Dietary calcium modulates renal BBM angiotensin II binding and Na+-H+ antiporter activity in SHR

Moshe Levi, William L Henrich, Paul V. Wilson, Mark S. Griggs, Elizabeth A. McAllister

Research output: Contribution to journalArticle

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Abstract

Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 ±50 in 0.1% Ca vs. 784 ±61 ng angiotensin I (ANG I)·mg-1·h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 ± 52 in 0.1% Ca vs. 1,104 ±59 ng ANG I·mg-1·h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 ±50 in 0.1% Ca vs. 411 ±39 ng ANG I·mg-1·-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 ±14 in 0.1% Ca vs. 234 ±6 fmol ANG II/mg BBM protein in 3.6% Ca, P < 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 ± 1.4 in 0.1% Ca vs. 13.4 ±2.8 nM ANG II in 3.6% Ca, P = NS]. In addition, increasing dietary Ca caused a significant decrease in BBM vesicle Na+-H+ antiport, which was mediated by a decrease in the maximal activity (Vmax) (13.53 ±0.17 in 0.1% Ca vs. 11.35 ±0.21 nmol Na·5 s-1·mg BBM protein-1 in 3.6% Ca, P < 0.05) and no change in the affinity [Michaelis constant (Km), 8.65 ±0.41 in 0.1% Ca vs. 8.64 ±0.35 mM Na in 3.6% Ca, P = NS]. Our study therefore indicates that increasing dietary Ca causes decreases in renal BBM ANG II binding sites and Na+-H+ antiport activity without changing intrarenal renin secretion. These intrarenal effects of dietary Ca on ANG II binding and Na+-H+ antiport may be important mechanisms of the blood pressure-modulating effect of dietary Ca in the SHR.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume260
Issue number5 29-5
StatePublished - 1991
Externally publishedYes

Fingerprint

Dietary Calcium
Sodium-Hydrogen Antiporter
Inbred SHR Rats
Microvilli
Angiotensin II
Kidney
Membranes
Ion Transport
Blood Pressure
Renin
Membrane Proteins
Binding Sites
Angiotensin I
Isoproterenol
Diet
Hypertension

Keywords

  • Brush-border membrane
  • Hypertension
  • Renin release
  • Sodium ion-hydrogen ion antiport

ASJC Scopus subject areas

  • Physiology

Cite this

Dietary calcium modulates renal BBM angiotensin II binding and Na+-H+ antiporter activity in SHR. / Levi, Moshe; Henrich, William L; Wilson, Paul V.; Griggs, Mark S.; McAllister, Elizabeth A.

In: American Journal of Physiology - Renal Fluid and Electrolyte Physiology, Vol. 260, No. 5 29-5, 1991.

Research output: Contribution to journalArticle

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abstract = "Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6{\%} Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 ±50 in 0.1{\%} Ca vs. 784 ±61 ng angiotensin I (ANG I)·mg-1·h-1 in 3.6{\%} Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 ± 52 in 0.1{\%} Ca vs. 1,104 ±59 ng ANG I·mg-1·h-1 in 3.6{\%} Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 ±50 in 0.1{\%} Ca vs. 411 ±39 ng ANG I·mg-1·-1 in 3.6{\%} Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 ±14 in 0.1{\%} Ca vs. 234 ±6 fmol ANG II/mg BBM protein in 3.6{\%} Ca, P < 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 ± 1.4 in 0.1{\%} Ca vs. 13.4 ±2.8 nM ANG II in 3.6{\%} Ca, P = NS]. In addition, increasing dietary Ca caused a significant decrease in BBM vesicle Na+-H+ antiport, which was mediated by a decrease in the maximal activity (Vmax) (13.53 ±0.17 in 0.1{\%} Ca vs. 11.35 ±0.21 nmol Na·5 s-1·mg BBM protein-1 in 3.6{\%} Ca, P < 0.05) and no change in the affinity [Michaelis constant (Km), 8.65 ±0.41 in 0.1{\%} Ca vs. 8.64 ±0.35 mM Na in 3.6{\%} Ca, P = NS]. Our study therefore indicates that increasing dietary Ca causes decreases in renal BBM ANG II binding sites and Na+-H+ antiport activity without changing intrarenal renin secretion. These intrarenal effects of dietary Ca on ANG II binding and Na+-H+ antiport may be important mechanisms of the blood pressure-modulating effect of dietary Ca in the SHR.",
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AU - McAllister, Elizabeth A.

PY - 1991

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N2 - Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 ±50 in 0.1% Ca vs. 784 ±61 ng angiotensin I (ANG I)·mg-1·h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 ± 52 in 0.1% Ca vs. 1,104 ±59 ng ANG I·mg-1·h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 ±50 in 0.1% Ca vs. 411 ±39 ng ANG I·mg-1·-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 ±14 in 0.1% Ca vs. 234 ±6 fmol ANG II/mg BBM protein in 3.6% Ca, P < 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 ± 1.4 in 0.1% Ca vs. 13.4 ±2.8 nM ANG II in 3.6% Ca, P = NS]. In addition, increasing dietary Ca caused a significant decrease in BBM vesicle Na+-H+ antiport, which was mediated by a decrease in the maximal activity (Vmax) (13.53 ±0.17 in 0.1% Ca vs. 11.35 ±0.21 nmol Na·5 s-1·mg BBM protein-1 in 3.6% Ca, P < 0.05) and no change in the affinity [Michaelis constant (Km), 8.65 ±0.41 in 0.1% Ca vs. 8.64 ±0.35 mM Na in 3.6% Ca, P = NS]. Our study therefore indicates that increasing dietary Ca causes decreases in renal BBM ANG II binding sites and Na+-H+ antiport activity without changing intrarenal renin secretion. These intrarenal effects of dietary Ca on ANG II binding and Na+-H+ antiport may be important mechanisms of the blood pressure-modulating effect of dietary Ca in the SHR.

AB - Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 ±50 in 0.1% Ca vs. 784 ±61 ng angiotensin I (ANG I)·mg-1·h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 ± 52 in 0.1% Ca vs. 1,104 ±59 ng ANG I·mg-1·h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 ±50 in 0.1% Ca vs. 411 ±39 ng ANG I·mg-1·-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 ±14 in 0.1% Ca vs. 234 ±6 fmol ANG II/mg BBM protein in 3.6% Ca, P < 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 ± 1.4 in 0.1% Ca vs. 13.4 ±2.8 nM ANG II in 3.6% Ca, P = NS]. In addition, increasing dietary Ca caused a significant decrease in BBM vesicle Na+-H+ antiport, which was mediated by a decrease in the maximal activity (Vmax) (13.53 ±0.17 in 0.1% Ca vs. 11.35 ±0.21 nmol Na·5 s-1·mg BBM protein-1 in 3.6% Ca, P < 0.05) and no change in the affinity [Michaelis constant (Km), 8.65 ±0.41 in 0.1% Ca vs. 8.64 ±0.35 mM Na in 3.6% Ca, P = NS]. Our study therefore indicates that increasing dietary Ca causes decreases in renal BBM ANG II binding sites and Na+-H+ antiport activity without changing intrarenal renin secretion. These intrarenal effects of dietary Ca on ANG II binding and Na+-H+ antiport may be important mechanisms of the blood pressure-modulating effect of dietary Ca in the SHR.

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