 Angiotensin-Converting Enzyme Protein 2,ACE2 Enzyme,ACE2 Protein,Angiotensin Converting Enzyme 2,Angiotensin-Converting Enzyme-Related Carboxypeptidase,ACE Related Carboxypeptidase,ACE2 Angiotensin Converting Enzyme Protein 2,Angiotensin Converting Enzyme Related Carboxypeptidase,Carboxypeptidase, ACE-Related,Carboxypeptidase, Angiotensin-Converting Enzyme-Related
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D000959 Antihypertensive Agents Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. Anti-Hypertensive,Anti-Hypertensive Agent,Anti-Hypertensive Drug,Antihypertensive,Antihypertensive Agent,Antihypertensive Drug,Anti-Hypertensive Agents,Anti-Hypertensive Drugs,Anti-Hypertensives,Antihypertensive Drugs,Antihypertensives,Agent, Anti-Hypertensive,Agent, Antihypertensive,Agents, Anti-Hypertensive,Agents, Antihypertensive,Anti Hypertensive,Anti Hypertensive Agent,Anti Hypertensive Agents,Anti Hypertensive Drug,Anti Hypertensive Drugs,Anti Hypertensives,Drug, Anti-Hypertensive,Drug, Antihypertensive,Drugs, Anti-Hypertensive,Drugs, Antihypertensive
D044139 Receptor, Angiotensin, Type 2 An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR. Angiotensin II Type 2 Receptor,Angiotensin Type 2 Receptor,Receptor, Angiotensin II Type 2,Angiotensin AT2 Receptor,AT2 Receptor, Angiotensin,Receptor, Angiotensin AT2

Related Publications

Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
June 1989, Hypertension (Dallas, Tex. : 1979),
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
February 2022, Journal of hypertension,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
June 1994, Journal of hypertension,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
January 2013, Clinical and experimental hypertension (New York, N.Y. : 1993),
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
November 1998, The American journal of physiology,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
May 2020, Disease models & mechanisms,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
June 1993, Hypertension (Dallas, Tex. : 1979),
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
December 1998, Physiology & behavior,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
April 2012, American journal of physiology. Regulatory, integrative and comparative physiology,
Lusi Xu, and Gaizun Hu, and Jiahe Qiu, and Takahiro Miura, and Seiko Yamakoshi, and Asako Namai-Takahashi, and Masahiro Kohzuki, and Osamu Ito
March 2020, Scientific reports,
Copied contents to your clipboard!