Calcium antagonism and protection of tissues from calcium damage.
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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000378:metabolism / Q000633:toxicity*; D002121:Calcium Channel Blockers / Q000009:adverse effects / Q000627:therapeutic use*; D004353:Drug Evaluation, Preclinical; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000401:mortality / Q000517:prevention & control; D008297:Male; D010280:Parathyroid Glands / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR; D012965:Sodium Chloride / Q000008:administration & dosage
D002121:Calcium Channel Blockers; D012965:Sodium Chloride; D002118:Calcium