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High calcium diet, different antihypertensive agents, and cytosolic free Ca2+ in spontaneously hypertensive rats
Insights
High dietary calcium intake and quinapril reduce blood pressure (BP) and intracellular calcium ([Ca2+]i) in hypertensive rats. This suggests calcium normalization, not just BP reduction, is key to hypertension management.
Area of Science:
- Cardiovascular Physiology
- Hypertension Research
- Mineral Metabolism
Background:
- Increased dietary calcium intake is linked to lower blood pressure (BP) in spontaneously hypertensive rats (SHR).
- The precise mechanisms underlying calcium's antihypertensive effects remain unclear.
- Lymphocyte intracellular free calcium concentration ([Ca2+]i) may serve as a biomarker for systemic calcium regulation.
Purpose of the Study:
- To investigate the effects of a high-calcium diet and various antihypertensive agents on BP and lymphocyte [Ca2+]i in SHR.
- To determine if observed reductions in [Ca2+]i are a consequence of lowered BP or an independent mechanism.
Main Methods:
- Adult SHR and Wistar-Kyoto (WKY) rats were fed either standard (1.1% calcium) or high-calcium (2.5%) diets for 14 weeks.
- Antihypertensive treatments included trichlormethiazide, atenolol, and quinapril administered in drinking water.
- Systolic blood pressure (SBP) and lymphocyte [Ca2+]i (measured using quin-2) were assessed.
Main Results:
- Untreated SHR exhibited higher SBP and [Ca2+]i compared to WKY rats.
- High-calcium diet, trichlormethiazide, atenolol, and quinapril all reduced SBP in SHR.
- Only the high-calcium diet and quinapril significantly reduced lymphocyte [Ca2+]i concurrently with BP reduction.
Conclusions:
- The reduction in lymphocyte [Ca2+]i associated with high calcium intake is independent of the decrease in blood pressure.
- Normalization of [Ca2+]i may play a crucial role in the antihypertensive effects of oral calcium and ACE inhibition.
- These findings suggest potential therapeutic implications for managing genetic hypertension through calcium modulation and ACE inhibition.
Abstract:
Several studies have shown that increased dietary calcium decreases blood pressure (BP) in spontaneously hypertensive rats (SHR), but the underlying mechanisms are not fully understood. We compared the effects of a high calcium diet and different antihypertensive agents on BP and intracellular free Ca2+ concentration ([Ca2+]i) in lymphocytes of adult SHR. The calcium content of the normal chow was 1.1% and that of the high calcium chow was 2.5%. Antihypertensive drug treatments were performed by giving the animals trichlormethiazide (2 mg/kg/day), atenolol (25 mg/kg/day), and quinapril (10 mg/kg/day) in drinking water. Untreated SHR and normotensive Wistar-Kyoto (WKY) rats served as controls. After 14 weeks of study systolic BP (SBP) and [Ca2+]i in blood lymphocytes, measured with a fluorescent indicator quin-2, were higher in untreated SHR than in WKY rats. Trichlormethiazide, atenolol, quinapril, and the high calcium diet all decreased BP in SHR, but only quinapril and calcium-rich diet concurrently reduced [Ca2+]i. We conclude that the reduction in [Ca2+]i during high calcium intake does not result from decreased BP itself. If the changes in lymphocyte [Ca2+]i reflect Ca2+ metabolism in other tissues as well, especially in vascular smooth muscle, the normalization of [Ca2+]i may be involved in the BP-lowering mechanisms of oral calcium loading and angiotensin-converting enzyme (ACE) inhibition in genetic hypertension.