Renal arteriolar injury by salt intake contributes to salt memory for the development of hypertension

Hideyo Oguchi, Hiroyuki Sasamura, Kazunobu Shinoda, Shinya Morita, Hidaka Kono, Ken Nakagawa, Kimiko Ishiguro, Kaori Hayashi, Mari Nakamura, Tatsuhiko Azegami, Mototsugu Oya, Hiroshi Itoh

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The role of salt intake in the development of hypertension is prominent, but its mechanism has not been fully elucidated. Our aim was to examine the effect of transient salt intake during the prehypertensive period in hypertensive model animals. Dahl salt-sensitive rats and spontaneously hypertensive rats were fed from 6 to 14 weeks with lowsalt (0.12% NaCl), normal-salt (0.8% NaCl), high-salt (7% NaCl), or high-sodium/normal-chloride diet and returned to normal-salt diet for 3 months. Rats in the high-salt group saw elevations in blood pressure (BP) not only during the treatment period but also for the 3 months after returning to normal-salt diet. We named this phenomenon salt memory. Renal arteriolar injury was found in the high-salt group at the end of experiment. Dahl salt-sensitive rats were fed from 6 to 14 weeks with high-salt diet with angiotensin receptor blocker, vasodilator, calcium channel blocker, and calcium channel blocker+angiotensin receptor blocker and returned to normal-salt diet. Although BP was suppressed to control levels by vasodilator or calcium channel blocker, elevated renal angiotensin II and renal arteriolar injury were observed, and salt memory did not disappear because of sustained renal arteriolar injury. Calcium channel blocker+angiotensin receptor blocker suppressed renal arteriolar injury, resulting in the disappearance of salt memory. Cross-transplantation of kidneys from Dahl salt-sensitive rats on high salt to control rats caused increase of BP, whereas control kidneys caused reduction in BP of hypertensive rats, inducing the central role of the kidney. These results suggest that renal arteriolar injury through BP and renal angiotensin II elevation plays important roles in the development of salt memory for hypertension.

Original languageEnglish
Pages (from-to)784-791
Number of pages8
JournalHypertension
Volume64
Issue number4
DOIs
Publication statusPublished - 2014

Fingerprint

Salts
Hypertension
Kidney
Wounds and Injuries
Inbred Dahl Rats
Angiotensin Receptor Antagonists
Diet
Blood Pressure
Calcium Channel Blockers
Calcium Channels
Vasodilator Agents
Angiotensin II
Inbred SHR Rats
Sodium Chloride
Kidney Transplantation
Animal Models

Keywords

  • Hypertension
  • Kidney transplantation
  • Renin-angiotensin system
  • Vascular system injuries

ASJC Scopus subject areas

  • Internal Medicine
  • Medicine(all)

Cite this

Renal arteriolar injury by salt intake contributes to salt memory for the development of hypertension. / Oguchi, Hideyo; Sasamura, Hiroyuki; Shinoda, Kazunobu; Morita, Shinya; Kono, Hidaka; Nakagawa, Ken; Ishiguro, Kimiko; Hayashi, Kaori; Nakamura, Mari; Azegami, Tatsuhiko; Oya, Mototsugu; Itoh, Hiroshi.

In: Hypertension, Vol. 64, No. 4, 2014, p. 784-791.

Research output: Contribution to journalArticle

Oguchi, Hideyo ; Sasamura, Hiroyuki ; Shinoda, Kazunobu ; Morita, Shinya ; Kono, Hidaka ; Nakagawa, Ken ; Ishiguro, Kimiko ; Hayashi, Kaori ; Nakamura, Mari ; Azegami, Tatsuhiko ; Oya, Mototsugu ; Itoh, Hiroshi. / Renal arteriolar injury by salt intake contributes to salt memory for the development of hypertension. In: Hypertension. 2014 ; Vol. 64, No. 4. pp. 784-791.
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AU - Sasamura, Hiroyuki

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AU - Morita, Shinya

AU - Kono, Hidaka

AU - Nakagawa, Ken

AU - Ishiguro, Kimiko

AU - Hayashi, Kaori

AU - Nakamura, Mari

AU - Azegami, Tatsuhiko

AU - Oya, Mototsugu

AU - Itoh, Hiroshi

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N2 - The role of salt intake in the development of hypertension is prominent, but its mechanism has not been fully elucidated. Our aim was to examine the effect of transient salt intake during the prehypertensive period in hypertensive model animals. Dahl salt-sensitive rats and spontaneously hypertensive rats were fed from 6 to 14 weeks with lowsalt (0.12% NaCl), normal-salt (0.8% NaCl), high-salt (7% NaCl), or high-sodium/normal-chloride diet and returned to normal-salt diet for 3 months. Rats in the high-salt group saw elevations in blood pressure (BP) not only during the treatment period but also for the 3 months after returning to normal-salt diet. We named this phenomenon salt memory. Renal arteriolar injury was found in the high-salt group at the end of experiment. Dahl salt-sensitive rats were fed from 6 to 14 weeks with high-salt diet with angiotensin receptor blocker, vasodilator, calcium channel blocker, and calcium channel blocker+angiotensin receptor blocker and returned to normal-salt diet. Although BP was suppressed to control levels by vasodilator or calcium channel blocker, elevated renal angiotensin II and renal arteriolar injury were observed, and salt memory did not disappear because of sustained renal arteriolar injury. Calcium channel blocker+angiotensin receptor blocker suppressed renal arteriolar injury, resulting in the disappearance of salt memory. Cross-transplantation of kidneys from Dahl salt-sensitive rats on high salt to control rats caused increase of BP, whereas control kidneys caused reduction in BP of hypertensive rats, inducing the central role of the kidney. These results suggest that renal arteriolar injury through BP and renal angiotensin II elevation plays important roles in the development of salt memory for hypertension.

AB - The role of salt intake in the development of hypertension is prominent, but its mechanism has not been fully elucidated. Our aim was to examine the effect of transient salt intake during the prehypertensive period in hypertensive model animals. Dahl salt-sensitive rats and spontaneously hypertensive rats were fed from 6 to 14 weeks with lowsalt (0.12% NaCl), normal-salt (0.8% NaCl), high-salt (7% NaCl), or high-sodium/normal-chloride diet and returned to normal-salt diet for 3 months. Rats in the high-salt group saw elevations in blood pressure (BP) not only during the treatment period but also for the 3 months after returning to normal-salt diet. We named this phenomenon salt memory. Renal arteriolar injury was found in the high-salt group at the end of experiment. Dahl salt-sensitive rats were fed from 6 to 14 weeks with high-salt diet with angiotensin receptor blocker, vasodilator, calcium channel blocker, and calcium channel blocker+angiotensin receptor blocker and returned to normal-salt diet. Although BP was suppressed to control levels by vasodilator or calcium channel blocker, elevated renal angiotensin II and renal arteriolar injury were observed, and salt memory did not disappear because of sustained renal arteriolar injury. Calcium channel blocker+angiotensin receptor blocker suppressed renal arteriolar injury, resulting in the disappearance of salt memory. Cross-transplantation of kidneys from Dahl salt-sensitive rats on high salt to control rats caused increase of BP, whereas control kidneys caused reduction in BP of hypertensive rats, inducing the central role of the kidney. These results suggest that renal arteriolar injury through BP and renal angiotensin II elevation plays important roles in the development of salt memory for hypertension.

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KW - Kidney transplantation

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