Insulin and blood pressure responses to changes in salt intake

Cubeddu, LX; Hoffmann, I S; Jiménez, Elio; Roa, C.; Cubeddu, RJ; Palermo, Coromoto; Baldonedo, RM

doi:10.1038/sj.jhh.1000984

Cited by 6 publications

(5 citation statements)

References 24 publications

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“…However, it is not clear whether in vivo Ang II or cyclical stretch or both are involved in the augmented oxidative stress observed in the 2K1C mice. In a hypertension rat model of infused Ang II, was demonstrated that this peptide, but not blood pressure is responsible for ROS production (Cubeddu et al, 2000).…”

Section: K1c Hypertension Affects Bone Marrow Cellsmentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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Angiotensin II (Ang II), which plays a pivotal role in the pathophysiology of the two-kidney, one-clip (2K1C) Goldblatt hypertension, has been associated with augmented generation of reactive oxygen species (ROS) in some cells and tissues. In the present study, we evaluated the influence of 2K1C hypertension on oxidative stress, DNA fragmentation, and apoptosis of bone marrow (BM) cells. Two weeks after the renal artery clipping or Sham operation, flow cytometry analysis showed a higher production of superoxide anions (approximately sixfold) and hydrogen peroxide (approximately twofold) in 2K1C hypertensive than in Sham normotensive mice. 2K1C mice also showed an augmented DNA fragmentation (54%) and apoptotic cells (21%). Our data show that the 2K1C renovascular hypertension is characterized by an increased production of ROS, DNA damage, and apoptosis of BM, which is a fundamental source of the cells involved in tissue repair.

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Section: K1c Hypertension Affects Bone Marrow Cellsmentioning

confidence: 99%

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Campagnaro

Tonini

Doche

et al. 2013

DNA and Cell Biology

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“…The present study has been performed to explore the influence of SGK1 on renal function and systolic blood pressure during a high-fat and high-salt diet, both of which have been shown to favor an increase in blood pressure (13,20,21,27,34,41,44,53,59). Surprisingly, lack of SGK1 does not affect systolic blood pressure after a high-fat diet alone, but it completely abrogates the increase in systolic blood pressure after additional high-salt treatment.…”

mentioning

confidence: 99%

Resistance of mice lacking the serum- and glucocorticoid-inducible kinase SGK1 against salt-sensitive hypertension induced by a high-fat diet

Huang

Boini²,

Oßwald³

et al. 2006

American Journal of Physiology-Renal Physiology

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of mice lacking the serum-and glucocorticoid-inducible kinase SGK1 against salt-sensitive hypertension induced by a high-fat diet. Am J Physiol Renal Physiol 291: F1264 -F1273, 2006; doi:10.1152/ajprenal.00299.2005.-Mineralocorticoids enhance expression and insulin stimulates activity of the serum-and glucocorticoid-inducible kinase SGK1, which activates the renal epithelial Na ϩ channel (ENaC). Under a salt-deficient diet, SGK1 knockout mice (sgk1 Ϫ/Ϫ ) excrete significantly more NaCl than their wild-type littermates (sgk1 ϩ/ϩ ) and become hypotensive. The present experiments explored whether SGK1 participates in the hypertensive effects of a high-fat diet and high-salt intake. Renal SGK1 protein abundance of sgk1 ϩ/ϩ mice was significantly elevated after a high-fat diet. Under a control diet, fluid intake, blood pressure, urinary flow rate, and urinary Na ϩ , K ϩ , and Cl Ϫ excretion were similar in sgk1 Ϫ/Ϫ and sgk1 ϩ/ϩ mice. Under a standard diet, high salt (1% NaCl in the drinking water for 25 days) increased fluid intake, urinary flow rate, and urinary Na ϩ , K ϩ , and Cl Ϫ excretion similarly in sgk1and sgk1 ϩ/ϩ mice without significantly altering blood pressure. A high-fat diet alone (17 wk) did not significantly alter fluid intake, urinary flow rate, urinary Na ϩ , K ϩ , or Cl Ϫ excretion, or plasma aldosterone levels but increased plasma insulin, total cholesterol, triglyceride concentrations, and systolic blood pressure to the same extent in both genotypes. Additional salt intake (1% NaCl in the drinking water for 25 days) on top of a high-fat diet did not affect hyperinsulinemia or hyperlipidemia but increased fluid intake, urinary flow rate, and urinary NaCl excretion significantly more in sgk1

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“…Similarly, no association was found between fasting or post-load insulin and systolic or diastolic BP in a healthy Hispanic population under low and high salt intake conditions. 15 A major problem with most of these studies is the poor stratification of the study patients. 5,[11][12][13][14] The presence of confounding variables such as older age, obesity, visceral or abdominal fat accumulation, salt sensitivity, dyslipidaemia and others, complicates the interpretation of the results.…”

Section: Journal Of Human Hypertensionmentioning

confidence: 99%

Insulin resistance and upper-normal glucose levels in hypertension: a review

Cubeddu

Hoffmann

2002

J Hum Hypertens

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Reduced insulin-mediated glucose disposal, indicative of insulin resistance, has been demonstrated in lean male hypertensives both with the hyperinsulinaemic euglycaemic clamp and the insulin suppression test. In lean hypertensives, insulin resistance was not accompanied by increases in fasting plasma insulin and glucose levels; but with modest hyperglycaemia and hyperinsulinaemia after a glucose load. Population studies (no stratification) reveal that: (1) insulin sensitivities vary widely in normotensives and hypertensives, (2) there are hypertensives and normotensives with similar degrees of insulin resistance, (3) not all hypertensives are insulin resistant, and (4) insulin resistance does not contribute to the blood pressure level of the hypertensive population. In large cross-sectional studies, the clustering of obesity, dyslipidaemia and type 2 diabetes is largely responsible for the observed associations between insulin or insulin resistance and hypertension. Recent studies indicate a role of glucose in blood pressure control. Glucose has been shown to

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Insulin and blood pressure responses to changes in salt intake

Cited by 6 publications

References 24 publications

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Renovascular Hypertension Leads to DNA Damage and Apoptosis in Bone Marrow Cells

Resistance of mice lacking the serum- and glucocorticoid-inducible kinase SGK1 against salt-sensitive hypertension induced by a high-fat diet

Insulin resistance and upper-normal glucose levels in hypertension: a review

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