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Calcium antagonism and protection of tissues from calcium damage
1Institute of Pharmacology, Bayer AG, Wuppertal, Federal Republic of Germany.
Abstract:
Calcium antagonism of nifedipine, nitrendipine or nisoldipine prevented salt-induced hypertension, renovascular damage and mortality in Dahl salt-sensitive (S) rats. The calcium agonist BAY K 8644 accelerated the development of salt-induced hypertension in S rats. In some S rats on a low-salt diet BAY K 8644 induced renovascular damage without sustained hypertension. In stroke-prone spontaneously hypertensive rats (SHRSP) on a normal diet the natural appearance of stroke was correlated with an increased calcium content in brain and kidney tissue. Nimodipine prevented stroke and the increase in brain calcium content without affecting the high blood pressure. A similar protective effect without substantial influence on high blood pressure was achieved by bilateral parathyroidectomy. Hypertension-associated vascular damage does not necessarily depend on the systemic intravascular pressure. In malignant hypertension the deleterious calcium overload in tissues may be activated or inhibited independently of the regulation of arterial blood pressure.
Insights
Calcium channel blockers prevented hypertension and related damage in rats. However, calcium overload in tissues, not just high blood pressure, may drive vascular damage in conditions like malignant hypertension.
Area of Science:
- Cardiovascular Pharmacology
- Renal Physiology
- Hypertension Research
Background:
- Hypertension is often associated with increased calcium levels in tissues.
- The role of calcium in hypertension-related organ damage requires further elucidation.
Purpose of the Study:
- To investigate the effects of calcium antagonism and agonism on salt-induced hypertension and organ damage in Dahl salt-sensitive rats.
- To explore the relationship between tissue calcium content, stroke, and hypertension in stroke-prone spontaneously hypertensive rats.
Main Methods:
- Administration of calcium channel blockers (nifedipine, nitrendipine, nisoldipine) and a calcium agonist (BAY K 8644) in Dahl salt-sensitive rats.
- Monitoring of blood pressure, mortality, and renovascular damage.
- Measurement of calcium content in brain and kidney tissue of stroke-prone spontaneously hypertensive rats.
- Intervention with nimodipine and bilateral parathyroidectomy in stroke-prone spontaneously hypertensive rats.
Main Results:
- Calcium antagonism prevented salt-induced hypertension, renovascular damage, and mortality in Dahl rats.
- The calcium agonist BAY K 8644 accelerated hypertension and caused renovascular damage in Dahl rats.
- In stroke-prone spontaneously hypertensive rats, stroke correlated with increased brain and kidney calcium; nimodipine and parathyroidectomy prevented stroke without lowering blood pressure.
Conclusions:
- Hypertension-associated vascular damage may not solely depend on systemic blood pressure.
- Tissue calcium overload can be a critical factor in malignant hypertension and associated organ damage, potentially independent of blood pressure regulation.