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Dietary calcium modulates renal BBM angiotensin II binding and Na(+)-H+ antiporter activity in SHR
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
Insights
Increasing dietary calcium in spontaneously hypertensive rats lowered blood pressure by reducing angiotensin II binding sites in kidney membranes. This suggests a novel renal mechanism for calcium
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Nutritional Science
Background:
- Dietary calcium intake significantly influences blood pressure regulation.
- The kidney is a critical organ in the development and management of hypertension.
- Understanding renal mechanisms is key to explaining calcium's blood pressure-lowering effects.
Purpose of the Study:
- To investigate the renal mechanisms underlying the blood pressure-lowering effects of increased dietary calcium.
- To examine the impact of dietary calcium on renin release and angiotensin II binding in the kidney.
Main Methods:
- Spontaneously hypertensive rats (SHR) were fed diets with varying calcium content (0.1% vs. 3.6%).
- Renal superficial cortical slice renin release was measured under basal, stimulated, and inhibited conditions.
- Apical brush-border membrane (BBM) vesicles were isolated to assess angiotensin II binding characteristics.
Main Results:
- Elevated dietary calcium did not alter basal, isoproterenol-stimulated, or angiotensin II-inhibited renin release from renal slices.
- In contrast, increased dietary calcium significantly reduced angiotensin II binding in renal BBM vesicles.
- This reduction in binding was attributed to a decrease in the number of binding sites (Bmax), not a change in affinity (Kd).
Conclusions:
- Dietary calcium's blood pressure-lowering effect in SHR may involve modulating renal angiotensin II binding.
- The primary mechanism appears to be a reduction in the number of angiotensin II binding sites in the kidney's BBM.
- This study highlights a potential renal pathway through which dietary calcium impacts hypertension.
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.h-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 less than 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].(ABSTRACT TRUNCATED AT 250 WORDS)